Monday, October 5, 2026

Wuyi Mountains, China: Sunday 10/4/26 open @WorldUnivAndSch #WUaSNewsAndQA @WUaSPress #WUaSWBM #HarvardAARD #VirtualCellInTime * * * * * Harvard Aging Research and Drug Development conference Th 10/1/26-Sat 10/3/26 - ARDD 2026 — Day One Recap ... Days One through Three Recaps

 

Sunday 10/4/26 open @WorldUnivAndSch #WUaSNewsAndQA @WUaSPress #WUaSWBM #HarvardAARD #VirtualCellInTime 

https://youtu.be/lf77X55TTIE 





Recording of (newly) SUNDAY 10/4/26 open @WorldUnivAndSch #WUaSNewsAndQA @WUaSPress #WUaSWBM
-https://youtu.be/lf77X55TTIE
-https://worlduniversityandschool.blogspot.com/2026/09/sacajawea-peak-wallowa-mountains-or-m.html
-https://scott-macleod.blogspot.com/2026/09/sacajawea-peak-wallowa-mountains-or.html
-https://www.youtube.com/@ScottMacLeodWorldUniversity/videos #HarvardAARD #VirtualCellInTime #AvatarAgentEHR #DigitalHealthTwins #MITOCWinRVE ?

https://x.com/WorldUnivAndSch/status/2106902274186621149

https://x.com/WUaSPress/status/2106902555859312964

https://x.com/sgkmacleod/status/2106902497269096568

https://x.com/Q_YogaMacFlower/status/2106902416985833931

https://x.com/HarbinBook/status/2106902641410535788

https://x.com/scottmacleod/status/2106904103871824286 








* * * * 


Dear Universitians, World University and School networks & friends, World Universitians, all,  


Friendly NtF (Nontheist Friends) Quaker & Yoga (as in 8 limbs of Yoga) greetings! How are you? 

Glad to be traveling from the SF Bay Area to the Harvard Aging Research and Drug Development (ARDD) conference in Boston, from Thursday, 10/1-10/3/26 - https://agingpharma.org/program2026 - and staying at the Friends' Meeting House at Cambridge. 

I'm planning to hold the next open World Univ & Sch Weekly Business Meeting WUaS News and Q & A on Sunday afternoon October 4, 2026 at 4pm Eastern Time (1pm Pacific Time) ... and potentially or possibly in conversation with the Harvard Quaker Chaplin John Bach there. 


Here are a possible Sun 10/4/26 WUaS Agenda and News, and the Zoom URL for this -


Topic: Sun 10/04/26 open best STEAM Creative Commons' licensed OpenCourseWare wiki World Univ & Sch WUaS News and Q&A, with Zoom URL
Time: Oct 4, 2026 04:00 PM Eastern Time (US and Canada)

Join Zoom Meeting
https://us04web.zoom.us/j/72834561360?pwd=paJIK8N8TPKSnBFUAAw9SC4hdZMjTn.1

Meeting chat link
https://us04web.zoom.us/launch/jc/72834561360

Meeting ID: 728 3456 1360
Passcode: 722MMJ




AND 

here is the WUaS Agenda for M September 28, 2026 - 


Topic: M 9/28/26 open best STEAM Creative Commons' licensed OpenCourseWare wiki World Univ & Sch WUaS News and Q&A, with Zoom URL
Time: Sep 28, 2026 10:00 AM Pacific Time (US and Canada)

Join Zoom Meeting
https://us04web.zoom.us/j/71228313741?pwd=xUnQd2lQ4K4dvIASJTgZqZUCWTYDmQ.1

Meeting chat link
https://us04web.zoom.us/launch/jc/71228313741

Meeting ID: 712 2831 3741
Passcode: V9GckN



World University & School is growing daily, and Weekly Business Meeting by Weekly Business Meeting - https://worlduniversityandschool.blogspot.com/search/label/Business%20Meeting AND https://scott-macleod.blogspot.com/search/label/Business%20Meeting - (and before these, with WUaS Monthly Business Meeting by Monthly Business Meeting, loosely conducted in the Manner of unprogrammed Friends NtFs Quakers) and blog post by blog post too ... And waiting, I think, for accreditation opportunities to further develop, and in WUaS seeking to Deploy with the Full US Federal Toolkit as well. 



And WUaS is waiting for money ... from Grants.gov initially or https://simpler.grants.gov/? ...  or some other grant somehow ? (MacArthur foundation, Nobel foundation, or?)  And how to grow a flourishing, engaged and engaging research community online? MIT and Harvard's "How to Grow Almost Anything" synthetic biology course online as a model - https://worlduniversityandschool.blogspot.com/search/label/HTGAA and https://scott-macleod.blogspot.com/search/label/HTGAA? 


And how best to grow an engaged and engaging WUaS wiki-teaching and wiki-learning community - with wiki-teachers and wiki-learners teaching and learning in any of these subjects - https://wiki.worlduniversityandschool.org/wiki/Subjects - or beginning new wiki subjects (first in English but then in all 200 countries' main languages, and then for speakers of all 7159 living languages to do this, in all these languages, and again with wiki-subjects one can create ... for example about what one loves to do, teach or learn about) - and both online with a 2D-3D computer screen & in our homes in a developing realistic virtual earth in VR goggles, and digital glasses and similar hardware AND especially in WUaS Multimedia Rooms (in our homes and which we create or eventually are able to purchase), a WUaS Hospital Multimedia Room, & at the WUaS Academic Medical Center, (eg out of 670 Ridgecrest Rd, Canyon 94516 potentially too)?  And see: "Google Earth in an Immersive Meeting Room" 
https://youtu.be/KjUHngd5fDk - 


AND for a #RealisticVirtualHarbin Hot Springs as ethnographic and STEM field sites, and classrooms -  


... enter into this #RealisticVirtualEarth here at the Harbin Hot Springs' gate house - 
{and see Peter Norvig's INCREDIBLE #ToolifyAIWUaS article Revolutionizing Education with Machine Learning and AI - https://www.toolify.ai/ai-news/revolutionizing-education-with-machine-learning-and-ai-2574306 - which mentions a RVE for the first time other than WUaS that I know of} 

and with a #RealisticVirtualEarth a #RealisticVirtualEarthFor, a #RVEforSTEM, a #RVEforIndustrialProduction, a #RVEforAgenticAI, a #RVEforEverything ... and see 

Experience the real power of Industrial AI with Siemens

https://youtu.be/O3Sj0Ab9q3s



All the best, abolition-ally - and with ~50 million people enslaved or caught in human  trafficking  - https://www.modernslaverycommission.org/ &  https://share.google/aimode/Wi9Zp8zsytD4mU08C (a best STEAM Creative Commons' licensed OpenCourseWare wiki @WorldUnivAndSch #WUaSabolition movement continues to grow to protect people ... https://worlduniversityandschool.blogspot.com/2025/10/eagle-aquila-world-university-and.html 
... and in WUaS seeking to code for all 7.9 billion people on the planet from here -https://wiki.worlduniversityandschool.org/wiki/You_at_World_University - to facilitate wiki free universal education, and potentially to end poverty worldwide), Yogically (8 limbs of Yoga & see tree of 8 limbs of yoga picture - https://x.com/Q_YogaMacFlower/status/2044848212360753480), Friendly NtF NtQ Quaker (& re Quaker SPICES - https://www.friendsjournal.org/s-p-i-c-e-s-quaker-testimonies/) & Unitarian Universalist church (re 7 or 8 UU Principles' https://www.uua.org/beliefs/what-we-believe/principles) greetings, kind regards, 

Scott
Scott GK MacLeod
Founder, President, CEO & Professor, Yoga teacher, Presiding and Recording Clerk (loosely in the manner of unprogrammed NtF Friends / Quakers), 

Recording will be posted here -




TwitterX and LinkedIN - 

Announcement - 

Announcement - 

#HarvardAARD #VirtualCellInTime to #AvatarAgentEHR as #DigitalTwins for 7.9B people in #RealisticVirtualEarthForGenetics ...at #WUaSunivs







* * * * 

World University and School / WUaS 


1st of 2 WUaS wings - 

World Univ & Sch wing - 
a 501 c 3 / similar non-profit - 
building on CC licensed best STEAM OpenCourseWare and which is wiki:  


World University and School 
http://worlduniversityandschool.org/ (and see both exempt legal entities' tax IDs at bottom here)




Agenda item 0 
As video minutes - 


Monday, September 21, 2026
Anamudi mountain, India: M 9/21/26 recording of @WorldUnivAndSch @WUaSPress #WUaSNewsAndQA #WUaSWBM #MITAS #MITAlumniStartups * (was - M 9/21/26 & M 9/28/26 open best STEAM Creative Commons' licensed OpenCourseWare wiki World Univ & Sch WUaS News and Q&A, with Zoom URL)
 


M 9/21/26 recording of @WorldUnivAndSch @WUaSPress #WUaSNewsAndQA #WUaSWBM #MITAS #MITAlumniStartups

https://youtu.be/cJkMi9pPOqk

-https://worlduniversityandschool.blogspot.com/2026/09/anamudi-mountain-india-m-92126-m-92826.html

-https://scott-macleod.blogspot.com/2026/09/anamudi-mountain-india.html

w Tue 9/14 #WUaSAgenda

-https://worlduniversityandschool.blogspot.com/2026/09/tushar-mountains-ut-m-91426-m-92126.html

-https://scott-macleod.blogspot.com/2026/09/tushar-mountains-ut.html

-https://www.youtube.com/@ScottMacLeodWorldUniversity/videos

#MITAS #MITAlumniStartups




*

M 9/21/26 recording of @WorldUnivAndSch @WUaSPress #WUaSNewsAndQA #WUaSWBM
-https://youtu.be/cJkMi9pPOqk
-https://worlduniversityandschool.blogspot.com/2026/09/anamudi-mountain-india-m-92126-m-92826.html
-https://scott-macleod.blogspot.com/2026/09/anamudi-mountain-india.html
w M 9/14 #WUaSAgenda
-https://worlduniversityandschool.blogspot.com/2026/09/tushar-mountains-ut-m-91426-m-92126.html
-https://scott-macleod.blogspot.com/2026/09/tushar-mountains-ut.html
-https://www.youtube.com/@ScottMacLeodWorldUniversity/videos

#MITAS #MITAlumniStartups ~


https://x.com/WorldUnivAndSch/status/2102121398168871236

https://x.com/Q_YogaMacFlower/status/2102122158210371695

https://x.com/WUaSPress/status/2102122759405089155

https://x.com/HarbinBook/status/2102122941832147359

https://x.com/sgkmacleod/status/2102123511775121665

https://x.com/scottmacleod/status/2102123999056785552

https://x.com/TheOpenBand/status/2102124083664363665

https://lnkd.in/p/dpXVsrrk = https://lnkd.in/p/dpXVsrrk

https://www.linkedin.com/posts/world-university-and-school_the-open-band-berkeley-theopenband-on-activity-7507890560322408449-Y_bJ ~


https://scott-macleod.blogspot.com/2026/09/anamudi-mountain-india.html




Agenda item 1 

Harvard ARDD Aging Research and Drug Development conference 10/1/26-10/3/26 in the TreeHouse in Allston, MA




Dear George, All, 

Greetings. Looking forward to meeting you in the Harvard TreeHouse. 

In thinking through some of my and World University and School's goals for the

Harvard ARDD 2026 
Aging Research and Drug Development conference 10/1/26-10/3/26 in Boston 

& re also 



these include 

1
Develop 3 WUaS aging reversal OSK pharmaceutical gene drug therapies initially with research, and then produce and manufacture them & with a realistic virtual earth for OSK, a digital-physical #RVEforGenetics on the digital or in-silico side - and in collaboration with possibly 3 different companies too (initially) ...that would all successfully become FDA approved ...

and then upload them to our body minds via the eRapid Fouling Resistant sensor or similar - 

#eRapidFoulingResistantSensor-https://wyss.harvard.edu/technology/erapid-multiplexed-electrochemical-sensors-for-fast-accurate-portable-diagnostics/ WITH #AgingReversal & #ExtremeLongevity #AvatarAgentElectronicHealthRecords?



(Interoperate with the Flywire Connectome Project re Drosophila fly brain, and newly develop this for aging reversal and longevity and for humans, and with 'citizen science' .... and in a #RVEforFlywireConnectome ?)


AND -

At #HarvardAgingResearch & #HarvardDrugDiscovery conf 10/1-10/3/26
https://agingpharma.org/program2026#virtual-cell-in-time & re  #VirtualAgingCell from #InsilicoMedicine https://youtu.be/vufvnB1R1xM #PetrinaKamya & #FedorGalkin Interoperate e.g. the years 2007, '12 & '24 #GStreetView w #GTimeSlider in https://goo.gl/maps/7gSsSTweRCBo9gf87 @ #GCellViewLevel @ #HarbinGateHouse WITH #AgingReversal & #ExtremeLongevity #AvatarAgentEHR from #GPegman?


AND





1 a
to reverse muscle wasting with an OSK drug - system wide for the whole body 

eg for muscle wasting aging reversal (eg for my 91 year old mother)


1 b
to help people become ~25 years old in a 150 year old (or a 1500 year old) bodymind  ... and with a realistic virtual earth too, so digitally create this pharmaceutical in something like a FORKED Google Street View with time slider AND adding the G cell and G molecule view etc levels and even possibly interoperating with Radical Numerics' General Biological Intelligence AI ... and with Insilico Medicine's 'virtual cell in time' potentially and Pharma AI - https://pharma.ai/ ... 


1 c
to reverse my right ear, what I'm calling "eustachian tube dysfunction" - possibly targeting the cells involved with an OSK gene drug therapy ... including for pressure and nerves in the area ..  and such that I could play the Scottish Highland Bagpipes' again, and put my head underwater etc and wouldn't have to sleep only on my right side (since pain occurs if I sleep on my left side)





2
Create a

realistic virtual earth & Harbin for aging reversal with Harbin gate house's 3 dates, & 3 years too to time slide cells And molecules back & with pegman as a avatar agent ehr by FORKING from Google Street View and adding the G Cell G Molecule, and even the G Qubit levels 


2 a
and even with the Google UCSB Quantum Computer and re - 


Super: #QuantumEchoes including running simulations FWD & in reverse #ReversingTheArrowOfTime

Reversing The Arrow Of Time 



2 b i
Could the ink drop become our "avatar agent electronic health records" as digital twins?

2 b ii 
or a digital cell interoperating with Insilico Medicine's virtual cell in time? 




3
Prove aging reversal - at Harvard ARDD 2026 itself 

per Anthonio Regalado's Tweet (scibrazil@gmail.com.- above) a few weeks ago 


Antonio Regalado
@antonioregalado

Age reversal remains unproven. Yet that is the goal of the healthspan XPRIZE pretty much. The purse is $81 million to the team able "restore" the cognitive & physical function of a person by 20 years, after 1 year of treatment. Finalists to be announced this summer
4:48 AM · Jun 9, 2026

https://x.com/antonioregalado/status/2064313678250332350




4
Create 

Courseware for aging reversal and extreme longevity and related research 

1-3 aging reversal genetics and or research courses for WUaS, with parallels to MIT OCW courses and to add here too -



5

Yoga ...

Develop a realistic virtual earth for Yoga (as in 8 limbs of Yoga) and Yoga asana perhaps interoperating with our avatar agent electronic health records or digital twins and for research too 

since 
Scientists discover why exercise reverses muscle aging | ScienceDaily



Incredible: A response to how #AgingReversal of #MuscleWasting works with movement at molecular level from #DukeUniversityNUS :
Scientists discover #WhyExerciseReversesMuscleAging | #ScienceDaily 

Researchers have uncovered a molecular “switch” that helps explain why exercise keeps aging muscles healthy. By reducing levels of a gene called DEAF1, physical activity allows older muscles to clear out damage, repair themselves, and maintain strength.

How to develop with #YogaAsana for 80 & 90 year olds esp in #RealisticVirtualEarthForMolecules etc and so as to live to 150 years of age and even 1500 years of age and well beyond?


Retweeting - 

#WUaSpharma 1st 2 #OSKGeneDrugTherapies w #EpigeneticReprogramming? 1) #AgingReversal of #MuscleWasting & #BoneDensityLoss before eg 70s, 2) #AgingReversalGenetics of #earENT #EustachianTubeDysfunction / sim w #OSKdrugs in #RealisticVirtualEarthForGenetics w #AvatarAgentEHR How?



Scientists discover why exercise reverses muscle aging | ScienceDaily 


Researchers have uncovered a molecular “switch” that helps explain why exercise keeps aging muscles healthy. By reducing levels of a gene called DEAF1, physical activity allows older muscles to clear out damage, repair themselves, and maintain strength.


5 A


As #aKindOfYoga, how @demishassabis to join or align (#YogaWUaS) #eRapidSensor https://wyss.harvard.edu/technology/erapid-multiplexed-electrochemical-sensors-for-fast-accurate-portable-diagnostics/ w #IF1ProteinControlsAgingRate = gene https://x.com/geochurch/status/1993414908600299747 - to our #AvatarAgentElectronicHealthRecords re Pegman in #GStreetView #GCellView w #GTimeSliders to #ReverseAging?

https://x.com/Q_YogaMacFlower/status/1998169594750754829?s=20

https://x.com/WorldUnivAndSch/status/1998167467076849702

https://x.com/HarbinBook/status/1998169340332671133?s=20

https://x.com/WUaSPress/status/1998169186212962672?s=20

https://x.com/scottmacleod/status/1998168989575635272?s=20

https://x.com/sgkmacleod/status/1998169416492830929?s=20

https://x.com/TheOpenBand/status/1998169517445529801?s=20



Retweeting -

Jay Jin
@JayJin_JJ
·
Dec 6
Replying to @Q_YogaMacFlower and @demishassabis

Oh wow, molecular health visualization in Street View?. 🤯 That's absolutely wild - imagine zooming from your neighborhood straight into your DNA. This AI + biotech combo is exactly where breakthroughs happen. #HealthTech

https://x.com/JayJin_JJ/status/1997353871052509632?s=20




Expanded - 
Further as #aKindOfYoga, how @demishassabis to join or align (#YogaWUaS) #eRapidSensor https://wyss.harvard.edu/technology/erapid-multiplexed-electrochemical-sensors-for-fast-accurate-portable-diagnostics/ #IF1ProteinControlsAgingRate = gene https://x.com/geochurch/status/1993414908600299747 - to a #RealisticVirtualEarthForMolecules https://blog.google/technology/ai/google-deepmind-isomorphic-alphafold-3-ai-model/ to our #AvatarAgentElectronicHealthRecords re Pegman @ #GMoleculeLevel in #GStreetView w #GTimeSliders to #ReverseAging for #ExtremeLongevity?




Bring in Friends NtFs Quaker geneticists affiliated with the Friends Meeting at Cambridge, all over the world, and in Great Britain as well.


https://scott-macleod.blogspot.com/2026/09/deinandra-increscens.html





1 A

How best could a MIT Prof like Dr @GeoChurch develop a 1st #MITOCW #AgingReversalGenetics' course IN A #RealisticVirtualEarth ?


https://scott-macleod.blogspot.com/2026/09/sunda-pangolin-manis-javanica.html







Agenda item 2 

Thursday, September 24, 2026
Deinandra increscens: 

[Air-L] Open Position at UCSB Dept. of Communication * Thanks, Amy (Gonzales, Assistant Professor at UCSB), I may add this to the upcoming free-to-students' startup World University and School, building on CC-4 MIT OCW in 7 languages, and wiki, WUaS Weekly Business Meeting Agenda and News (loosely conducted in the manner of unprogrammed NtF Friends / Quakers) ... and as an UCSB alumnus, in Sociocultural Anthropology with a Master's degree focus on the Internet and virtual UNESCO World Heritage Sites, having taken Communication classes too, and worked as a TA in both departments * Working on writing "Society, Information Technology and the Global University" in the new Academic Press at WUaS (planned in all 7159 known living languages with machine and human translation) but am postponing publication of it until at least 2027. Friendly regards, Scott * * *


 

The UCSB Department of Communication is recruiting for a tenure-track/tenured open rank faculty position. We seek a scholar who conducts innovative, theoretically grounded, and empirically rigorous research using quantitative, qualitative, or mixed-method approaches that addresses the social consequences of AI from an organizational communication perspective. All courses are taught in-person on campus. A reasonable estimated full-time rate for this position is $95,000-$435,000 annually. The University of California is an Equal Opportunity Employer. All qualified applicants will receive consideration for employment without regard to race, color, religion, sex, sexual orientation, gender identity, national origin, disability, age, protected veteran status, or other protected status under state or federal law.

Link to Job Advertisement: https://recruit.ap.ucsb.edu/JPF03137


--
Amy Gonzales, Ph.D. (she/her)
Associate Professor, Department of Communication
Interim Co-Director, Chicano Studies Institute
UC Santa Barbara 

_______________________________________________
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Join the Association of Internet Researchers:
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Thanks, Amy (Gonzales, Assistant Professor at UCSB),
https://www.comm.ucsb.edu/people/amy-gonzales
https://www.linkedin.com/in/amylgonzales

I may add this to the upcoming free-to-students' startup World University and School, building on CC-4 MIT OCW in 7 languages, and wiki, WUaS Weekly Business Meeting Agenda and News (loosely conducted in the manner of unprogrammed NtF Friends / Quakers) ... and as an UCSB alumnus, in Sociocultural Anthropology with a Master's degree focus on the Internet and virtual UNESCO World Heritage Sites, having taken Communication classes too, and worked as a TA in both departments (I think there's a UCSB video of my teaching ... part of an UCSB program for learning to teach). (I was also active in the little Quaker Meeting in Santa Barbara. Do you know UCSB's Stephen Pope for example - also a Cornell alumnI think?) Juan-Vicente Palerm was my main professor at the end of my time at UCSB, before heading to Edinburgh, Scotland potentially to do a PhD ... with my MSc dissertation there about virtual St. Kilda as a nascent place. 

Thanks for this -

Profs at the Pub - Amy Gonzales

https://youtu.be/YNGNRMeytrc

Working on writing "Society, Information Technology and the Global University" in the new Academic Press at WUaS (planned in all 7159 known living languages with machine and human translation) but am postponing publication of it until at least 2027.  

Friendly regards,
Scott

https://scott-macleod.blogspot.com/search/label/society%20and%20information%20technology (in daily blog)


PS
Just TweetedX this, with many implications for reversing the digital divide -

Excited about #CFOs #QuakerCFOs for the #nonprofit #501c3 @WorldUnivAndSch wing - https://app.candid.org/profile/9121509/world-university-and-school-27-3105368 & https://worlduniversityandschool.org/ emerging (as #ForProfitinCA general stock company wing @WUaSPress http://worlduniversityandschool.org/AcademicPress.html waits) re coding for all 7.9B people https://wiki.worlduniversityandschool.org/wiki/You_at_World_University ~

https://x.com/Q_YogaMacFlower/status/2102964248964219382

https://x.com/WorldUnivAndSch/status/2102963894805463498

https://x.com/scottmacleod/status/2102964171700924788

https://x.com/sgkmacleod/status/2102964576723812735

https://x.com/HarbinBook/status/2102964478635876360

https://x.com/WUaSPress/status/2102964347551260731

https://x.com/TheOpenBand/status/1683154436514893825



https://scott-macleod.blogspot.com/2026/09/deinandra-increscens.html






Agenda item 3 

The Moonshot Podcast regarding the Moonshot Factory - Internet access for the remaining 2.6 billion people who don't have it yet! How could @WorldUnivAndSch facilitate #FreeUniversalEducation for all 7.9B in 7K langs & #EndPoverty w #Pi too? * * * 




Zoom conference call time newly ran out after the above - 

....





* * * * * ~

Harvard Aging Research and Drug Development conference Th 10/1/26-Sat 10/3/26 -

ARDD 2026 — Day One Recap



Dear Scott Gordon Kenneth MacLeod,

ARDD 2026 — Day One Recap

Aging Research and Drug Discovery Meeting · Thursday, October 1, 2026 · David Rubenstein Treehouse, Harvard University, Cambridge, MA

 

Opening

09:00–09:35 · Canopy Hall

George Daley — Dean, Harvard Medical School

“Opening remarks”

Key takeaway: Aging research has immense potential, but the field must resist hype, uphold rigor and communicate responsibly.

•     Goal should be extending healthspan, not lifespan alone, as age-related disease burden rises globally.

•     Optimistic claims in longevity often exceed what current science can support.

•     Epigenetic clocks are exciting, but their causal link to aging is unclear; their clinical and ethical use is uncharted.

•     Premature commercialization of cellular reprogramming risks repeating the unproven stem cell clinic era.

•     Warned of “therapeutic misconception”; cited a recent death after an IV infusion of NAD marketed for anti-aging.

•     Scientists should avoid financial conflicts of interest and communicate in measured, fact-based terms.

Jamie Justice — Executive Director, XPRIZE Healthspan

“Welcome & XPRIZE Healthspan overview”

Key takeaway: The $101M, seven-year XPRIZE Healthspan creates a standardized, transparent framework for early-stage healthy-aging trials.

•     Teams must restore muscle, cognitive and immune function in older adults within a one-year trial; function is used as the measure of clinical benefit.

•     Finalists run one-year trials on common protocols with centralized resources, enabling head-to-head comparison and biomarker development.

•     96% of semifinalist teams are now in early-stage clinical testing, up from ~65% the previous year.

•     “Plurality of effect”: >70% of awarded teams showed effects across multiple functional systems.

•     Top 20 finalists announced; 10 awarded a share of $10M to run one-year trials.

•     Approaches span lifestyle, supplements, biologics, repurposed and novel drugs, and AI platforms; strong representation from North America and Asia.

Chair introductions by Evelyne Bischof, Alex Zhavoronkov, Vadim Gladyshev, Morten Scheibye-Knudsen and Jesse Poganik, followed by the ribbon-cutting ceremony.

Policy, Regulation & Trials for Aging

09:35–10:50 · Canopy Hall

ADM Brian Christine — Assistant Secretary for Health, U.S. Department of Health and Human Services

“Policy & regulatory address”

Key takeaway: Health policy should shift from reactively treating individual diseases to proactively preserving health and extending healthspan.

•     The U.S. “health paradox”: great wealth and capability, but life expectancy lags peer nations amid rising obesity and diabetes.

•     Targeting the biology of aging could delay multiple age-related diseases at once.

•     Framed within the HHS “Make America Healthy Again” agenda: breaking down silos between NIH, FDA, CDC and other agencies.

•     Government role: fund rigorous trials, develop biomarkers that predict meaningful outcomes (e.g., mobility), translate evidence into practice.

•     Examples of updating practice: testosterone labeling after the TRAVERSE trial; removal of the boxed warning on menopausal hormone therapy.

•     Peptides need rigorous study; personally supports access to safely compounded peptides in the meantime.

•     Basic pillars: nutrient-dense diet (2025–2030 Dietary Guidelines), physical activity, muscle mass, sleep, avoiding tobacco.

Andrew Brack — Program Manager, Proactive Health, ARPA-H

“ProSPR: Building regulatory-grade endpoints and trials to develop medicines for healthspan”

Key takeaway: ProSPR is building validated functional measures, anchored in intrinsic capacity, to open a clear regulatory path for aging therapeutics.

•     Central bottleneck: no clear FDA pathway for aging medicines. The endpoint landscape:

–   Upstream biomarkers (e.g., epigenetic): fast-moving but not yet predictive of clinical outcomes.

–   Hard endpoints (e.g., mortality): favored by FDA but slow and costly.

–   Functional measures (e.g., grip strength): promising middle ground, but not standardized.

•     Five-year program of up to $144M integrating academia, startups, pharma, FDA and CMS.

•     Building a sex-specific ProSPR Intrinsic Capacity (ProSPR IC) score from harmonized longitudinal datasets (15 integrated so far), plus an at-home kit (Mike Snyder, Stanford; Buck Institute).

•     Pursuing FDA qualification of a Clinical Outcome Assessment, which would be public and usable by any sponsor.

•     Repurposing trial led by Elena Volpi (UT Health San Antonio): ~1,200 participants over three years testing dapagliflozin and GLP-1 agents; oral semaglutide arm started.

•     Phase 1b novel therapeutics include Cambrian Bio’s mTORC1-selective rapalog, a GPER agonist, a brain-penetrant 17α-estradiol, and a LINE-1-targeting reverse transcriptase inhibitor (Gorbunova/Sedivy).

Panel: Matching Clinical Trials of Therapeutics & Regulatory Mandates — Moderated by Andrew Brack (ARPA-H)

Key takeaway: FDA officials signaled that progress does not hinge on calling aging a disease; validated, function-based endpoints and shared data are the way forward.

•     Lowell Zeta (Acting Chief of Staff, Office of the Commissioner, FDA):

–   Longevity and healthspan are high priorities for FDA and HHS.

–   Defining aging as a disease is not necessary and conventional tools may constrain innovation; focus on endpoint science, including digital measures of function and “feeling well.”

•     Steven Kozlowski (Chief Scientist, FDA):

–   Proposed quantifying a shared “g factor” of aging underlying multiple chronic diseases as a pre-competitive, qualified endpoint.

–   Called for large longitudinal control datasets, standardized mechanistic-evidence frameworks and a few reliable “anchor” markers.

–   Aging and longevity will be a priority in FDA’s upcoming regulatory science focus areas; new trial guidance planned for early FY2027.

•     Jeffrey Siegel (Director, Office of Drug Evaluation Sciences, FDA):

–   Pathway 1: show benefit across two or three distinct age-related diseases.

–   Pathway 2: a broad aging indication measured by a composite across functional domains (cognition, frailty, vision, etc.).

–   Validated surrogates support traditional approval; “reasonably likely” surrogates can support accelerated approval with confirmatory trials.

•     Justin Penzenstadler (Associate Director, Office of Cardiology, Hematology, Endocrinology and Nephrology, FDA):

–   Near term: enriched older, multimorbid populations with hard endpoints, while collecting intrinsic capacity data to validate faster endpoints later.

–   Repurposed drugs (SGLT2i, GLP-1s) need careful design so known cardiovascular benefits are not mistaken for broad aging effects.

–   Urged a pre-competitive consortium to build a “cookbook” of validated biomarkers; best route to feedback is a protocol under an IND.

AI & Clinical Trials in Healthspan

13:00–14:00 · Canopy Hall · Moderator: Andrew Shin, Mass General Brigham

Elena Bonfiglioli — Global Business Leader, Healthcare & Pharma, Microsoft

“AI clinical trials and the longevity discovery loop”

Key takeaway: Agentic AI and privacy-preserving data ecosystems can link R&D, diagnostics, care and consumer health to enable earlier prevention.

•     Discovery loop across four phases: research and drug discovery, diagnostics, care delivery and consumer health.

•     Microsoft Discovery: agentic AI platform for reasoning, simulation and iteration over molecules.

•     AI retrosynthesis work published in Nature with Novartis and GSK to predict synthesizability.

•     Population programs: UK’s Our Future Health; Abu Dhabi (health authorities and M42) 360° longitudinal datasets to predict disease earlier.

•     Emphasis on confidential computing, responsible AI and pre-competitive regional longevity data hubs.

•     Consumer health: ~50M daily health queries; U.S.-only Health Copilot connected to wearables and EMRs.

•     Mission: “Compress 250 years of research into the next 25.”

Wei-Wu He — CEO, Human Longevity, Inc.

“Human Longevity Longitudinal Cohort: From Genome to Digital Health Twin: Building the Future of Precision Longevity”

Key takeaway: Whole-genome sequencing plus AI enables earlier prediction and prevention of disease, potentially pushing average life expectancy toward 100.

•     Next leap after germ theory: cheap, massive data (genomics, imaging) combined with AI.

•     Clinical-grade whole-genome sequencing now ~$599.

•     Heart attack risk is ~50–60% heritable; genomic analysis reported as 61% more sensitive than standard of care for predicting CAD.

•     Genomics could flag predicted non-responders to GLP-1 drugs before costly treatment.

•     Case: 72-year-old with positive methylation cancer test and negative colonoscopy; AI pointed to the appendix, where a 7 cm tumor was found; signal turned negative after surgery.

•     Goal: reduce “sick span” (~15 years for a U.S. newborn girl) to one or two years.

Evelyne Bischof — Medical Director, Sheba Longevity Center

“Clinical Trials for Healthspan: Lessons from the ELITE Trial”

Key takeaway: Adaptive, responder-based trials that pair continuous digital phenotyping and omics with an AI copilot can tune polytherapy day by day.

•     ELITE (XPRIZE Healthspan semifinalist): 31 participants, 8 weeks, N-of-1 approach.

•     Two arms: metformin + GLP-1, or metformin + SGLT2 inhibitor, each with supplements and prebiotics; no lifestyle changes.

•     Continuous phone/multispectral scans and daily micro-surveys; omics at weeks 0, 4 and 8.

•     Significant gains in cognitive and muscular function and improved immune signals; favorable shifts in GlycanAge, proteomic, methylation and organ clocks and oral microbiome diversity.

•     Two metformin reactions; retrospective pharmacogenomics suggested they were predictable.

•     Next: a two-year definitive study adding lifestyle interventions.

•     Biggest need for longevity doctors: an AI “orchestrator” acting as a virtual multidisciplinary team.

Healthspan in Leading Industries

14:00–15:00 · Canopy Hall · Moderator: Sri Devi Narasimhan, Cell Press

Stephanie Manson-Brown — Head of Clinical Development, AbbVie

“Connecting Aging Biology to Skin Health”

Key takeaway: Skin is a neuroendocrine immune organ; keeping it healthy may have systemic benefits for inflammation and cognition.

•     Skin barrier breakdown (e.g., from UV) releases cytokines that can drive systemic inflammaging.

•     Small studies: twice-daily emollients lowered circulating IL-6 and TNF-alpha.

•     A three-year study in China: older adults using emollients twice daily avoided the cognitive decline seen in controls.

•     Healthy adults over 60 share an inflammatory signature with atopic dermatitis patients.

•     A 15-attribute lexicon now defines “skin quality”; validated objective tools and PROs are still lacking.

•     GLP-1 paradox (“Ozempic face”): volume loss vs. reduced systemic inflammation; more research needed.

Laure Crabbe-Vert — Senior Life Science Innovation Manager, LVMH Research

“The Skin Aging Journey”

Key takeaway: An integrated pipeline from single-cell clocks to bioprinted skin and in vivo imaging is used to validate interventions against skin aging.

•     Skin clocks built from single-nucleus transcriptomics (ages 25–80) with Vadim Gladyshev’s lab; keratinocytes and fibroblasts were most informative.

•     With age: senescence markers (p16) rise; ECM, oxidative-stress detoxification and circadian pathways decline; inflammation rises.

•     Bioprinted full-thickness skin models (with LabSkin Creations), including a new immunocompetent, vascularized model.

•     Rose de Granville extract restored fibronectin after laser wounding and matched dexamethasone against chronic UV inflammation.

•     Aged skin is markedly stiffer (atomic force microscopy); peptides plus the extract restored younger mechanics.

•     LC-OCT “optical biopsies” plus AI estimate the age of the dermis in vivo.

Philipp Gut — Adult Health Lead, Nestlé Research

“Nutritional approaches to improve healthspan”

Key takeaway: Weight loss lowers biological age, but GLP-1 users face “hidden malnutrition” that calls for targeted nutritional support.

•     Up to 40% of community-dwelling older adults may face malnutrition.

•     UK Biobank: higher BMI tracks with accelerated biological aging; a one-year meal-replacement trial lowered PhenoAge.

•     Survey of ~220 GLP-1 users: 20–40% lower food intake with no improvement in diet quality.

•     47% missed 1 g/kg protein, 75% missed 1.2 g/kg; >95% had inadequate vitamin D intake.

•     NHANES: lower dietary nutrient density correlates with faster PhenoAge and worse survival.

•     NAD+ precursors (NR, NMN) raised NAD+ and unexpectedly boosted microbial short-chain fatty acid production.

•     New: Nestlé Nutrition Institute’s Longevity Academy and a five-year partnership with NTU Singapore.

Selected Short Talks (parallel track)

13:00–15:15

Anastasia Shindyapina — Staff Scientist, Retro Biosciences

“Scalable platform to produce hematopoietic stem cells”

•     End-to-end iPSC-to-HSC pipeline; ~2–4M HSCs per mL of media at high purity.

•     Derived HSCs engrafted in immunodeficient mice over 20 weeks (success varied across donor lines) and kept an epigenetic age of ~0.

•     Telomeres lengthen at the iPSC stage and are preserved in HSCs.

•     Multiple clones screened to minimize CHIP and oncogenic mutations (final product also screened); initial indication bone marrow failure, later immune aging.

Christopher Petty — Graduate Student, Sinclair Lab, Harvard Medical School

“Chemical epigenetic reprogramming mitigates signatures of aging”

•     SL100, a chemical cocktail found by screening for nuclear-integrity restoration, lowers transcriptomic age.

•     In aged mice: no toxicity after one month of oral dosing; blunted frailty; youthful frailty and blood clocks.

•     In a progeroid Lmna model: preserved weight, fat and muscle, prevented kyphosis; trend toward longer lifespan.

•     Engineered to avoid full reprogramming; no teratomas observed; no human dosing yet.

Michael Corley — Associate Professor, UC San Diego

“Same Target, Different Pharmacology, Different Aging Effects?”

•     NRTIs also inhibit HERV-K and LINE-1; tenofovir comes as TAF or TDF.

•     TAF (higher intracellular levels at a lower plasma dose) shifted epigenetic and transcriptomic clocks down and suppressed CD8 T-cell aging programs.

•     TDF was neutral or adverse and raised GDF15, consistent with its bone and metabolic toxicities.

•     Lesson: target engagement alone does not guarantee benefit; tissue pharmacology matters.

Wayne Mitchell — Instructor, Harvard Medical School

“CROP-seq CRISPRi and CRISPRa screens identify p53 knockdown”

•     Single-cell CRISPR screen of 274 transcription factors in aged mouse fibroblasts; p53 knockdown consistently lowered transcriptomic age.

•     Modest lifespan/healthspan gains in worms; ~20% median lifespan increase in female flies with mid-life knockdown, but shorter lifespan in males with lifelong knockdown.

•     AAV9 p53 knockdown in mice reduced liver senescence, lowered heart transcriptomic age and strongly reduced frailty.

•     Key caveat: cancer risk.

David Tingley — Co-founder, Olio Labs

“An experimental platform to accelerate aging research”

•     196 sensor-equipped cages produce ~5,000 hours of behavioral data per day.

•     Behavioral clock predicts mouse age with ~14-day median absolute error.

•     Detected effects of a rapamycin combination (11 days), calorie restriction (19 days) and GLP-1 drugs (8 days).

•     Can run ~80 intervention studies in ~25 days; sleep architecture is a key feature.

Fridolin Haug — Graduate Student, Mass General Brigham / Harvard Medical School

“FaceAge as a biomarker of aging and health”

•     Model trained on >30M photos estimates age from a single selfie.

•     In >37,000 cancer patients, looking older predicted worse survival (HR 1.06 per year).

•     Looking older associated with hypertension, depression, cancer and heart disease.

•     A clinical trial is testing FaceAge to guide individualized treatment decisions.

John C. Martinez — Postdoctoral Researcher, Gorbunova Lab, University of Rochester

“Knockdown of LINE1 transposable elements extends lifespan”

•     Systemic shRNA knockdown of the youngest L1 families (Rosa26-driven).

•     Longer lifespan, lower frailty and reduced systemic inflammation in old mice.

•     Males fertile at 18–24 months; females fertile to ~12–13 months vs. ~9 months in controls, with more follicles and less fibrosis.

Dan Liu — Longevity Virtual Cell R&D Center, Tsinghua University

“Cross-Species Single-Cell AI Identifies Multi-Target Interventions”

•     Integrates human, mouse, dog and C. elegans single-cell data to rank conserved, druggable targets.

•     A two-agent treatment improved ovarian markers (more secondary follicles, higher AMH) in aging mice; fertility not tested.

•     A dual-target intervention lowered frailty and raised grip strength beyond single-target treatment.

Aging Research and Pharma R&D Productivity

15:30–16:30 · Canopy Hall · Moderator: Lisa Melton, Nature Biotechnology

Michael Li — Assistant Professor, Harvard Business School

“Insilico’s Rentosertib Dilemma”

Key takeaway: AI speeds discovery but shifts the bottleneck to clinical development; portfolio decisions must weigh the value of information for future AI learning.

•     HBS case on Insilico Medicine’s AI-discovered TNIK inhibitor rentosertib for idiopathic pulmonary fibrosis: license out or self-develop?

•     AI discovery: ~1.5 years vs. ~6.5 traditionally, at perhaps one-third of the cost.

•     Ten similar trials ≈ one unique data point for model learning; prioritize assets that generate novel data.

•     Phase 3 estimated at ≥$91M, roughly Insilico’s total prior R&D spend (≈18 targets to PCC).

•     Phase 2a signals: improved lung function trajectories and favorable proteomic aging clock effects.

•     Insilico kept the asset; Phase 3 initiated July 2026 (planned N=320, 52 weeks).

•     Insilico response (Alex Zhavoronkov): kept the asset to retain data and publish openly; more than 40 follow-on drugs on similar paths.

Alexander Schuhmacher — Professor, Technische Hochschule Ingolstadt

“Rethinking Pharma R&D Performance”

Key takeaway: Sustainable R&D productivity requires balancing efficiency and effectiveness, investing in internal capabilities and cutting commercially unsuccessful launches.

•     Dataset: 18 top pharma companies, ~17 years, ~2,000 candidates, ~20,000 trials, 274 FDA approvals.

•     Average likelihood of first approval: 14.3%, with wide variation between companies.

•     65% of drugs launched by leading companies originated externally.

•     About one-third of approved drugs never recouped their own R&D costs; internally discovered drugs had higher commercial value on average.

•     Only blockbusters reliably sustain the research-driven big pharma model.

•     Recommendations: pair AI efficiency gains with effectiveness, build absorptive capacity through internal research, reduce unsuccessful launches.

Michael Ringel — COO, Life Biosciences

“Epigenetic Restoration to Reverse Age-Related Diseases”

Key takeaway: ER-100, an OSK-based epigenetic reprogramming therapy, restores visual function preclinically and is now in Phase 1.

•     Targets glaucoma and NAION, both of which damage retinal ganglion cells.

•     Reverts DNA methylation toward a youthful pattern via OSK (Oct4, Sox2, Klf4) expression.

•     Non-human primates: pattern ERG recovered toward baseline after induced damage.

•     Mice: optic nerve axon regrowth after crush; vision restored to baseline in a glaucoma model.

•     GLP NHP toxicology showed no significant adverse events; Phase 1 dosing began Q1 2026; first-cohort data being presented at AAO.

•     Preclinical signals in MASH, RPE cells (AMD), brain, heart, endothelium and cartilage.

Clinical Healthspan Trials and Practice

16:30–17:30 · Canopy Hall · Moderator: Barbara Cheifet, Nature Biotechnology

Vishwa Deep Dixit — Professor, Yale School of Medicine

“Inflammaging Checkpoints”

Key takeaway: Cysteine restriction, not methionine restriction, drives longevity effects via adipose thermogenesis, and taurine acts as a metabolic signal regulating the NLRP3 inflammasome.

•     NLRP3 inflammasome in tissue macrophages drives IL-1β/IL-18 inflammation and predicts mortality.

•     CALERIE participants achieved ~14% calorie restriction (target 25%); adipose metabolomics pointed most strongly to taurine/cysteine metabolism.

•     In animal models, cysteine restriction caused ~30% weight loss in six days by converting white fat to thermogenic brown fat.

•     Earlier methionine restriction diets also lacked cysteine; new worm data show cysteine, not methionine, restriction extends lifespan.

•     Cystine was the top metabolite predictor of mortality in a large human cohort.

•     Taurine inhibits NLRP3 in old mice; taurine efflux from macrophages is the metabolic sensor regulating NLRP3 assembly.

James Kirkland — Professor, Cedars-Sinai Medical Center

“New Clinical Trials Strategies for Gerotherapeutics”

Key takeaway: Small, coordinated trials are showing safety and early efficacy of targeting fundamental aging processes while building responsive biomarker sets.

•     “Intermediate hypothesis”: targeting one fundamental aging process can beneficially affect many others.

•     Translational Geroscience Network: year seven, 13 U.S. centers, central biobank (~45,000 samples/year) and data and statistics core; 128 trials underway.

•     Biomarker strategy: intervention-responsive body-fluid markers suitable as surrogates, not predictive clocks; alpha-Klotho increased in all 20 participants of an IPF senolytic trial.

•     Across ~25 senolytic trials in older, multimorbid participants: no serious adverse events reported for certain senolytics.

•     Early signals strongest in participants with the highest senescent cell burden (hints of MoCA improvement in MCI/early Alzheimer’s; osteoporosis phase 2a); improved biopsy scores in non-alcoholic cirrhosis.

•     Next: biomarker-guided adaptive trials, donor-kidney rehabilitation for transplant, perioperative delirium, influenza and N-of-1 healthspan clinic trials.

Nicole Sirotin — CEO, Institute for Healthier Living Abu Dhabi

“Advancing Longevity Therapeutics Through Clinical Trials”

Key takeaway: Abu Dhabi’s government-backed ecosystem combines population genomics, data infrastructure and trial capacity for longevity medicine.

•     >800,000 Emiratis sequenced, 400,000 with genomes linked to clinical data; Malafi health exchange holds >5M records.

•     Described as the world’s first government-mandated regulatory framework for healthy longevity medicine, with the Department of Health and the Healthy Longevity Medicine Society.

•     Projects: polygenic risk score validation with the Buck Institute; Ramadan fasting study with Harvard and Oura; Human Phenotype Project with Weizmann’s 10K project.

•     Model-of-care study (22-week intervention) funded by the national insurer could become a scalable care bundle.

•     Invited international partners to run multi-site trials in Abu Dhabi.

Talk: GLP-1 and Healthy Ageing

18:10–18:30 · Canopy Hall

Nikolaj Roed — Global Project Leader, Novo Nordisk

“GLP-1 and healthy ageing”

Key takeaway: Clinical, observational and proteomic data support semaglutide as a contributor to healthspan; muscle health and women’s health are key unmet needs.

•     Disclosure: Novo Nordisk employee and shareholder.

•     UK cohort applying SELECT criteria: lifelong semaglutide estimated to add ~2 years of life.

•     Reduced risk of infection-related outcomes, including COVID; cancer effects appear type-dependent.

•     SELECT: benefits consistent across frailty levels; the frailest reported the largest quality-of-life gains (not proposed as a frailty treatment).

•     Proteomic clocks: 2–3 years lower biological age, with onset at 13–20 weeks.

•     Unmet needs: muscle health (frailty, sarcopenia, malnutrition) and women’s health; study underway comparing hormone therapy, semaglutide and both combined.

•     Whether GLP-1 counts as a “longevity” therapy remains debatable.

ARDD 2026
Organizer,
13th Aging Research and Drug Discovery Meeting






* * ~


ARDD 2026 — Day One Recap: Additional Sessions


13th Aging Research and Drug Discovery Meeting

Dear Scott Gordon Kenneth MacLeod,

ARDD 2026 — Day One Recap: Additional Sessions

Aging Research and Drug Discovery Meeting · Thursday, October 1, 2026 · David Rubenstein Treehouse, Harvard University, Cambridge, MA

 

Clinical Trials in Diseases of Aging: From Evidence to New Therapeutics and Regulatory Pathways

11:20–12:00 · Canopy Hall · Panel

Sebastien Thuault (moderator) — Editor, Nature Medicine

Key takeaway: Panelists saw several routes to approval for aging-related therapies, from surrogate endpoints and comorbidity-focused trials to patient-relevant function measures, and agreed that biomarkers must be tied to outcomes people can feel.

•     Steven Quay (Founder & CEO, Atossa Therapeutics):

–   HHS and FDA are receptive to novel approaches in aging.

–   Developing mammographic breast density as a surrogate marker for breast cancer prevention via accelerated approval: conditional market access on the surrogate, with hard endpoints confirmed later.

–   “Wedding cake” approach: define the indication, population and condition, then select a biomarker suitable for accelerated approval.

–   Patient-reported outcomes can show benefit within 2–3 weeks, which can support access.

•     Jill Lee (Director, Regulatory Policy, Novo Nordisk):

–   The field is trailblazing, with many open questions; the ultimate goal is preventing chronic disease.

–   Three paths: develop aging biomarker pathways; target aging-related comorbidities (obesity is linked to more than 200 age-related conditions); and prioritize measures of how patients feel, function and survive, likely faster than validating new biomarkers.

–   Example: the cardiovascular benefits of GLP-1 drugs were discovered in diabetes safety trials.

•     Calum MacRae (Professor, Mass General Brigham):

–   Called for inverting the pyramid from a disease-centric focus to healthspan.

–   Adherence is a major challenge: only 55% of patients remain on statins one year after a heart attack; perceived benefit drives uptake, as seen with GLP-1 drugs.

–   Cardiology took decades to turn cholesterol and blood pressure from risk markers into targets, and some LDL-lowering agents worsened outcomes, so surrogates must be linked to outcomes.

–   Molecular insights should connect to measures people can feel or see, such as sleep metrics and intrinsic capacity.

•     Steve Horvath (Professor, UCLA):

–   Advocates recognizing aging as a disease, with clear definitions.

–   Molecular biomarkers are essential alongside functional and disease assessments.

–   Companies are reluctant to collect extra biomarker data for fear of negative signals, so incentives are needed to collect it in interventional trials.

–   A qualified surrogate endpoint for aging may be achievable within about 10 years.

–   Proposed tiered, pre-specified biomarker panels in trials (Tier 1 must-have, Tier 2 nice-to-have), drawing on DNA methylation, proteomics, metabolomics and imaging.

From Healthspan Trials to Clinical Practice: Building the Path to Patient Access

17:30–18:10 · Canopy Hall · Panel

Michael Basson (moderator) — Editor, Nature Medicine

Key takeaway: Personalized, preventive healthspan care is emerging, but it needs standardized outcomes, shared data and reimbursement frameworks to scale and to reduce disparities.

•     David Dodick (CMO, Atria Health; Professor, Mayo Clinic):

–   Atria Health Institute is building a preventive ecosystem with deep phenotyping, with a focus on preventive neurology and brain health.

–   Three tiers of measures: conventional endpoints (glucose, blood pressure, cholesterol, sleep, weight, cognition, coronary CT angiography, cancer screening); emerging disease biomarkers (p-tau217, polygenic risk scores) as research; and aging biomarkers (epigenetic and proteomic organ clocks) as research.

–   Process of deep phenotyping, risk stratification, early intervention and multidisciplinary follow-up, with a de-identified registry intended as a “Framingham for prevention”; aims to scale to Medicare Advantage and employer plans.

–   Running an IRB-approved trial of GLP-1 effects on a proteomic brain clock; uses evidence-informed, risk-adjusted off-label treatment for high-risk patients.

–   Wearables are mostly motivating; the team is building dashboards that integrate wearable and EHR data with preset alerts.

•     Sara Bonnes (Professor, Mayo Clinic):

–   Longevity medicine lacks clinical standards, and reimbursement is difficult when aging is not a disease.

–   Focuses on healthspan, patient goals and avoiding harm; primary care time constraints make communication central.

–   Wearables help many patients but can harm some, for example those with eating disorders or body image concerns, so the approach must be tailored.

–   Objective data such as body composition can reveal gaps between reported and actual exercise: “This doesn’t let you lie.”

•     Erwin Tan (Senior Director, AARP):

–   AARP’s geroscience principles focus on healthspan and avoid labeling aging a disease because of the risk of ageism; perceptions of aging affect health.

–   AARP provides a consumer voice and aims to democratize interventions and reduce disparities.

–   Brain health motivates lifestyle change; AARP’s Global Council on Brain Health produces accessible summaries for the public.

–   Interested in scaling clinic insights into remote tools for broader population engagement.

Selected Short Talks

13:00–13:15 · Parallel track

Albert Higgins-Chen — Assistant Professor, Yale University

“The POLARIS Platform for Omics, Longevity and Aging Biomarker Insights”

•     POLARIS is an ecosystem of five interconnected tools to help researchers select, interpret and understand aging biomarkers, especially DNA methylation clocks, for clinical trials.

•     methylCIPHER v2: software that calculates up to 143 DNA methylation clocks, with metadata to guide selection.

•     A benchmarking platform evaluates clocks across 179 datasets on four dimensions: stability, treatment response, associations and risk prediction (STAR).

•     Treatment response arm: covers 88 interventions; mortality and pace-of-aging clocks such as GrimAge and DunedinPACE were the most responsive. Results are available on an interactive website.

•     CpG Atlas: a SQL database annotating individual CpG sites, queryable in natural language, to explain the biology behind clocks.

•     CpG Library: a curated library of 2,500 papers on aging biomarkers, mined with LLMs, with an AI chat function.

•     The platform is continuously updated by AI agents with human review.

XPRIZE Healthspan: Meet the Finalists — Group A: Multimodal & Clinical Approaches

09:35–10:00 · Parallel workshop · Cedar Grove

Stefanie Morgan — VP Operations & Applied Science, AgelessRx

“AgelessRx: a multimodal approach to improving healthspan”

•     Premise: monotherapy is insufficient for the multimodal nature of aging.

•     90-day randomized pilot with three arms: placebo, a medium-sized intervention and a comprehensive “more is more” stack.

•     Safety: blood biomarkers stayed within healthy ranges, with no clinically concerning adverse effects.

•     Both intervention arms improved biological age on a plasma proteomics test versus placebo; in the comprehensive arm, 5 of 6 participants had lower biological age.

•     DEXA: lean mass improved in both intervention arms; bone mineral density improved in the comprehensive arm.

•     SF-36 well-being scores improved significantly in both intervention arms versus placebo.

•     The finals trial will use the comprehensive stack, with low-dose GLP-1s and sermorelin added after other internal trials.

Zahi Fayad — Director, BioMedical Engineering, Mount Sinai

“NYC VITA 2030: a randomized trial to improve healthspan by targeting inflammation”

•     Targets chronic low-grade systemic inflammation as a primary driver of aging.

•     Intervention: exercise (two 20-minute HIIT and three 40-minute resistance sessions per week, guided by videos and wearables), spermidine (40 mg daily) and weekly rapamycin.

•     A pilot confirmed positive signals from each component; an antiviral drug was dropped after showing no effect.

•     Design: 365-day, 2:1 randomized trial with 180 participants (120 intervention, 60 control receiving lifestyle counseling).

•     XPRIZE success requires improvement in all three domains: muscle (six-minute walk and power), cognition (4 of 6 tests) and immune age, which the speaker called a very high bar.

Judith Klein-Seetharaman — Professor, Arizona State University

“ASU Team Healthspan: a multimodal intervention and a new integrated age metric”

•     Centerpiece is oxygen as hormetic stress: hyperbaric oxygen therapy and simulated altitude.

•     Adds AI-governed adaptive resistance training, a multimodal recovery protocol and personalized nutrition guided by metabolomics and a digital twin model.

•     Collects more than 500 parameters, including digital biomarkers, blood assays, multi-omics and physiological measures.

•     Developed “reserve energy,” an integrated age metric derived from age-dependent physiological biomarkers, to capture declining intrinsic capacity.

•     Over an 8-week intervention, most participants improved on reserve energy; strong gains in muscle function and a significant improvement in Rapid Visual Information Processing (CANTAB).

Bruno Balen — Founder, ANI AI

“ANI AI: adaptive polytherapy and a world model of human biology”

•     Eight-week, non-adaptive pilot at Sheba Medical Center in Israel combining GLP-1-class drugs, GLP-2, metformin and proprietary supplements, with no lifestyle changes.

•     Very deep profiling: multi-omics, glycomics, metagenomics, functional and cognitive tests, and daily multispectral scans with an in-house device.

•     Responses were strong but heterogeneous: about half of participants improved in two domains and about one-third (“super responders”) in all three XPRIZE domains.

•     No participant showed agreement across all aging clocks tested; argued for treating clocks as multidimensional rather than a single number.

•     Proposes AI as therapy: per-person in silico trials using a world model of human biology, a 90-second daily digital check-in (97.7% adherence reported), and treatment adapted mid-trial.

Panel Discussion: Group A — Multimodal & Clinical Approaches

10:05–10:25 · Parallel workshop · Cedar Grove · Panel

Group A finalists — AgelessRx, NYC VITA, ASU Team Healthspan, GOQii, ANI AI

Key takeaway: Multimodal interventions cannot yet be separated into the effects of individual components, so teams are measuring the combined effect and expect AI models to untangle individual contributions later.

•     Isolating effects: factorial designs would be ideal but are too complex and costly now; trials test the combination against controls.

•     Antagonism vs. synergy: one team tested its combination empirically and found the effects complementary; another deliberately chose a small number of orthogonal modalities to limit risk.

•     Bruno Balen (ANI AI):

–   Called drug interactions a “mess” that cannot be predicted without data; deep, repeated omics plus AI world models can reconstruct the biology, and near-real-time measurement allows dynamic adjustment.

•     Partnerships: needed for financing and running trials; requests included a wearable and sensor company and compute partners for AI costs.

•     Commercialization: one team pointed to existing commercial operations and approved therapeutics as a shorter path to return; NYC VITA emphasized scalable modalities (exercise, rapamycin, spermidine); one team plans a Series A in early 2027.

XPRIZE Healthspan: Meet the Finalists — Group B: Drugs & Biologics

10:25–10:55 · Parallel workshop · Cedar Grove

Reenie McCarthy — CEO, Mighty Therapeutics

“Mitochondrial All Stars: targeting mitochondrial dysfunction to improve healthspan”

•     Mitochondrial dysfunction is a central driver of aging; age disrupts the cardiolipin-dependent inner mitochondrial membrane.

•     Elamipretide is the first FDA-approved mitochondria-targeted therapy (accelerated approval for Barth syndrome) and normalizes mitochondrial structure and function in preclinical models.

•     In a fully enrolled Phase 3 trial in dry AMD, it showed a protective effect on photoreceptors.

•     SHAPE trial (4 weeks, open-label, 23 older adults, with the University of Washington): improvements in strength, six-minute walk, peak VO2, cognition and inflammatory markers.

•     Finals study: 120 participants with the University of Washington, expected to begin enrolling in 2026.

Takahiro Karasaki — Associate Professor, University of Tokyo

“Goda Lab: engineering extracellular vesicles for rejuvenation”

•     Natural extracellular vesicles (EVs) from young plasma can rejuvenate aged mice, but deliver poorly to target cells.

•     “Super EVs” have engineered surfaces that improve targeting and uptake.

•     Rejuvenation in vitro comparable to rapamycin; in aged mice, hair regeneration and improved frailty index; in fruit flies, average lifespan extended by four days.

•     No major safety concerns in mice; plans to engineer EVs from cultured stem cells for aged individuals; seeking clinical development partners.

Brian Rash — VP Research & Discovery, Longeveron

“Longeveron: laromestrocel for aging frailty and Alzheimer’s disease”

•     Laromestrocel is an allogeneic, off-the-shelf bone marrow-derived mesenchymal stem cell infusion with anti-inflammatory and pro-vascular effects; given to 644 participants across six randomized trials.

•     Aging frailty Phase 2b: 63-meter (~20%) improvement in six-minute walk distance.

•     Alzheimer’s Phase 2a (CLEAR MIND): 48% slower brain atrophy on MRI and improved MoCA scores versus placebo; brain inflammation (free water) stayed flat versus a rise with placebo.

•     Finals trial planned for mid-2027.

Bae Hoon Kim — Research Director, PRG S&T

“RPRGAON-Progeria: targeting progerin to address aging”

•     Progerin, a toxic lamin A variant that deforms the nucleus, drives Hutchinson-Gilford progeria syndrome and is also found in naturally aged people.

•     In progeria mice, treatment removed progerin, restored the nuclear envelope, doubled body weight, recovered muscle strength by 80% and extended lifespan by 60%.

•     Phase 1 safety trials are complete.

•     Plans a Phase 2 trial in the U.S. and South Korea, possibly from Q2 2027, and a five-subject Werner syndrome study at the University of Michigan.

Tomonari Abe — CEO, Abeyoando Pharma Co.

“Abeyoando Pharma: Yojyo Plus, bridging longevity science and daily health habits”

•     Yojyo Plus is a 28-ingredient daily supplement designed to target the 12 hallmarks of aging, including NMN, ginsenoside, spermidine and Okinawa fucoidan.

•     In a 42-day, double-blind, placebo-controlled trial of 42 people, functional age fell by 2.8 years (vs. 0.6 with placebo) and PhenoAge by 4.1 years.

•     A weaker effect on immune function led to an AI-guided formula revision; the next trial will enroll 125 people for one year.

•     Opening a $7.5 million seed round.

Eunjae Yang — Principal Investigator, Lono Jaeyak Inc.

“Lono Jaeyak: cellular rejuvenation with senotherapeutic cocktails”

•     Single-pathway interventions fail because senescence is sustained by multiple interacting pathways.

•     Synthetic and natural cocktails target four senescence pathways at once.

•     Restored proliferation in senescent cells, reduced epigenetic age by 10–27 years, normalized gene expression and rejuvenated MSCs from an 86-year-old donor.

•     Aims to use rejuvenated autologous MSCs for regenerative medicine.

Panel Discussion: Group B — Drugs & Biologics

11:00–11:20 · Parallel workshop · Cedar Grove · Panel

Group B finalists — Mitochondrial All Stars, Goda Lab, Longeveron, RPRGAON-Progeria, Abeyoando Pharma, Lono Jaeyak

Key takeaway: Teams described their regulatory footing, partnership needs and closing messages.

•     Reenie McCarthy (Mighty Therapeutics):

–   FDA acceptance of an imaging marker of photoreceptor function in dry AMD offers a hard endpoint for an aging-related disease.

–   Revenue from the approved Barth syndrome product helps, but additional trial funding is welcome; closing message: “recharging bioenergetics” to add life to years.

•     Goda Lab:

–   Super EVs affected multiple aging phenotypes (frailty, hair regeneration, fly lifespan), evidence of a broad platform rather than a single disease pathway.

•     Brian Rash (Longeveron):

–   Preparing to meet FDA on endpoints for aging frailty; manufactures in-house at its Miami GMP facility; open to partnerships; stressed rigorous randomized designs.

•     Bae Hoon Kim (PRG S&T):

–   Measuring progerin in natural aging requires a more sensitive plasma assay; the company is pre-IPO and seeking co-development and licensing partners.

•     Tomonari Abe (Abeyoando Pharma):

–   Seeking investors and research partners; cited diet’s effect on Okinawan longevity.

ARDD 2026
Organizer,
13th Aging Research and Drug Discovery Meeting




* * ~

ARDD 2026 — Day Two Recap


ARDD 2026 — Day Two Recap

ARDD 2026 <event-noreply@whova.io>Sat, Oct 3, 2026 at 4:31 AM
Reply-To: stephanie@insilicomedicine.com
To: president@worlduniversityandschool.org
13th Aging Research and Drug Discovery Meeting

Dear Scott Gordon Kenneth MacLeod,

ARDD 2026 — Day Two Recap

Aging Research and Drug Discovery Meeting · Friday, October 2, 2026 · David Rubenstein Treehouse, Harvard University, Cambridge, MA

 

MAIN TRACK — CANOPY HALL

Chair Opening Introduction

09:00–09:15 · Canopy Hall

Chairs — Alex Zhavoronkov, Vadim Gladyshev, Morten Scheibye-Knudsen, Daniela Bakula, Jesse Poganik

•     Zhavoronkov: the meeting aims to showcase early signals from pharma and frontier companies on interventions that could extend healthy life; nothing has yet been proven to add even one year of life in healthy people.

•     Gladyshev and Poganik pointed attendees to the parallel sessions and posters, with talks running concurrently across floors.

•     Sponsors and partners thanked included Novo Nordisk, AstraZeneca, AbbVie and Nestlé.

Reimagining Drug Discovery Through the Lens of Aging Biology

09:15–09:35 · Canopy Hall

Fiona Marshall — President, Biomedical Research, Novartis

Key takeaway: Single-target regenerative approaches have not translated into clinical benefit, so Novartis is moving to a systems-based approach built on longitudinal human data and resilience biology.

•     LNA043 (osteoarthritis): MRI evidence of cartilage regeneration, but no improvement in pain or mobility, the endpoints regulators require.

•     Bimagrumab (sarcopenia): increased muscle mass, but no improvement in mobility, frailty or function in sarcopenia patients.

•     New Diseases of Aging and Regenerative Medicine department organized around the hallmarks of aging rather than siloed disease areas.

•     Uses the Data42 repository (decades of clinical trial data, e.g., CANTOS) plus external data such as Our Future Health and BioAge.

•     Focus on resilience: why some people avoid disease despite high cholesterol or brains full of amyloid.

•     Goal is not an “aging” approval: target specific aging-driven diseases and add aging-relevant secondary or exploratory endpoints.

•     AI-based predictive safety models used to balance anti-aging efficacy against proliferation and genotoxicity risks.

Pharma Chief Executive Panel

09:35–10:20 · Canopy Hall · Moderator: Alice Park, TIME

Panel — Christophe Weber (Takeda, former CEO), Elcin Barker Ergun (Menarini), Fiona Marshall (Novartis), Ariel Feldstein (Pfizer), Stéphane Bancel (Moderna)

Key takeaway: Pharma strategies are converging on prevention, earlier intervention and multi-system mechanisms enabled by AI, but trial timelines, endpoints and reimbursement remain barriers.

•     Christophe Weber (former CEO, Takeda):

–   Prevention already exists (statins, blood pressure control), but health systems remain treatment-oriented.

–   AI is multiplying research productivity; the bottleneck is shifting to clinical development.

–   Serious prevention requires a “completely different paradigm.”

•     Elcin Barker Ergun (Menarini):

–   Portfolio targets leading causes of death: cardiovascular disease, cancer, respiratory illness, neurodegeneration and infection.

–   Launching a CETP inhibitor in the EU that raises HDL and lowers LDL; oncology shifting toward earlier-stage intervention.

–   Menarini licensed two cancer molecules from Insilico Medicine’s AI platform, now in clinical trials.

•     Fiona Marshall (Novartis):

–   Prevention is ideal but limited by long trials and reimbursement; targets early disease stages with measurable outcomes.

–   Novartis uses AI foundation models in a “lab in the loop” cycle to propose cross-disease targets.

–   Novartis licensed a Chinese CAR-T therapy, going “where there’s good science”; would join a pre-competitive consortium to validate aging biomarkers.

•     Ariel Feldstein (Pfizer):

–   GLP-1 drugs show the value of treating cardio-renal-metabolic-neuro axes together.

–   Real-world data at scale plus AI can explain why aging trajectories diverge; next wave of innovation is prevention.

•     Stéphane Bancel (Moderna):

–   “Health stack”: genomic knowledge, prevention (lifestyle, vaccines) and early intervention.

–   Lynch syndrome cancer-prevention vaccine program; Phase 3 study of an individualized mRNA cancer vaccine in early-stage lung cancer.

•     Cross-cutting: China’s clinical trial system is becoming markedly more efficient; regulators and payers must evolve to accept biomarker-based and preventive strategies.

Longevity Therapeutics as the Most Impactful Trillion-Dollar Industry in Biotechnology: How to Discover and Develop Them in the Most Credible and Equitable Way with AI

10:20–10:40 · Canopy Hall

Alex Zhavoronkov — CEO, Insilico Medicine

Key takeaway: AI-discovered rentosertib showed Phase 2 functional and biological-age signals, supporting a “dual-purpose” route from disease approval to longevity.

•     Dual-purpose strategy: pick targets shared by aging and disease, win approval where standard of care can be beaten, then expand; ~70% of Insilico programs are designed this way.

•     IPF Phase 2: high dose produced a 98 mL increase in FVC over 12 weeks (small study; no definitive claims).

•     Trial proteomics (Nature Biotechnology, published ~two weeks earlier): 758 UK Biobank aging-associated proteins showed trajectory reversal consistent with a senomorphic effect.

•     Independent groups, including Gladyshev’s lab, applied six clocks: ~3–6 years lower biological age after four weeks; largest organ effect in arterial aging (−16.57 years at 60 mg QD).

•     Phase 3 now ongoing; Insilico reported profitability in the first half of the year and 34 developmental candidates to date.

Modulation of Aging Clocks by the GLP-1/GIP dual agonist, Tirzepatide

10:40–11:00 · Canopy Hall

Kevin Duffin — VP, Aging Research, Eli Lilly

Key takeaway: In a SURMOUNT-5 sub-study, 72 weeks of tirzepatide slowed multiple epigenetic clocks, including organ-specific clocks, though some methylation-based predictions missed.

•     Tirzepatide arm only, participants over 50; whole blood at baseline and 72 weeks; analyzed independently by Zymo Research and TruDiagnostic (Illumina EPIC v2) with consistent results.

•     First-generation clocks: ~0.5 year reduction; second-generation: >1.5 years; third-generation pace clocks: slower rate of aging.

•     TruDiagnostic organ clocks (SYMPHONYAge): heart, immune, kidney and liver ages decreased.

•     Methylation correctly predicted falls in BMI, waist-to-hip ratio, HbA1c, glucose and lipid changes, but wrongly predicted rises in SHBG, TNF receptor and VCAM.

•     Limitations: small single-arm analysis, 72 weeks, clocks not trained on treatment effects; findings are hypothesis-generating.

New Technology Partnering & Licensing

11:30–12:10 · Canopy Hall · Moderator: Alex Philippidis, GEN

Panel — Morten Sogaard (Astellas), Christopher Austin (GSK), Alex Cogdill (Daiichi Sankyo), Vishnu Sresht (Genentech), Carl Gordon (OrbiMed)

Key takeaway: Pharma interest in aging biology is strong, but deals hinge on disease-specific efficacy, clear mechanisms and sound AI and data governance.

•     Sogaard (Astellas): partnering spans asset licensing, modality platforms and AI; priority access to high-quality human biology datasets; actively partnering in China.

•     Austin (GSK): aging increasingly seen as unifying biological principles, especially immune aging and inflammaging; warned of “irrational exuberance” and unsupported valuations among some longevity biotechs.

•     Austin: “Everything at GSK has become AIified”; keeps data and models in controlled internal environments to prevent leakage; biology is AI’s main frontier.

•     Attractive first indications cited by Austin: fibroinflammation in lung (IPF, COPD), liver, kidney, brain and cancer.

•     Sresht (Genentech): shift toward collaborative learning partnerships and pre-competitive data consortia; unsettled IP ownership for AI-assisted work creates friction.

•     Gordon (OrbiMed): 2026 strong for pharma acquisitions, but few in aging; licensing follows demonstrated efficacy in a specific disease, not preclinical aging signals.

•     China: Chinese biotechs deliver comparable or better quality faster and cheaper; data and sample export limits are a constraint.

Multiplex testing of de-aging polypharmacy & targeted delivery

12:10–12:30 · Canopy Hall

George Church — Professor, Harvard Medical School

Key takeaway: Multi-gene therapies, ML-designed delivery vectors and engineered organs aim to address aging across several pathways at once.

•     Single-pathway interventions may yield only ~2–20% effects; combinations (e.g., alpha-Klotho, TGF-beta receptor 2, FGF21) showed synergy in mouse diabetes and kidney models.

•     OSK delivered in a single AAV to mice late in life (after half the cohort had died) increased longevity.

•     Machine learning plus multiplex libraries: Dyno Therapeutics AAV capsids reported with 280× higher brain delivery and 50× lower liver targeting.

•     Herpesvirus-based vectors under development to carry dozens of genes.

•     iPSC-derived oligodendrocyte precursor cells rescued mice from an MS-like demyelinating disease; heading to clinical trials.

•     Xenotransplantation: pig organs with 69 edits (retrovirus knockouts, glycan removal, seven human transgenes) in an FDA-cleared trial; later patients have fared better than the first.

•     Allogeneic CAR-T programs from companies co-founded by Luhan Yang (e.g., QT-019B, QN-139b) are in FDA clinical trials for autoimmune disease.

Session

13:30–14:50 · Canopy Hall · Moderator: Scotch McClure, Maxwell Biosciences

Sophie Lemire-Brachat & Naisha Shah — Novartis; BioAge

“APEx (Aging and Physical Exercise): A Human Longitudinal Engine for Novel Target Discovery”

Key takeaway: Combining decades of longitudinal human data with exercise biology aims to find targets that mimic the protective effects of physical activity.

•     Novartis–BioAge collaboration, started ~1.5 years ago, focused on resilience rather than only disease pathology.

•     Cohorts with decades of follow-up: 25k+ serial proteomic profiles, genome-wide genotyping and deep phenotyping (VO2 max, grip strength, walking speed, pTau217, NfL).

•     Heart failure: kidney, cardiac and metabolic signals ~20 years before diagnosis; fibrosis biology and NT-proBNP ~4 years before.

•     Alzheimer’s: distinguishes resistance (no pathology despite risk) from resilience (pathology without cognitive decline).

•     Knowledge graph ranks targets by evidence across metabolic, muscle, cardiac and neuro domains.

Scotch McClure — CEO, Maxwell Biosciences

“Nature’s Youth Peptide: Reversing Immunosenescence, Restoring Youth”

Key takeaway: Maxwell is developing stabilized synthetic versions of the human peptide LL-37 to control pathogen burden, which it frames as foundational to longevity.

•     LL-37 (cathelicidin) production declines sharply with age, according to the speaker.

•     Claromers: peptoid-style molecules with side chains moved from carbon to nitrogen, resisting enzymatic degradation (DARPA-funded origin).

•     Reported activity against all fungi and enveloped viruses tested and >400 bacterial strains, without harming the gut microbiome.

•     FDA Qualified Infectious Disease Product designation for pneumonia (bacterial and fungal), with Fast Track and Priority Review eligibility.

•     Company described work with the government of India on drug-resistant infections and a potential U.S. Ebola stockpile; 11 issued and 48 pending patents.

Yuelei Shen — President & CEO, Biocytogen

“Advancing Aging Therapeutics Across the Discovery-to-Translation Continuum”

Key takeaway: Humanized mice, AI-guided antibody discovery and companion-animal studies are combined to close the mouse-to-human translation gap.

•     Target-humanized mice allow anti-human antibodies to be tested in aged mice; fully human antibody mice (RenMice) generate human antibodies directly.

•     AI pipeline from immunized mice to sequencing to binding prediction; automated facility producing up to ~800 antibody samples per day.

•     Candidate aging targets include IL-11, IL-6 receptor, FAP, CD38 and CD39.

•     Veterinary hospital in China with ~3,000 dogs, ~350 of them aged; an anti-IL-11 antibody will soon be tested in aged dogs.

Tony Wyss-Coray — Professor, Stanford University

“Circulating proteins reveal and regulate cell and organ function”

Key takeaway: Plasma proteomics can estimate the age of individual cell types and organs, and these ages predict disease and mortality.

•     Liver-derived proteins such as ApoA1 can be taken up by microglia in mice and improve their phagocytic function.

•     BONCAT labeling tracks proteins made by specific cell types (e.g., neurons) in blood.

•     UK Biobank (~44,000 people): astrocyte age was the strongest cellular predictor of Alzheimer’s; extremely old astrocytes ≈5× risk, very young ≈40% lower risk.

•     Among APOE4 carriers, none with very young astrocytes developed Alzheimer’s.

•     Smokers with old alveolar type 2 cells had double the lung cancer risk; skeletal muscle cell age was the strongest mortality predictor.

•     1946 British birth cohort: protective lifestyle factors associated with up to ~70% lower risk of having an “old” organ.

Diseases as a Pathway to Longevity Therapeutics: Which age-related disease resembles aging most closely?

14:50–15:30 · Canopy Hall · Moderator: Barbara Cheifet, Nature Biotechnology

Panel — Ruth Gimeno (Eli Lilly), Ariel Feldstein (Pfizer), Carine Boustany (Boehringer Ingelheim)

Key takeaway: No single disease models aging; some (IPF) share its mechanisms directly, while others (obesity) act as systemic accelerated-aging models.

•     Gimeno: distinguishes specific diseases with targetable risk factors (atherosclerosis, osteoporosis) from systemic diseases (obesity, IPF) that mirror aging; protective alleles such as PCSK9 point to “one and done” therapies.

•     Gimeno: the field has “almost too many biomarkers”; the challenge is validating the right ones, and outcome studies remain necessary.

•     Feldstein: obesity (“adiposity-based chronic disease”) as systemic accelerated aging; GLP-1 use in millions of people is a unique research opportunity; favors proteomic biomarkers.

•     Boustany: IPF (median diagnosis ~67–70) shares hallmarks with aging, including senescence, telomere shortening and impaired epithelial repair; telomere shortening is causal in IPF.

•     Shared view: aging clocks are useful for organ-specific insight; human-centric data such as UK Biobank and combination studies (e.g., GLP-1s with senolytics) are priorities.

Early Stage Investor Panel

16:00–16:40 · Canopy Hall · Moderator: Amol Pawar, UBS

Panel — Sergey Jakimov (LongeVC), Arie Belldegrun (Vida Ventures), Yan Lei (Synaro Capital), Gérôme Guiot (LVMH), Chuen Yan Leung (Value Partners Group)

Key takeaway: Early-stage longevity companies should work within existing regulatory frameworks by targeting specific diseases, raise from patient and appropriate capital, and deliver on milestones rather than overpromise.

•     Jakimov: LongeVC shifted to age-related diseases to align with regulators and pharma buyers; cited Rubedo reaching Phase 2 by focusing on specific indications; founders should learn to speak the FDA’s language.

•     Belldegrun: aging drugs must meet standard drug criteria (defined mechanism, defined population, FDA-recognized endpoints); the biggest founder mistake is to overpromise and underdeliver; the field lacks a clear regulatory “finish line.”

•     Belldegrun: raise money when it is available, not when it is needed; roughly $50M is typically needed to reach IND and early clinical stage.

•     Yan Lei: diligence focuses on biology, animal data, target validity and team; a common mistake is focusing on an exit too early.

•     Guiot: treat aging drugs as drugs; keep most of a portfolio on de-risked regulated paths with a limited allocation to moonshots; the Series A bar has risen.

•     Leung: inflated boom-time valuations harm the ecosystem; founders should raise realistic amounts at disciplined valuations.

•     Family offices can offer patient capital, but may underestimate drug development timelines compared with experienced institutional investors.

Full-Stack and Growth Stage Investor Panel

16:40–17:20 · Canopy Hall · Moderator: Patrick Temple-West, Financial Times

Panel — Jim Flynn (Deerfield), Alfredo Viegas (Oaktree Capital Management), Kan Chen (Qiming Venture Partners)

Key takeaway: AI is driving a “golden age” of biotech innovation, but investors favor proprietary data and practical applications over pure software, amid rising low-cost competition from China.

•     Flynn: Deerfield follows a “data first strategy empowered by software”; proprietary data is the real moat; small-molecule “tokenization” and slow synthesis cycles limit AI learning loops.

•     Viegas: invests in AI “picks and shovels”; sees wearables plus data as the next frontier; advised companies to raise money now.

•     Viegas warned China is becoming the “Costco of biotech,” licensing molecules at a fraction of U.S. cost; Flynn countered that U.S. companies can combine university-sourced targets with licensed Chinese assets.

•     Chen: Qiming backs foundation-model companies and AI-native biotechs; AI will “eat the preclinical end” of the industry, but impact on P&L will take time.

•     Chen called GLP-1 drugs the “first longevity medicine” that is not “snake oil”; Viegas stressed healthspan’s economic value; Flynn noted longevity investments increasingly start with acute or orphan indications.

From Infrastructure to Insight: A Large-Scale DNA methylation Asset and Epigenetic Insights from a Longitudinal GLP-1 Trial

17:20–17:40 · Canopy Hall

Kirsten Seale — Scientist, TruDiagnostic

Key takeaway: A single DNA methylation assay can serve as a broad trial endpoint, tracking biological age, surrogate biomarkers and future disease risk, as shown in a tirzepatide trial.

•     TruDiagnostic database: >140,000 methylation samples, ~87,000 with deep phenotypes; pipeline computes >2,500 metrics per sample.

•     Analyzed ~100 participants from the tirzepatide arm of the 72-week Eli Lilly trial (overweight or obesity without diabetes).

•     Favorable (younger) signal across 26 age-related clocks; strongest for outcome-trained second-generation and organ-specific clocks; robust to immune cell shifts.

•     18 of >2,000 methylation surrogates changed significantly, matching known pharmacology (e.g., type 2 diabetes risk score, BMI, HbA1c, GlycA, CRP proxies).

•     Methylation “disease modes” shifted away from patterns linked to type 2 diabetes and mortality.

•     Steve Horvath suggested repeating the study with a control arm; individual-level responder data were not yet available.

Skin Deep: Clinical Translation of a GPX4-Targeted SenoAdaptive Medicine for Skin Aging, Alopecia and Actinic Keratoses

17:40–18:00 · Canopy Hall

Marco Quarta — Co-Founder & CSO, Rubedo Life Sciences

Key takeaway: Topical GPX4-targeting RLS-1496 kills senescent cells while inducing protective hormesis in stressed cells, with early clinical benefit across several skin conditions.

•     GPX4 found via single-cell multi-omics distinguishing senescent from stressed cell states: triggers ferroptosis in senescent cells, autophagy and redox reset in stressed cells.

•     4-week trials (European basket trial in psoriasis, atopic dermatitis and photoaged skin; U.S. open-label trial in actinic keratosis): well tolerated, including in atopic dermatitis skin.

•     Actinic keratosis: 50% mean lesion reduction (some complete clearance) vs. ~14% natural resolution; effects persisted up to 4 months.

•     Photoaged skin: ~10% increase in multiple collagens; psoriasis lesions fell ~20% vs. a ~30% increase with vehicle.

•     Plasma proteomics showed reduced systemic inflammatory markers despite negligible systemic drug exposure.

•     Skin methylation clock (with Mitra Bio): mean 2.1-year reduction after 4 weeks.

•     Ex vivo balding scalp: matched or numerically exceeded finasteride; Phase 1a androgenic alopecia trial starting end of October 2026; oral GPX4 program for eye and metabolic disease to follow.

Using buccal methylomic data to generate novel insights into epigenetic aging

18:00–18:20 · Canopy Hall

Adiv Johnson — CSO, Tally Health

Key takeaway: Epigenetic clocks become more reliable and useful by suppressing technical noise and explaining age predictions through modifiable biomarker proxies.

•     Tally Health (cheek-swab test) has >25,000 buccal methylation datasets, ~10,000 longitudinal; now part of Infinite Epigenetics, TruDiagnostic’s parent company.

•     CheekAge: exercise linked to younger epigenetic age; poor sleep, smoking and any alcohol to older; validated in external cohorts for mortality and disease associations.

•     For shared CpGs, Twist methylation sequencing was noisier than Illumina EPIC v2 arrays; PC clocks reached ICC >0.99 on both platforms, while uncorrected replicate differences reached 15.5–20+ years.

•     Proof-of-concept deep learning clock using biomarker proxies: ICC ~0.996, mean absolute error near 2 years.

•     BMI was the strongest driver of epigenetic age; higher omega-3 intake linked to younger age; ultra-processed foods, high resting heart rate and poor dental health to older.

Leveraging Glycans in Precision Longevity: From Individualized Monitoring to Targeted Intervention

18:20–18:40 · Canopy Hall

Gordan Lauc — Professor, University of Zagreb; Co-founder, GlycanAge

Key takeaway: IgG glycans are modifiable biomarkers that track biological age, predict disease years ahead and act as effectors of inflammation.

•     His lab has profiled glycans in >300,000 people across major cohorts.

•     Glycan profiles become more pro-inflammatory with age: linearly in men, while women are protected until menopause and then age rapidly.

•     Each additional year of GlycanAge corresponds to ~1% higher all-cause mortality hazard; largely additive to standard blood biomarkers and uncorrelated with epigenetic clocks.

•     Pro-inflammatory glycan changes appear up to a decade before diagnosis of diabetes, cardiovascular and inflammatory disease.

•     Weight loss and calorie restriction improve GlycanAge; hormone therapy reverses the perimenopausal rise in most women; metformin, SGLT2 inhibitors and GLP-1s help some but not all patients.

AI IN DRUG DISCOVERY FORUM — CEDAR GROVE (PARALLEL TRACK)

Session I: Super Intelligence & Computational Design in Drug Discovery

09:10–10:30 · Cedar Grove · AI in Drug Discovery Forum · Chair: Max Unfried, The Thalion Initiative

Prashanth Vishwanath — Director, AI/ML Biologics, Takeda

“From Targets to Biologics: AI Powering the Next Leap in Discovery at Takeda”

•     “Lab of the future”: agentic decision support, automation, ML-ready data and hybrid wet/dry-lab scientists.

•     AI agents score target viability across six dimensions: biology, translation, druggability, clinical, commercial and safety.

•     Generative design fixed an Fc-fusion protein’s aggregation and stability issues in two design cycles.

•     AI-guided preclinical design first asks whether existing data can answer the question, reducing animal use.

Alex Zhavoronkov — CEO, Insilico Medicine

“Aging-first Drug Discovery with MMAI and Longevity Foundation Models”

•     Aging clocks have evolved from “mechanical watches” (early epigenetic clocks) to multi-omic foundation models such as Insilico’s Precious GPT series.

•     Benchmark of 25,000 prompts across 18 frontier models: smaller fine-tuned models outperformed large LLMs on biological tasks.

•     Future: large orchestrator models coordinating many specialized agents for continuous research.

•     AI is validated only when it repeatedly yields successful drug candidates; ~$5M estimated to reach a developmental candidate.

Peter Clark — VP, Computational Drug Design, Novo Nordisk

“Therapeutic Discovery in the Agentic Era”

•     Agentic tools nearly doubled scientist bandwidth; reported hit rates of 20–60% depending on target interface.

•     Agents predict the best modality per target (e.g., small molecules for deep pockets, VHH or cyclic peptides for shallow interfaces); 60–70% faster time to portfolio entry.

•     Chat-based design system connecting ~300 applications.

•     Humans still decide on target nomination, synthesis, in vivo work and clinical development.

Alex Voda — CEO, Cat Health Company

“Reproducibility-Aware AI for Drug Discovery: Purrsistence as a Service”

•     Fraud and reproducibility index screens the literature; image manipulation estimated in ~10% of published studies.

•     Expanding DrugAge from ~1,000 to ~9,000 compounds.

•     Full-stack, in-house development without CROs; veterinary trials (1–2 years) as a faster route to validation.

•     Case: a 22-year-old cat with late-stage CKD improved substantially, with SDMA falling from 24 to ~13–14.

Session II: Large Scale Datasets to Feed Future AIs

10:45–11:45 · Cedar Grove · AI in Drug Discovery Forum · Chair: H.E. Sahia Ahmad, Dubai Department of Economy and Tourism

H.E. Sahia Ahmad — Dubai Department of Economy and Tourism; Dubai Longevity Authority

“Session introduction: Dubai’s role in advancing longevity and healthspan”

•     The Dubai Longevity Authority, established in 2026, aims to reduce friction from lab to patient without lowering standards.

•     Dubai’s population (~200 nationalities, ~90% international residents) enables validation across diverse groups.

•     AI in longevity needs privacy-preserving governance, representative data and shared standards and benchmarks.

Jon Gootenberg — Professor, Harvard

“Proteomic Clocks for Target Nomination”

•     Proteomics offers interpretable, organ-resolved signals that correlate strongly with age and disease risk.

•     Clocks built on biologically defined protein subsets transfer between UK Biobank and All of Us; organ clocks best predict related outcomes (e.g., heart clock for cardiovascular mortality).

•     Drug effects need careful interpretation: metformin raises clock age through GDF15 induction, a marker effect.

•     Mendelian randomization separates drivers from markers: GDF15 is strongly linked to mortality but appears non-causal, while FES and FURIN show causal evidence.

•     Clocks may serve as surrogate endpoints only after rigorous validation, since they can move without outcomes changing, and vice versa.

Joe Betts-LaCroix — CEO, Retro

“AI for rejuvenation & replacement therapies”

•     Two strategies: replacement (young HSCs, microglia) and rejuvenation in place, aiming to add ~10 healthy years.

•     An autophagy-restoring small molecule is in Phase 1 in Australia, with a Phase 2 in Alzheimer’s planned for 2027.

•     A generative protein model produced engineered reprogramming transcription factors with improved performance; ~50% functional hit rate, with variants up to ~80% dissimilar from wild type.

•     Proposed that the FDA run predictive models confidentially on undisclosed trials to build trust in AI predictions.

Max Unfried — Scientific Director, The Thalion Initiative

“Biomedical Mega Projects: The Necessary Infrastructure To Understand The Biology Of Aging and Maximum Lifespan”

•     Curing age-related diseases alone is unlikely to extend maximum human lifespan (~120 years).

•     Called for long-horizon, internationally funded “mega projects” on the scale of physics.

•     Thalion plans standardized tissue sampling across all organs from ~200 mammal species (~60 specimens per species, across ages) with multi-omics, to build an AI-ready comparative dataset.

What does AI in Longevity Biotech really need? And how can private capital markets and philanthropy fill this gap?

11:45–12:30 · Cedar Grove · AI in Drug Discovery Forum · Moderator: Uli Stilz, Flagship Pioneering

Panel — Youssof Mal (Hevolution), Sergey Jakimov (LongeVC), Martin Borch Jensen (Gordian Biotech), Todd White (The Thalion Initiative), Michelle Kwok (Draper Associates)

Key takeaway: AI alone is not a moat; investors want proprietary, human-relevant data, validated assets in specific indications and causal, longitudinal data generation.

•     Mal: a single healthspan biomarker is unlikely; a composite intrinsic capacity score, or an intrinsic capacity digital twin, is more feasible; federated cross-border training can avoid moving raw data.

•     Jakimov: AI is a standard tool; pure AI drug discovery companies without assets will become redundant; there is no investable “fighting aging” category, only specific indications.

•     Borch Jensen: stop building unvalidated models; ask a specific question, generate causal data (Gordian’s in vivo screens) and prove the model yields a useful medicine.

•     White: static, low-resolution snapshot data limits models; information density matters more than data volume; biobanks need future-proofing.

•     Kwok: met with 286 AI-bio companies in the past year; the “best model” is not a moat; backs proprietary data generation and in-house validation, and early, unconventional frontier bio ideas.

Session III: Targeting Neurodegeneration with AI

13:40–14:40 · Cedar Grove · AI in Drug Discovery Forum · Chair: Morten Scheibye-Knudsen, University of Copenhagen

Feixiong Cheng — Director, Genome Center, Cleveland Clinic

“AI4Cure-AD Platform for Alzheimer’s Disease Drug Development”

•     Combines human genetics and multi-omics, deep phenotypes, AI target prediction, EHR data and validation in iPSC neurons and organoids.

•     Single-cell atlas of >2,200 individuals and ~40 million nuclei.

•     AI flagged sildenafil for repurposing; EHR analysis linked it to 30–40% lower Alzheimer’s risk, leading to a Phase 2 trial.

•     Genetics pointed to EPHB2 as a causal target; editing in human iPSC neurons was neuroprotective and reduced tau hyperphosphorylation.

•     An EPHB2 inhibitor reduced amyloid and neuroinflammation in mice, completed Phase 1a and is in a ~30-person Phase 1b pilot focused on CSF and plasma biomarkers.

Jacqueline Lam — Visiting Associate Professor, University of Cambridge

“DeepDrugX for Alzheimer’s Disease Drug Discovery”

•     Causal AI platform seeks upstream “bottleneck genes” where inflammatory, metabolic and vascular pathways converge, and ranks drug combinations.

•     From 107 Alzheimer’s GWAS genes, a graph neural network ranked the top 50 approved drugs; in UK Biobank (~500,000 people), two blood pressure drugs and one statin were linked to lower odds of Alzheimer’s.

•     Reported link-prediction AUC of 0.98; independent groups have tested 11 of the top 20 candidates, four of which have entered human trials.

Gerald Lushington — Qnapsyn Biosciences Inc.

“LLMs to Flip the Script on Neuroimmune Aging Targets”

•     A human-led “committee” of LLMs from different vendors, with advocacy, counter-advocacy and devil’s-advocate rounds, to reduce confirmation bias.

•     Applied to the link between immunosenescence and neurocognitive decline, the process converged on thymic involution as a unifying driver.

•     Proposed targets around thymic epithelial cell biology (Foxn1/cTEC and AIRE/mTEC), upstream stress signaling and downstream proteostasis (PSMB11).

AI-enabled Next-Generation Targets in Neuro Aging

14:40–15:20 · Cedar Grove · AI in Drug Discovery Forum · Moderator: Iosif M. Gershteyn, ImmuVia

Panel — Derek M. Huffman (Albert Einstein College of Medicine), Feixiong Cheng (Cleveland Clinic), Mahdi Moqri (Harvard Medical School), Alexander Amini (Liquid AI)

Key takeaway: AI can help find neurodegeneration targets and biomarkers, but black-box behavior, siloed models and weak causal reasoning remain limits.

•     Huffman: use AI to prevent disease by targeting aging itself; models need single-cell CNS and longitudinal data; sex differences matter (e.g., low IGF-1 may benefit females but not males).

•     Cheng: EPHB2 took 3–4 years of lab validation; targets backed by human genetics have higher clinical success; network- and pathway-based methods make AI more explainable.

•     Moqri: AI-scientist tools matched or beat senior postdocs at predicting early Alzheimer’s signs from omics, but lack causal explanation; p-tau with APOE status and age is a leading early-detection candidate.

•     Amini: current models are siloed by biological scale; called for vertically integrated multimodal foundation models and both language-based and computational ways to decide when to trust them.

•     Discussion: AI is strongest at “one-to-ten” optimization rather than true “zero-to-one” discovery, and randomized trials remain the gold standard for causality.

Session IV: AI for Systems Immunology & Immune Aging

15:35–16:35 · Cedar Grove · AI in Drug Discovery Forum · Chair: Derya Unutmaz, Jackson Laboratory

Gang Liu — Director of Discovery Services, BioIntron

“RushData: High-Throughput Experimental Data for AI-Driven Antibody Discovery”

•     AI has made antibody hits abundant; wet-lab validation is now the bottleneck.

•     Tests ~3,000 sequences per batch in CHO-K1 cells; supernatant data in 7 days, purified-sample affinity and developability data in 14 days.

•     Built on a facility producing >150,000 antibodies per year; outputs structured for retraining AI models.

Jamie Heywood — CEO & Founder, Alden Scientific

“Reproducibility and scale bound Individual Physiology AI: integrating genomic, antibody, protein and clinical data over time”

•     ~60,000 integrated samples, including ~3,000 replicates to quantify measurement variance; better sample handling reduced replicate CV from 33% to 23%.

•     Of the clocks tested, a protein age model was most accurate (~0.94) but offered little actionable guidance; glycan age tracked trajectory rather than position.

•     First antibody-based age clock built on 1,600 antigens in ~2,500 people.

•     UK Biobank variation compresses to ~256 latent variables; >90% of signal in his cohorts sits in core proteomic assays.

Immunity as the Longevity Lever: What AI can see in the aging immune system, and what we can do about it

16:35–17:20 · Cedar Grove · AI in Drug Discovery Forum · Moderator: Derya Unutmaz, Jackson Laboratory

Panel — Andrea Cipriano (Eli Lilly / Stanford), Tina Ziainia (Human Longevity), Fiona Miller (quadraScope Ventures), Xian Zeng (Byterna Therapeutics)

Key takeaway: Immune aging is central to age-related disease but hard to measure; functional readouts currently beat omics clocks.

•     Unutmaz: immune cells do not “retire” but become dysregulated; naive T cell decline tracks with all-cause mortality; CRP is only a crude proxy.

•     Cipriano (personal capacity): defines immune aging as loss of function and resilience; proteomic clocks trained on chronological age are not reliable for immune rejuvenation; prefers functional readouts such as vaccine response.

•     Ziainia: clocks can mislead if major disease is missed; sex differences and menopause shape immune trajectories; more evidence needed on hormone therapy’s immune effects.

•     Miller: invests across the hallmarks of aging (14 portfolio companies) with the immune system as a central driver; science must connect to economic value.

•     Zeng: AI-designed in vivo CAR-T using circular RNA and LNP delivery; AI needed to define targets for cell states such as senescence.

•     Jamie Heywood also contributed, arguing for “distance to adverse outcome” metrics over age correlation.

Session V: Accelerating Translational Longevity Research Through Artificial Intelligence

17:35–18:35 · Cedar Grove · AI in Drug Discovery Forum · Chair: Max Unfried, The Thalion Initiative

Derya Unutmaz — Professor, Jackson Laboratory for Genomic Medicine

“How AI can help defeat aging: Roadmaps, breakthroughs and what’s next”

•     Four pillars: high-dimensional data, clinical digitization, AI and lab automation.

•     Goal: probabilistic digital twins enabling in silico trials on millions of virtual patients.

•     Predicts virtual cells and digital twins within 5–10 years and “longevity escape velocity” within 10–15 years.

•     Argued regulators should account for the “lost potential” of approval delays.

Kia Winslow — Sr. Director, BioAge

“BioLens: An LLM-Enabled Literature Database for Systematic Analysis of Mouse Lifespan Research”

•     LLM pipeline screened ~270,000 PubMed records to ~3,300 papers with Kaplan-Meier plots; database covers ~1,200 papers, including negative results.

•     ~70% of interventions genetic, ~20% pharmacological; >70% in B6 mice and >90% include males; accelerated-aging models tend to overstate life extension.

•     Average median lifespan gains: ~16% genetic, ~11% pharmacological; robust, replicated pharmacological findings come largely from the ITP.

•     Database is public and downloadable.

Salah Mahmoudi — CEO, SAISHO

“AlphaForge predicts clinical outcomes through multi-domain scientific reasoning”

•     Predicts clinical success and primary failure drivers from structure, target and disease alone.

•     Retrospective AUC 0.90 on 391 small-molecule programs; prospective AUC 0.886 on 83 programs after the model was frozen in January 2025.

•     Reported to outperform general LLMs by ≥29 points; identifies the primary failure reason in most cases (e.g., liver toxicity of sitaxentan).

•     Performance similar in trials of patients over 60.





* * ~


ARDD 2026 — Day Three Recap



ARDD 2026 — Day Three Recap

ARDD 2026 <event-noreply@whova.io>Sun, Oct 4, 2026 at 4:29 AM
Reply-To: stephanie@insilicomedicine.com
To: president@worlduniversityandschool.org
13th Aging Research and Drug Discovery Meeting

Dear Scott Gordon Kenneth MacLeod,

I hope you all got some good rest last night and enjoyed the last day of ARDD 2026!

ARDD 2026 — Day Three Recap

Aging Research and Drug Discovery Meeting · Saturday, October 3, 2026 · David Rubenstein Treehouse, Harvard University, Cambridge, MA

 

Chair Opening Introduction

09:00–09:15 · Canopy Hall

Chairs: Alex Zhavoronkov, Vadim Gladyshev, Morten Scheibye-Knudsen, Daniela Bakula and Jesse Poganik. (Not captured in the notes.)

Morning Talks

09:15–10:15 · Canopy Hall

The 09:15–09:35 slot is listed on the agenda as "Speaker TBC"; no notes match it (see the cross-check section at the end).

Vadim Gladyshev — Professor, Harvard Medical School

09:35–09:55 · Measuring, targeting and understanding aging (no title on the agenda; topic from the notes)

Key takeaway: Aging should be modeled as systemic biological states using multimodal, multispecies, longitudinal data; actionable biomarkers such as transcriptomic clocks can find interventions that lower biological age even while the underlying trajectory continues.

•     Three intervention tiers: physiological remodeling for modest lifespan gains (near term); time-targeted, organ-specific interventions before disease; radical extension by breaking systemic barriers (e.g., coordinated tissue replacement).

•     In silico-to-in vivo pipeline: ~4,000 compounds screened computationally, profiled in cells, then tested in mice; of 10 advanced, 5 extended lifespan, and short 5-day dosing improved frailty (Anastasia Shindyapina's work, under review).

•     Transcriptomic clocks predict age and time-to-death and replicate across mouse, rat, macaque and human; TACO is a public tool that runs them across datasets with cross-platform normalization.

•     Multi-agent mining of GEO-scale data: most perturbations raise biological age; rare rejuvenating hits were validated, including a compound that lowered biological age and frailty over 3 months in old mice.

•     Heterochronic heart transplantation: a young heart in an old host ages faster, an old heart in a young host rejuvenates; human donor data agree, supporting wider use of older donor hearts. One transplanted organ barely changed systemic age.

•     ~50 clocks for organs, cell types and organelles; models now span up to eight modalities (transcriptomics, proteomics, metabolomics, MRI, DEXA, retinal imaging, EHR, plus voice, photo and video).

•     Menopause time-to-event clocks show a sharp transition around age 50, with no analogous pattern in men.

•     Q&A: cross-platform bias persists but shrinks with larger datasets; immune infiltration is a fair concern for the heart data, but single-cell imaging suggests the heart cells themselves rejuvenate.

Mark Cobbold — SVP IO Discovery & Cell Therapy Oncology, AstraZeneca

09:55–10:15 · Genetic strategies to prevent T cell senescence for scalable allogeneic CAR T (topic from the notes)

Key takeaway: Knocking out CDKN2A, CDKN2B and MTAP together prevents replicative senescence in T and NK cells, potentially enabling off-the-shelf CAR T at massive scale from a single donor.

•     Autologous CAR T has treated ~80–90k patients but is too infrastructure-heavy for common autoimmune diseases (lupus, RA, MS) now in CAR T trials.

•     Borrowing from tumor biology: genomics of 21 T-cell lines and lentiviral screens in donor T cells pointed to the chromosome 9p locus (CDKN2A/B, MTAP), often co-deleted in T-cell malignancies.

•     Triple knockout in CD8, CD4, γδ T and NK cells turned limited proliferators into cells expanding up to ~10^20-fold; lower β-gal, higher Ki-67; all three knockouts together performed best.

•     Combined with allogeneic safety edits (HLA and TCR knockouts) in a "universal" cell platform.

•     Safety: no accumulation of deleterious mutations across runs; in mice, edited cells did not persist without cytokines and were rejected after weeks.

•     HER2 (solid tumor) and BCMA (myeloma) CARs controlled patient-derived xenografts as well as standard CAR T; ~10^9-fold expansion could treat thousands per batch, ~10^20-fold potentially millions.

•     Q&A: iPSC-derived T cells are hard to turn into authentic cytotoxic T cells, so gene editing was chosen over Yamanaka reprogramming; every T-cell subset tested responded to the edits.

Search & Evaluation Strategies for Longevity Therapeutics

10:15–11:00 · Canopy Hall · Panel

Lisa Melton (moderator) — Senior News Editor, Nature Biotechnology

Key takeaway: A "longevity" indication does not exist yet; the practical path is to win approval in a specific age-related disease and use it as a foothold to gather evidence of broader effects on aging.

•     Panelists: Thomas Marron (Eli Lilly), Jason Sanders (GSK), Tala Fakhouri (Parexel) and Zachary Cary (Takeda).

•     Tala Fakhouri:

–   Regulators are more engaged and open to real-world evidence for confirmatory purposes; aging endpoints need pre-competitive consortia.

–   AI can help build new biomarkers, ingest multimodal data and run digital-twin simulations, since 60-year studies are not feasible.

–   The science can take a systems view, but regulation still requires a single approvable indication first.

•     Jason Sanders:

–   Useful biomarkers must predict dynamic clinical outcomes (like the ASCVD risk score), not chronological age.

–   Even systemic approaches need specificity (senescent-cell clearance acts body-wide but targets one cell type); claims of working "all over the body" are a red flag.

–   Understanding healthy aging means deeply phenotyping adults aged ~40–90, not studying centenarians; the field lacks a strong model of "normal aging" and access to living human tissue is a bottleneck.

•     Thomas Marron: regulators and payers will get comfortable with new biomarkers gradually, from data collected alongside trials (as in IPF); for senolytics the question is still which indication can be approved and reimbursed.

•     Zachary Cary: unvalidated biomarkers add risk to an already expensive process; a drug must meet a clear unmet need to be reimbursed.

•     Target-based vs. systems biology is "and, not or"; advice to startups was to follow human biology (e.g., telomere disorders hit specific organs such as marrow and lung).

Panel: Metabolic Health and Longevity by Nestlé Research

11:30–12:10 · Canopy Hall · Panel

Philipp Gut (moderator) — Adult Health Lead and Research Lead Healthy Longevity, Nestlé Research

Key takeaway: GLP-1 drugs are transforming metabolic health, but nutrition, resistance exercise and individualized digital measurement are needed to protect lean mass and personalize response.

•     Panelists: Ryan Carvalho (Head of Nestlé Research), Calum MacRae (Mass General Brigham), Giulia Menichetti (Harvard Medical School) and Brianna Stubbs (Buck Institute).

•     Calum MacRae:

–   GLP-1 benefits reach beyond weight (cardiac, renal, inflammatory) and some appear before weight loss; one patient reported a 98% improvement in arthritis within a week.

–   Responses vary widely (lean vs. fat loss), so mechanism must be understood at the individual level; phones, wearables and even purchases can quantify health reserves.

•     Ryan Carvalho:

–   Nutrient needs persist or rise on GLP-1s; protein and amino-acid advice should be stratified (e.g., older adults with sarcopenia vs. postmenopausal women).

–   Million Veteran Program data (2026, Lancet family journal): healthy diet and lifestyle further reduce cardiovascular events during GLP-1 weight loss.

–   "Nutritional dark matter": food compounds missing from databases, some modulating GLP-1 pathways via bitter and xenobiotic receptors; microbiome function matters more than diversity.

–   With ~1 dietitian per 4,000 people in the U.S., AI tools that infer diet from blood metabolomics are needed.

•     Brianna Stubbs: resistance training attenuates GLP-1 lean-mass loss; an ARPA-H ProSPR-funded project (with Mike Snyder and David Furman) is building at-home intrinsic capacity measures to catch declines as early as the mid-40s, framing intrinsic capacity as a "vital sign."

•     Giulia Menichetti asked whether food labels could one day describe effects on molecular pathways; Carvalho said the data gap between model foods and branded products, plus the food "matrix effect," makes that hard.

Semaglutide and Healthspan: Decoding the Emerging Evidence

12:10–12:30 · Canopy Hall

Alejandro Aguayo-Orozco — Senior Scientific Director Diabetes Insights, Novo Nordisk

"From clinical outcomes to organ-specific biological age"

Key takeaway: Across major trials, semaglutide lowered proteomic organ-age scores, and the later effects are only partly explained by weight loss.

•     Outcome data from ~32,000 patients (SELECT, STEP-HFpEF, FLOW, SOUL): 20% MACE reduction in non-diabetic SELECT; 24% kidney composite reduction in FLOW (stopped early for efficacy); 18% lower all-cause mortality in a pooled six-trial analysis.

•     Proteomics from five trials: lower heart and kidney age scores from the earliest timepoint, broadening to multiple organs over time.

•     Organ-age reductions were not mediated by weight, HbA1c or hsCRP; the heart-age reduction mediated up to 40% of the reduction in cardiovascular death.

•     Early adipose signature paradoxically looks "older" during rapid weight loss and up-titration (leptin, FABP4), then turns neutral or better; a proteomic frailty score was lower from one year onward.

•     No clear dose dependence across doses and formulations (including oral); no data on microdosing; EVOKE (Alzheimer's) lean-cohort data not yet analyzed; glucose homeostasis as a mediator under study.

•     Sensitivity analyses show most clock proteins move coherently, not a few heavily weighted ones.

Panel: Aging Research in Pharma

13:30–14:10 · Canopy Hall · Panel

Sri Devi Narasimhan (moderator) — Deputy Editor, Cell Press

Key takeaway: Geroscience needs shared definitions, foundational discovery, functional trial endpoints and close academia–industry collaboration to overcome biological heterogeneity.

•     Panelists: Sophie Lemire-Brachat (Novartis), Maria Dermit (Novo Nordisk) and William Mair (Harvard).

•     Definitions: Dermit separates "aging" (biology) from "health" (patient-centric); Lemire-Brachat frames aging as functional decline across systems and calls for aligned data ontologies; Mair distinguishes gerontology from geroscience, which treats aging as a modifiable risk factor.

•     William Mair:

–   Discovery science not tied to profit is indispensable (GLP-1 traced to venom proteins, CRISPR to bacterial defense).

–   Preclinical results fail to translate because of heterogeneity (microbiome, environment, sex, strain) and incentives that reward discovery over validation.

–   Even mTOR/rapamycin is poorly understood; chronic inhibition may "break the system" rather than mimic youth. Psychosocial factors robustly affect aging biology. There is no single "golden window" for intervening.

•     Sophie Lemire-Brachat: human genetics and ultra-rare protective variants will reveal new mechanisms; multimodal data enables digital twins; objective endpoints need work (e.g., refining the six-minute walk test).

•     Maria Dermit: longevity claims need mortality, functional and validated clock evidence; AI speeds preclinical work but needs human oversight; personalization means matching indication, population and modality.

•     Consensus: Phase 2 success requires hard functional outcomes, surrogates alone are insufficient, and non-competitive consortia should be encouraged.

Therapeutic Assets & Licensing (Late Stage)

14:10–14:50 · Canopy Hall · Panel

Cailin McGurk (moderator) — Managing Director, Morgan Stanley

Key takeaway: Large longevity deals will follow translational confidence and regulatory clarity; until then, upfront payments stay modest.

•     Panelists: Mark Cobbold (AstraZeneca) and Phil McGurk (SVP, Head of Global Business Development, Takeda).

•     Mark Cobbold:

–   Early in vivo CAR T data showing robust expansion without lymphodepletion "rewrote the rules" and drove a rapid acquisition; internal champions mobilize organizations.

–   Expects genomic and epigenomic medicines to matter more than small molecules for aging; called aging the "mother of all diseases" and predicted a GLP-1-style frenzy for assets once the science matures.

–   Thinks China is likely to lead, given scale, sustained investment and long-term planning; prevention does not break pharma's model (the vaccine precedent).

•     Phil McGurk:

–   Allocate each risk to the party best placed to manage it; contrasted M&A (acquirer absorbs risk) with licensing (shared risk, milestones, royalties).

–   Best deals are championed by credible R&D leaders, not BD alone or top-down mandates.

–   Cited Takeda's orexin agonist program as a long academia–industry effort (described as the first orexin agonist approval after more than 20 years of research, starting in narcolepsy type 1 with broader indications possible).

•     Cailin McGurk: pharma partners in a "barbell," very early or very late; big upfronts go to validated biology (e.g., KRAS molecular glues, oral GLP-1s); for longevity, translation confidence is the main barrier.

•     Q&A: pharma–pharma pre-competitive consortia exist; results are mixed but they produce useful side insights.

In Vivo Validation Across the Target Landscape

14:50–15:10 · Canopy Hall

Martin Borch Jensen — Co-Founder & CSO, Gordian Biotechnology

Key takeaway: Mosaic in vivo screens with single-cell readouts map each target's effects across organs, de-risking target selection before committing to a drug.

•     AI lacks ground-truth biology; Gordian's aim is to scale in vivo validation.

•     Mosaic screens: low-dose AAV libraries up- or down-regulate single genes in scattered cells within an intact animal; single-cell transcriptomics compares perturbed cells with internal controls, then overlays human disease and healthy signatures.

•     Osteoarthritis: screens in horses with spontaneous OA (hundreds of targets per animal); validated in human tissue co-cultures and aged, obese mice; program now in IND-enabling studies.

•     Weight loss: one target gave ~10% weight loss alone; with semaglutide it deepened loss and prevented rebound for at least two months after semaglutide stopped; now in small-molecule lead optimization. Mechanism (increased lipolysis) confirmed in human adipocytes.

•     Cross-organ safety: the same target inhibited glycolysis in cardiomyocytes, flagging possible fibrosis risk and informing systemic vs. targeted delivery.

•     Q&A: robots for in vivo handling likely within ~3 years; a 10x jump in research capacity possible in the early 2030s.

Reversing Metabolic Decline Through AMPK Network Activation in Humans

15:10–15:30 · Canopy Hall

James Peyer — Cambrian Bio (listed on the agenda as "CB, Cambrian Bio")

Key takeaway: ATX-304 was presented as the first AMPK activator to translate into humans, raising metabolic rate and improving cardiometabolic markers with placebo-like safety.

•     Earlier AMPK approaches failed: metformin (complex I stress), Merck's MK-8722 (cardiac glycogen buildup), DNP-type uncouplers (metabolic collapse), AICAR (poor pharmacokinetics).

•     ATX-304, from a phenotypic screen in Umeå, raises both glucose uptake and mitochondrial demand without lowering ATP or building glycogen; drives mitochondrial biogenesis (believed ANT1-dependent).

•     Mice: in aged lean animals, ~30% higher cardiac output and more than double treadmill endurance after 8 weeks; in obese mice, ~20% weight loss in a month without eating less or losing lean mass; 30% in 11 days with semaglutide; continued loss after semaglutide stopped despite eating 30% more.

•     Phase 1: 23 subjects (2:1), 8 weeks plus 8-week open-label at 400 mg/day; placebo-like safety, no overheating; higher resting metabolic rate, large adiponectin rise, lower triglycerides, liver fat and visceral fat.

•     Up to six trials planned for 2027 (monotherapy, with semaglutide, fatty liver), then intrinsic capacity and broader metabolic decline.

•     Q&A: almost no blood-brain barrier penetration; no human weight-loss data yet.

Therapeutic Assets & Licensing (Early Stage)

16:00–16:40 · Canopy Hall · Panel

Brianna Stubbs (moderator) — Research Assistant Professor & Director of Translational Science, Buck Institute

Key takeaway: For pharma, "proof of concept" is not one milestone but a body of evidence that an asset can be best-in-class against a specific, high-value target product profile.

•     Panelists: Jonathan Levi (AstraZeneca), Claris Munksgaard (EMD Serono), Nikolaj Kulahin Roed (Novo Nordisk), David Berry (Averin Capital) and Avi Spier (Novartis).

•     Jonathan Levi: "validated" must be specific; a hit from a transcriptomic clock is not enough without a clear line of sight to an indication (AstraZeneca's "5R" framework). Study the partner's pipeline and propose concrete combination plays.

•     Avi Spier: proof of concept means showing an asset can beat the competition and become the new standard of care.

•     David Berry:

–   VCs need 10x+ returns; a preclinical partnership is a ~5-year "wedding," so trust and cultural fit matter.

–   IP is paramount, pharma will exploit any holes; bring both cutting-edge human data and the conventional mouse data conservative reviewers still expect.

–   Proposed a shared, AI-enabled data room for dynamic asset comparisons, since each static diligence can cost $1–3M.

•     Nikolaj Kulahin Roed: the "totality of data" (human genetics, animal data, safety) decides; package longevity assets inside established indications and flag cross-aging signals (e.g., pain, hearing loss) without spreading too thin.

•     Claris Munksgaard: rigor (gold-standard models, no cherry-picking), clean PK, safety and target engagement, clear differentiation and a credible path to IND and label; indications must be commercially compatible (a high-price rare disease and a low-price broad indication do not add up). AI tools such as AlphaSense speed commercial assessment, but AI-integrated data rooms remain aspirational.

What Can Be Done to the Aging Brain: Why Live Long When the Brain Is Gone?

16:40–17:00 · Canopy Hall

Johan Luthman — EVP R&D, Lundbeck

Key takeaway: Amyloid clearance and behavioral-symptom drugs are progress, but disease modification, prevention and biomarkers for other proteinopathies remain major unmet needs.

•     The brain ages on a largely fixed set of neurons; cortical loss and microbleeds accelerate around 60–65; no drugs target the "frail brain," and sleep is a key modifiable factor.

•     Anti-amyloid antibodies clear amyloid but slow progression only ~25–35%, a benefit patients do not readily feel; prevention trials in biomarker-positive, asymptomatic people are under way.

•     Blood biomarkers are transforming Alzheimer's diagnosis, reducing reliance on PET and CSF.

•     A program with Otsuka produced the first approved drug for agitation in Alzheimer's.

•     Biomarkers are lacking for tau and α-synuclein; tau antibodies disappointed while antisense shows promise; antisense works strikingly in SOD1 ALS; an anti-α-synuclein antibody is in Phase 3 for multiple system atrophy, chosen for its relatively pure pathology and fast progression.

•     Advocated Bayesian adaptive trial designs; credited Oskar Fischer and Solomon Carter Fuller as co-discoverers of Alzheimer's pathology.

Preserving and Restoring the Thymus for Healthspan Extension

17:00–17:20 · Canopy Hall

Francisco Leon — Tolerance Bio (listed on the agenda as "TB, Tolerance Bio")

Key takeaway: Thymic involution is a key driver of immune aging; Tolerance Bio aims to preserve the thymus with anti-IL-33 and regenerate it with IL-7.

•     A 2023 Harvard study found more cancer and autoimmunity after adult thymectomy.

•     Residual thymic function correlates with survival in older people and with epigenetic clocks (GrimAge); centenarians often keep good thymic function, and naked mole rats keep their thymus; an AI model scores thymus health from CT scans.

•     Preservation: an anti-IL-33 antibody for people with a functioning thymus. Regeneration: IL-7 for those with little left.

•     In HIV (a model of accelerated immune aging), IL-7 raises naive T cells, recent thymic emigrants and TCR diversity; restoring CD4 counts in HIV is a near-term approvable indication, run in parallel with aging trials.

•     In Alzheimer's mouse models, boosting thymic function improved cognition ~50% by helping T cells clear plaques; exploring iPSC-derived thymus and LNP delivery.

Removing Oxidized Cholesterol

17:20–17:40 · Canopy Hall

Matthew O'Connor — CEO, Cyclarity Therapeutics

"Clinical Trials for a New Approach to Cardiometabolic and Age-Related Disease"

Key takeaway: An engineered cyclodextrin dimer selectively clears oxidized cholesterol and reverses foam cells; Phase 1 showed excellent safety and dose-dependent target engagement.

•     Hypothesis: 7-ketocholesterol accumulates with age and turns macrophages into plaque-building foam cells.

•     The drug is a cyclodextrin dimer (>1,000 Da but regulated as a small molecule), designed with computational chemistry and AI to prefer oxidized over native cholesterol; the complex is cleared by the kidneys.

•     Preclinically, it reverses the foam-cell phenotype and restores reverse cholesterol transport.

•     Phase 1a (SAD/MAD, 72 healthy volunteers): "extraordinarily safe," ~3-hour half-life, dose-dependent rise in urinary oxidized cholesterol.

•     Phase 1b is dosing coronary artery disease patients with CT angiography; an international Phase 2 is planned. A 1% plaque reduction may mean ~20% fewer cardiovascular events; the goal is 5–10%.

•     Unpublished: partial rescue of fatty liver in rodents, doubled with another approved drug; a fatty-liver Phase 1b is under consideration.

ARTAN Bio: One Codon Therapy for Multiple Aging Diseases

17:40–18:00 · Canopy Hall

Brian Bodemann — CEO, ARTAN Bio

Key takeaway: One engineered suppressor tRNA could restore full-length protein at tens of thousands of age-associated CGA-to-stop mutation sites, treating a whole class of somatic mutations at once.

•     Deamination of methylated cytosine turns CGA (arginine) into TGA (stop): ~68,000 susceptible sites in ~16,000 genes, ~30% of somatic premature stops, reaching ~1 in 9 cells by age 80; UV accelerates it.

•     A suppressor tRNA inserts arginine at the premature UGA; tRNAs need no tissue-specific promoters.

•     AAV9 test-bed program reached all six tested mouse organs without significant toxicity and restored full-length p53 in Calu-6 cells.

•     Lentiviral HSC program: up to ~90% transduction of primary human HSCs; aiming for IND-enabling studies in 2027 in clonal hematopoiesis (~240,000 identifiable U.S. patients; drivers enriched 3.7x after chemotherapy).

•     A topical LNP for sun-exposed skin is planned as a cosmetic product.

•     Early science funded through VitaDAO's VitaRNA token (~$1M raised from the community).

Talk: David Sinclair

18:00–18:20 · Canopy Hall

David Sinclair — Professor, Harvard Medical School

NAD boosting and epigenetic restoration (no title on the agenda; topic from the notes)

Key takeaway: Two fronts: newly described NAD-consuming structures in aging cells, and OSK gene therapy plus the chemical cocktail SL100 reversing aging markers in animals.

•     Information theory of aging: DNA damage redeploys epigenetic modifiers, eroding cell identity; cells retain a backup of their youthful state.

•     NAD: the lab describes a new structure in aging cells (transcribed as "inflammasomes") that consumes NAD via PARP14 and drives inflammation; inhibiting PARP14 is a candidate way to raise NAD.

•     OSK restored vision in old mice and primates; first results from the ER-100 trial in glaucoma and NAION were expected around October 9, 2026.

•     Unpublished: OSK slowed and killed several cancer cell lines by re-differentiating them; xenograft tumors shrank or grew more slowly.

•     SL100, from a screen described as 80 billion molecules, preserved neurite length in ALS models and, in a progeroid mouse model, extended mean lifespan 25% and maximum lifespan 33%.

•     Q&A: SL100's downstream pathways overlap little with OSK's; the lab studies ECM glycation; pairing a senolytic with an NAD booster is logical but timing is unknown; a forthcoming paper shows chronic oral NMN extended lifespan in female mice.

Talk: Morten Scheibye-Knudsen

18:20–18:40 · Canopy Hall

Morten Scheibye-Knudsen — Professor, University of Copenhagen

Quantifying and targeting aging phenotypes driven by DNA damage (topic from the notes)

Key takeaway: Phenotypic biomarkers from photos and cell morphology predict hard outcomes, and compounds that trigger DNA-damage signaling without damage reversed senescence and rescued Alzheimer's-model mice.

•     Facial photos predict survival better than some clinical measures; a morphology classifier identifies senescent cells in skin and blood; very low skin senescence predicted higher future cancer risk.

•     People living at higher altitude in Ethiopia had fewer circulating senescent cells.

•     Single-cell data suggest most somatic mutations arise during development, so point mutations may not drive degenerative aging outside cancer.

•     DNA-damage signaling depletes NAD (countered by PARP1 inhibition or NR); in a COPD pilot, NR lowered lung inflammatory cytokines.

•     A screen for compounds that stimulate the damage response without damage found "Drug F," which reversed senescence markers and improved motor function in flies; a spinout is advancing it.

•     In 5xFAD and APP/PS1 mice, Drug F rescued learning and motor deficits and reversed weight loss; clinical trials may follow.

Closing Remarks

18:40–19:00 · Canopy Hall

Not captured in the notes. Followed by open-bar networking from 19:00.

Pet and Animal Longevity Forum — Session I: Canine Aging

09:00–10:30 · Cedar Grove · Parallel track

Opening Remarks & Welcome (09:00–09:10): Max Unfried, Scientific Director, The Thalion Initiative. (Not captured in the notes.)

Dan Promislow — Senior Scientist and Scientific Advisor, HNRCA Tufts University

09:10–09:30 · "The Companion Dog as a Translational Model of Aging"

Key takeaway: The Dog Aging Project bridges lab models and humans, and its findings translate: dog mortality markers predicted human mortality from far less follow-up.

•     More than 55,000 dogs enrolled since 2020; a Precision Cohort of ~1,000 dogs gives annual biospecimens; data shared via the Broad's Terra.

•     NIA renewed funding for five more years; a new cohort of ~1,000 of the oldest U.S. dogs will get 30x genomes; the Precision Cohort could grow to 3,000 and add transcriptome, proteome and lipidome with more support.

•     Dogs with lower epigenetic age live longer; genes hypomethylated with age in dogs tend to rise in expression in aging humans.

•     25 metabolites (enriched for kidney markers) predict mortality in dogs and in the same direction in humans, found with 2.6 years of follow-up vs. 8–25 in human studies.

•     GWAS linked a chromosome 25 SNP to kynurenic acid; coat "furnishing" genes (RSPO2, FGF5) also shift cystathionine, a cysteine precursor.

•     TRIAD rapamycin trial: target 580 dogs (≥7 years, >40 lb), over half enrolled, one year of drug and three years of follow-up, neurology and cardiology arms; safety excellent, efficacy in ~4 years.

•     Q&A: U.S. dogs are mostly sterilized, so intact-dog studies may suit France or Germany; owners skew white, wealthy and educated; no experimental drugs in owners' pets without lab-dog safety data.

Steve Horvath — Professor, UCLA

09:30–09:50 · "Surrogate endpoints for veterinary geroprotector trials: the case for methylation clocks"

Key takeaway: DNA methylation clocks are the strongest candidates for surrogate endpoints in veterinary longevity trials, which could speed conditional approval of geroprotectors for dogs.

•     Lifespan endpoints are impractical (the 14-year Purina Labrador calorie-restriction study); FDA's Center for Veterinary Medicine allows conditional approval on a "reasonable expectation of effectiveness."

•     A surrogate must predict survival and mediate the treatment effect (like LDL); methylation clocks are accurate, stable, mortality-predictive, responsive (GLP-1, calorie restriction) and conserved.

•     The Mammalian Methylation Array measures ~36,000 conserved CpGs; >15,000 samples from 348 species are public; dual human–dog clocks estimate relative age across species.

•     In the Purina study, clocks detected the benefit of calorie restriction seven years before the survival readout, more strongly in females.

•     A clock built on 742 dogs from 93 breeds was accurate but showed no breed differences in aging rate, perhaps because the array targets ultra-conserved sites.

•     Castration lowers epigenetic age in sheep; a single-CpG "androgen clock" tracks cumulative androgen exposure.

•     Q&A: the field needs "causal clocks" (a Mendelian-randomization-style approach); CpGs that predict a species' maximum lifespan do not overlap with those that track age; a turtle clock paper was days from publication.

Vicky Yang — Associate Professor, Tufts University

09:50–10:10 · "Mitral valve prolapse: studying aging-associated cardiac changes in the dog model"

Key takeaway: Canine myxomatous mitral valve disease is driven by a macrophage–fibroblast feedback loop, offering targets that translate to human mitral valve prolapse.

•     Common in small breeds: murmurs at 3–5 years, heart failure at 8–10, survival ~1 year after; surgery is costly and rare for dogs.

•     Valve interstitial cells become myofibroblasts; the disease is polygenic in dogs and humans.

•     Pro-fibrotic M2 (CD206+) macrophages increase, with TGF-β-linked signaling and higher pERK.

•     Extracellular vesicles carry miR-145 (from diseased valves) and miR-125b (from M2 macrophages), both activating fibroblasts.

•     Targets: M2 macrophages, EV signaling, MEK–ERK (current MEK inhibitors are too toxic).

•     Q&A: mechanical stress likely recruits monocytes; the disease is distinct from checkpoint-inhibitor myocarditis.

Philipp Gut — Adult Health Lead, Nestlé Research

10:10–10:30 · "Nutrition to slow biological aging in dogs"

Key takeaway: Phenotypic and epigenetic clocks respond to diet and predict outcomes in dogs, making them practical endpoints for longevity nutrition trials.

•     Used biobanked samples from Purina's 14-year calorie-restriction study.

•     A dog PhenoAge from routine chemistry predicts mortality and flags accelerated aging even within normal ranges; lean-fed dogs were biologically younger at mid-life.

•     Golden Retriever Lifetime Study (Morris Animal Foundation): more time overweight meant older biological age and more osteoarthritis; in an unpublished trial, a weight-loss diet normalized biological age within six months.

•     An EM-seq epigenetic clock tracks age and mortality, classifies breeds, detected calorie restriction earlier than PhenoAge, and was already elevated in dogs that later developed osteoarthritis; healthy "super seniors" were younger.

•     Moving from blood to buccal swabs; effects were significant in both sexes, stronger in females.

•     Urged industry to agree on "good enough" standard clocks for trials, with next-generation clocks as exploratory endpoints.

Pet and Animal Longevity Forum — Session II: Commercializing Pet Longevity

10:45–12:20 · Cedar Grove · Parallel track

Anna Skaya & Garri Zmudze — General Partners, AniVC

10:45–11:05 · Fireside chat: "From Shark Tank to a 9-Figure Exit: Building, Selling, and Backing Animal Longevity"

Key takeaway: Pet "humanization" is driving demand, but early-stage animal health remains underfunded; AniVC backs strong founders with human-grade products and therapeutics.

•     Skaya founded Basepaws (pet genomics, 2016), appeared on Shark Tank and sold it to Zoetis for "close to nine figures"; Zmudze was an early backer. She reinvested proceeds into AniVC.

•     Theses: founders first; "pet parenting" over pet ownership; real longevity innovation (therapeutics, AI drug discovery) without overclaiming; the animal regulatory path is an advantage.

•     Cancer needs diagnostics first; many clinics lack imaging, so human diagnostic tech could translate.

•     Audience: Lou Hawthorne said pet owners consistently ranked "fix cancer" above cloning or general longevity.

•     Practical: daily brushing remains the best dental prevention; no diabetes investments yet for lack of innovation.

Kevin Esch — EVP and President R&D, Zoetis

11:05–11:25 · "A Lifetime of Care for More Healthy Years"

Key takeaway: Pets are living longer, so veterinary medicine must shift to earlier detection and long-term management of chronic disease through genetics, diagnostics and therapeutics.

•     Zoetis "Prevent, Detect, Treat" continuum, with genetics from the Basepaws acquisition; goals include predicting progression (e.g., feline CKD) and treatment response.

•     Osteoarthritis pain affects ~40% of dogs and ~60% of cats (Librela, Solensia); longer-acting antibodies and later disease-modifying agents in development.

•     CKD is underdiagnosed early; cancer is the leading cause of death in dogs; obesity needs holistic management.

•     Anxiety drives pet surrenders; a non-sedative anxiolytic is planned for 2027.

•     Markets are built by demonstrating superior care, as JAK inhibitors did in dermatology.

Graeme Bainbridge — Senior Principal Scientist, Dechra

11:25–11:45 · "Feline Longevity: How an Animal Pharma company thinks about chronic diseases and Quality of Life"

Key takeaway: For cats, the goal is healthspan: shifting from symptom management to disease-modifying treatment of chronic disease.

•     More than 80 million pet cats in the U.S.; CKD affects 50% of cats over 10, hyperthyroidism 10% of seniors, and 60% of cats over 6 show osteoarthritis.

•     Barriers: multimorbidity, subtle onset, symptom-focused drugs, few validated biomarkers vs. dogs, and difficulty getting cats to the vet.

•     Monoclonal antibodies are promising; biological-age biomarkers could transform trials; oral inflammation is an overlooked contributor to CKD.

•     Q&A: feline CKD looks different from human and canine disease (possibly inflammation- or infection-driven); finding progressors for trials is key.

Panel: The Pet Longevity Revolution

11:45–12:20 · Cedar Grove · Panel

Anna Skaya (moderator) — General Partner, AniVC

Key takeaway: Pet longevity is large and underserved, but vet time, trial costs and public awareness are the bottlenecks.

•     Panelists: Dan Promislow (Tufts), Julie K. Spears (Nestlé Purina PetCare), Kevin Esch (Zoetis) and Alex Voda (CEO, Cat Health Company).

•     Alex Voda: in an early CKD proof-of-concept, a 22-year-old cat's SDMA fell from ~24–25 to ~13–14 within weeks (preprint coming); a sarcopenia program is licensed to pharma; Matt Kaeberlein joined the advisory board. Criticized the pace of the field (no product on shelves ~7 years after Loyal's founding) and advised working directly with vets instead of CROs.

•     Julie K. Spears: nutrition is foundational (Purina's lean-feeding lifespan study); connected devices such as smart collars and litter-box sensors detected micro-changes across feline CKD stages.

•     Are vets ready for longevity? Esch said no (disease-focused training); Promislow said yes but overworked; 10–15 minute appointments are the barrier, and at-home diagnostics can help.

•     With $100M: Promislow would scale the Dog Aging Project; Esch would fund early innovation; Spears would run more trials; Voda would cut trial costs.

•     Promislow proposed a national search for "supercentenarian" pets to drive shared biomarker work; Voda noted the pet market is cash-pay, aligning company and owner incentives.

Virtual Cell in Time Forum — Session I

13:30–15:00 · Cedar Grove · Parallel track · Chair: Max Unfried, The Thalion Initiative

Opening Remarks & Welcome (13:30–13:40): not captured in the notes.

Omar Abudayyeh — Professor, Harvard Medical School

13:40–14:00 · "Building virtual models of biology and health"

Key takeaway: Population-level generative models plus biology-trained language-model agents can predict perturbations and have already produced validated rejuvenation hits.

•     Many virtual-cell models fail to beat linear baselines and are judged only on mean expression, not distribution shape or cell-to-cell structure.

•     A population-encoding model (transcribed as "OmniCell") decodes back to realistic single-cell counts and folds in bulk data (~10x more training data).

•     New data on 731 transcription-factor perturbations in two primary cell types raised the top-20 DE-gene hit rate from ~53% to ~62%.

•     Generic LLMs get ~2% of top-20 gene changes right; fine-tuning with reinforcement learning on biology QA reached ~20%, with interpretable reasoning and no sign of saturation with scale.

•     With Google DeepMind's AI co-scientist and an in-house agent, genome-wide in silico screens for rejuvenating old fibroblasts validated ~2 of ~20 predictions (KDM2A, HSF1).

•     A co-scientist-nominated epigenetic factor (unnamed) cut DNA breaks and senescence and rejuvenated cells by ~15–25 years across eight clocks without pluripotency.

•     Next: "virtual humans" built from protein QTLs via Mendelian randomization.

Yuancheng (Ryan) Lu — K99 Research Fellow

14:00–14:20 · "Functional Genomics and Virtual Screening for Rejuvenation Factor Discovery"

Key takeaway: Functional genomics plus single-cell foundation models are finding rejuvenation factors safer than OSK that restore function in the eye and beyond.

•     The eye suits this work: ~300M patients with AMD or glaucoma, efficient AAV delivery and non-invasive vision readouts.

•     A downstream OSK factor that clears the lipid-peroxidation product 4-HNE (likely GSTA4; transcribed "TSG4") restored vision tracking in 13 of 14 mice; a small-molecule enhancer was found.

•     An ORF screen (~13,000 ORFs in ~160M RPE cells under oxidative stress) yielded nine hits; the cardiac factor NKX2-5 beat OSK in two protection assays without changing cell identity.

•     Long-term NKX2-5 was toxic; deleting its homeodomain kept protection with less toxicity, and 21-month-old mice regained vision and ERG comparable to 3-month-olds.

•     Systemic NKX2-5 improved grip strength and frailty index (including kyphosis).

•     A model trained on ~14M cells, using paired fibroblasts from the same donors ~20 years apart (Baltimore Longitudinal Study of Aging), gave ~2x enrichment of hits orthogonal to OSK.

Hao Pei — Founder & CEO, MobiDrop

14:20–14:40 · "Aging Is Multidimensional — So Must Be the Data: Co-registered Single-cell Readouts for Longevity Drug Discovery"

Key takeaway: Aging is dynamic and heterogeneous, so MobiDrop co-registers multiple readouts on the same single cells over time to generate AI-ready data.

•     Current assays capture one dimension at one timepoint, averaged across millions of cells.

•     The platform (transcribed as "NovaCell") stacks five layers on the same cells: live imaging, electrophysiology, Cell Painting, whole transcriptome and proteome panels (up to 6,000 proteins); epigenomics is next.

•     Plugs into a lab's existing incubators, microscopes and sequencers.

•     Uses: senolytic and inflammaging screens, an intermediate funnel before animal studies, and gene-therapy QC.

•     Goal: virtual cells trained on in vitro perturbations linked to aged-mouse outcomes; preliminary models were not shown.

Kejun Ying — Postdoctoral Scholar, Stanford University School of Medicine

14:40–15:00 · "An open world model for human health and mortality"

Key takeaway: World models borrowed from video generation and protein language models can forecast individual disease trajectories and link protein structure to species lifespan.

•     Treats health as a "movie," not a sentence: 11 data domains (EHR, labs, MRI, proteomics, genetics and more) merge into a joint health state evolving in continuous time.

•     State-of-the-art prediction for more than 1,000 diseases up to 20 years out; predicts unseen diseases from a text description; simulated drug effects (e.g., statins) were checked against 286 real trials.

•     Structural model of 2M proteins from 287 species found 170 proteins whose structural features track maximum lifespan, independent of expression; it predicts lifespan about as well as methylation clocks (Cape golden mole predicted at ~30 years).

•     Starting his own lab in January 2027.

Virtual Cell in Time Forum — Session II

15:15–16:45 · Cedar Grove · Parallel track · Chair: Max Unfried, The Thalion Initiative

Le Song — Professor, Mohamed bin Zayed University of Artificial Intelligence

15:15–15:35 · "A World Model of the Virtual Cell"

Key takeaway: A true virtual cell should be multiscale, multimodal and stateful, and should drive generative design toward desired cell states.

•     Current models handle one perturbation and one response in one cell type.

•     Needed: multiscale simulation (DNA to cell), a persistent state for sequential perturbations, and "inverse design" of molecules for a target cell state rather than a binding target.

•     Hybrid architecture: graph neural networks on pathway knowledge (Reactome, KEGG) plus transformers to learn what is missing.

•     Multi-stage training on single modalities, then paired data; temporal live imaging and perturbation data are crucial.

•     The field is at the "GPT-1 or AlphaFold 1" stage; GenBio AI released a model (transcribed "iCell") pitched as the first world model of a human cell.

Petrina Kamya — Global Head of AI Platforms, Insilico Medicine

15:35–15:55 · "Introducing Insilico Medicine's Virtual Aging Cell"

Key takeaway: The Virtual Aging Cell is a multi-agent system that simulates interventions across five biological scales, now undergoing prospective lab validation.

•     Insilico has 10 clinical-stage programs (one in Phase 3), 18 IND-enabling studies and more than 47 internal programs.

•     Frontier LLMs do well at single-step retrosynthesis but poorly at ab initio tasks; Insilico's Pharmaceutical Superintelligence framework trains and benchmarks models on 12 years of data.

•     Lineage: 2016 embryonic-development AI (COX7A1) and the Precious1GPT–3GPT models.

•     ~43 specialized agents per layer across molecular, intracellular, intercellular, tissue/organ and organism scales; a patient-seeded baseline graph is compared with the post-intervention graph.

•     Q&A: prospective validation on molecules with unknown mechanism, in Insilico's robotic lab, is the only way to rule out literature leakage.

Daniel Ives — CEO & Founder, Shift Bioscience

15:55–16:15 · "A single-cell clock and perturbation-model reveals anti-fibrotic targets for epigenetic rejuvenation"

Key takeaway: A single-cell aging clock combined with virtual-cell perturbations finds single-gene knockdowns that both rejuvenate cells and reduce fibrosis.

•     Clock trained on >300 aged dermal fibroblast lines with methylation and single-cell data (correlation >0.9).

•     Virtual perturbations scored by the clock showed single genes dominating top combinations, and that knockdowns (not just OSK-style overexpression) can rejuvenate.

•     In the lab, ~150 of ~190 targets lowered cellular age and ~40 raised it; mTOR inhibition was the positive control.

•     Lead target in the TGF-β pathway: dose-dependent age reduction in fibroblasts (stronger in keratinocytes) and anti-fibrotic effects in liver, lung and heart fibroblasts; expression tracks fibrosis in MASH, IPF, heart failure and systemic sclerosis.

•     Partnering on LNP/siRNA delivery; mouse fibrosis and lifespan studies under way.

•     Q&A: acknowledged circularity risk in training on methylation clocks; mitigated with aging hallmarks outside the clock and OSK benchmarks.

Science Panel: Aging as a Stress Test of the Virtual Cell

16:15–16:45 · Cedar Grove · Panel

Julian Issa (moderator) — Host, The Beyond Tomorrow Podcast

"From Perturbation Response to Health and Mortality"

Key takeaway: Panelists agree virtual cells are worth building, but success depends on new longitudinal, perturbational data and on experimental validation that convinces skeptics.

•     Panelists: Petrina Kamya (Insilico), Omar Abudayyeh (Harvard Medical School), Kejun Ying (Stanford), Le Song (MBZUAI) and Morgan Levine.

•     Definitions converged on a dynamic, multimodal, multiscale, stateful simulator that predicts a cell's next state and supports "what-if" experiments.

•     Missing data: longitudinal perturbations of aged cells or young cells in aged environments (Levine), longitudinal human proteomics, and donor heterogeneity (Kamya).

•     Synthetic data split the panel: Abudayyeh was skeptical (hard to verify, amplifies noise); Song saw a role (AlphaFold 2 precedent) and called the challenge engineering and economics.

•     Sharing: federated learning (Kamya) and pooled data such as Illumina's billion-cell project (Song).

•     Convincing skeptics takes experimental proof, e.g., a correctly predicted novel mechanism; protein design earned credibility the same way. Levine: an accurate model can be inverted to design interventions.

•     Asked which aging target they would edit first in a person, a panelist named APOE, GDF15 and Klotho as interesting but urged starting with a small molecule to establish safety.

Virtual Cell in Time Forum — Session III

17:00–18:00 · Cedar Grove · Parallel track · Chair: Dominika Wilczok, Qiming Venture Partners

Morgan Levine — Computational scientist and entrepreneur

17:00–17:20 · "Biology is Multiscale: Why Virtual Cells Are Not Enough"

Key takeaway: Generative models that reproduce noisy RNA-seq are not enough; biology needs models that learn a cell's latent state as the basis for reasoning and planning.

•     Most virtual cells are in silico Perturb-seq, trained on narrow data, failing out of distribution, and seeing the cell through only the RNA "lens."

•     Benchmarks are weak; a recent virtual cell challenge was "hackable."

•     Proposes a general "perception layer" that integrates modalities into an internal representation (the "sculpture," not its "shadows"); this is the focus of her new startup (formerly at Altos Labs).

•     Q&A: impose as little human prior knowledge as possible and let data drive the model.

Eric Sun — Assistant Professor, MIT

17:20–17:40 · "Measuring and Modeling Cell Aging"

Key takeaway: Single-cell and spatial aging clocks reveal which cells drive aging in their neighbors, guiding targeted interventions.

•     A single biological age hides variation across cell types and organs.

•     Spatial transcriptomic map of mouse brain across 20 ages (3–35 months) with spatial aging clocks.

•     T cells are broadly pro-aging to nearby cells, even controlling for inflammation; neural stem cells are pro-rejuvenating. The lab is engineering cytokines against the T-cell effect.

•     A spatial perturbation model (graph neural network) learns from natural microenvironment variation and distinguished causal sender–receiver signaling.

•     The field should fill the "off-diagonal": tissue-level consequences of cell-level perturbations.

Ava Amini — Principal Researcher, Microsoft

17:40–18:00 · "Multimodal models to understand and target cell states"

Key takeaway: AI world models can prioritize which experiments to run; Microsoft's Quine outperformed human experts at nominating compounds that shift cancer cell states.

•     Quine is a multiscale, multimodal world model that also draws on the literature; the goal is to guide experiments, not replace them.

•     Pancreatic cancer: ranked ~8,000 FDA-approved compounds for shifting classical vs. basal states; the top 20 produced the largest shifts tested and beat an expert-chosen set.

•     It predicted a third, novel cell state, and compounds predicted to induce it worked as expected.

•     A fellowship program will give researchers access; spatial data integration is next.

Panel: Virtual Cells — A Venture Capital Perspective

18:00–18:40 · Cedar Grove · Panel

Dominika Wilczok (moderator) — Entrepreneur in Residence, Qiming Venture Partners

Key takeaway: Investors want focused, problem-specific uses of virtual cells built on high-fidelity human data and a de-risked path to an asset, not an "all-seeing eye" platform.

•     Panelists: Anthony Philippakis (GV), Avak Kahvejian (Flagship Pioneering), Manish Sharma (Warburg Pincus) and Andrew Marshall (Haystack Sciences). Philippakis's remarks were not separately captured.

•     Avak Kahvejian: much high-throughput data is "contrived" and may not translate; proprietary human-relevant data is needed for training and validation. Cited Cellarity (fetal hemoglobin for sickle cell, now in the clinic); 99% of investors still want a defined target.

•     Andrew Marshall: start with a niche problem where data comes fast; a virtual cell may be a tool rather than a company.

•     Manish Sharma: private equity needs a "whole product" (workflow, proprietary data, IP); institutional exposure to aging will be staggered.

•     Discussion: causality over exhaustive mechanism; agreed benchmarks; near-term uses in diagnostics, cell-therapy manufacturing and engineered microbes; omics layers are correlated, so orthogonal data (new 3D microscopy, the "dark proteome") is needed; partnerships can bootstrap a pipeline with $20–50M rather than $1B, but unvalidated models will not sell.

Closing Remarks (18:40–19:00): Max Unfried, The Thalion Initiative. (Not captured in the notes.)

 

ARDD 2026
Organizer,
13th Aging Research and Drug Discovery Meeting






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