
CEO @cambrianbio | PhD | creating medicines to keep people healthy | opinions my own
New York, USA
Joined June 2014
- Tweets960
- Following280
- Followers3.8K
- Likes1.8K
I've been coming to ARDD for 10 years now, and I joke that every year it feels a little like going back to summer camp: familiar faces, conversations that pick up right where we left off, and a few more people in the room who weren't thinking about aging a decade ago.
Seeing that growth up close has been one of the real pleasures of my career. Ideas that once lived mostly in mouse studies and late-night conference debates are now in clinical trials, in pharma pipelines, and in serious conversations about how we treat chronic diseases.
This year I had the privilege of talking about Cambrian's lead asset, ATX-304, an AMPK network activator that could help restore the metabolic health we all lose with age, a decline that is accelerated in people with obesity.
AMPK is one of the last famous targets in biology still without a drug. We've known for years that it's the master regulator of the benefits of exercise, and until our data this year, there had been nothing in humans. I'll be sharing more from my talk over the next couple of weeks.
Thank you to the ARDD team for another great year!
Another outstanding ARDD meeting in the books!
On the Main Stage, our CEO @JamesPeyer presented “Reversing metabolic decline through AMPK Network Activation in humans,” sharing data on our lead asset, ATX-304, an AMPK Network Activator in clinical development for obesity and other forms of cardiometabolic disease.
At the poster sessions, our Director, R&D Project Management, Travis McQuiston, PhD, presented our TORnado platform of highly selective mTORC1 inhibitors.
Our CFO/COO, Juliette Han, PhD, and Chief Business Officer, Mark Nuttall, were also in attendance, connecting with colleagues across the field and taking in the week’s science.
Thank you to the @ARDD_Meeting team for another great event, and thank you to everyone who stopped by to connect. More to come!
Wouldn't it be amazing if there was a commercially available mTORC1 inhibitor that could actually improve biological function in humans? 🙃 👇
Very proud of the team at Rapalogix and Re-Q as we share our new publication in the Journal of Cosmetic Dermatology.
In a 12-week, randomized, double-blind study, a formulation containing RLX-201, the active ingredient in Re-Q, significantly improved skin firmness, elasticity and overall skin quality compared with the same formulation without the active ingredient.
As a co-founder, seeing the team put its science to the test and publish the results means a lot. Skin longevity deserves this kind of work.
Congratulations to everyone behind it.
@rapalogix @DrDorisDay @JamesPeyer
onlinelibrary.wiley.com/doi/…
James Peyer retweeted
Here's my conversation with @BrackLab on the FDA shift on longevity, and how his PROSPR program will sustain the momentum.
Highly positive panel on longevity trials at ARDD:
Lowell Zeta (chief of staff) says longevity is a priority for the current FDA.
There's now a point person for longevity trial design: Justin Penzenstadler (reviewer on GLP1s).
Steven Kozlowski (chief scientist) working on guidance and tech specs, to be released first half of next year.
Justin recommends the field forma precompetitive consortium for which biomarkers, how to include in trials. And to talk to regulators regularly.
Day 2 of ARDD is nearly done. It's always one of my favorite meetings of the year - it feels like coming home (even in Boston instead of Copenhagen).
For my talk tomorrow, I'm trying something different… along with our data, I want to help answer a question:
Why don't we already have a good drug for activating AMPK?
AMPK is one of the last famous targets in biology without a drug. We've known for years that it's the master regulator of the benefits of exercise, yet there's been nothing in humans (until our data this year).
Join me on the main stage at 3:10pm ET tomorrow, Oct 3, and strap in for a fun story =)
We are proud to sponsor the 13th @ARDD_Meeting at Harvard's David Rubenstein Treehouse, and thrilled to share that our CEO, @JamesPeyer, will be speaking.
James will present "Reversing metabolic decline through AMPK Network Activation in humans" on the Main Stage on Saturday, October 3 at 3:10 PM ET.
While you're there, visit the poster sessions to meet Travis McQuiston, PhD, our Director, R&D Project Management, and learn more about our TORnado platform of highly selective mTORC1 inhibitors.
See the full program and register: agingpharma.org/
#ARDD2026
James Peyer retweeted
We are proud to sponsor the 13th @ARDD_Meeting at Harvard's David Rubenstein Treehouse, and thrilled to share that our CEO, @JamesPeyer, will be speaking.
James will present "Reversing metabolic decline through AMPK Network Activation in humans" on the Main Stage on Saturday, October 3 at 3:10 PM ET.
While you're there, visit the poster sessions to meet Travis McQuiston, PhD, our Director, R&D Project Management, and learn more about our TORnado platform of highly selective mTORC1 inhibitors.
See the full program and register: agingpharma.org/
#ARDD2026
If @ARDD_Meeting was just one day longer @davidasinclair could show off new data on Oct4. A missed opportunity ;-)
Looking forward to ARDD in Boston this year!
Our lab’s v2 in vivo age-restoration technology is fundamentally different from the v1 technology now in human trials. We’ll reveal it publicly at @ARDD_Meeting: Chris Petty, Thurs 1:30 p.m. ET, and me, Sat 6 p.m. ET
James Peyer retweeted
Welcome to X, @rapalogix!
I co-founded Rapalogix because I believe a deeper understanding of how skin ages can lead to better ways to care for it. That curiosity, and the chance to turn serious science into something useful, drew me in.
We recently launched our first product, Re-Q, a step toward putting that science into people’s daily skincare routines.
My hope is that Rapalogix becomes a thoughtful voice for skin science here. Sharing what we’re learning, answering questions and being honest about what still needs to be understood.
There’s plenty of skincare advice on this platform. Good evidence deserves an audience too.
James Peyer retweeted
When we started Loyal there was no FDA pathway for a any lifespan extension drug.
Today the FDA accepted our third one!
LOY-003, our daily pill for helping large dogs live longer (and healthier) lives, has earned RXE efficacy approval.
James Peyer retweeted
We are on the cusp of a wave of new therapies for some of the worst diseases. But the world won’t benefit unless the US fixes its drug regulatory system. My new essay for @nytimes, on how slow clinical trials are now the biggest obstacle to curing cancer.
nytimes.com/2026/09/04/opini…
- I interviewed dozens of researchers, especially oncologists at leading U.S. centers. A striking consensus emerged: science is no longer the main bottleneck to new cancer drugs. It is our ability to test discoveries in patients through clinical trials.
- The cost of starting a Phase 1 trial in America has roughly doubled over the past decade. As a result, companies increasingly take early trials abroad: Australia’s Phase 1 trial volume has nearly doubled in a decade, driven mainly by U.S. companies.
- Unfortunately, the underlying incentives are badly asymmetric: Institutions can be blamed for harms caused by moving too fast, but almost no one is blamed when patients deteriorate during avoidable delays. One doctor called the emerging system “ritualized safety over actual risk assessment.” Or as, @DavidHongMD put it: "We often forget that the biggest risk is the cancer itself."
- This problem is becoming more urgent because medicine itself is changing. Sequencing, biological engineering and A.I. make increasingly personalized therapies possible. But our regulatory system was mostly built for standardized drugs tested in large populations.
- @sytse, the co-founder of GitLab, shows what personalized medicine can achieve: after relapsed osteosarcoma and being told there were no options left, he pursued a highly individualized approach and has now been cancer-free for a year. But doing so required extraordinary resources and regulatory expertise.
- Pierce Ogden’s father was less lucky. After molecular analysis identified a drug that might target his glioblastoma, the manufacturer agreed to provide it. But administrative barriers delayed access until it was too late. “My dad was ready to try anything,” Pierce told me. “But the system is paternalistic.”
- The A.I. revolution is making this bottleneck more important, not less. A.I. relies on relevant data. Information from early-stage trials could compound with A.I. tools to achieve truly revolutionary medicines. Without the data, this is far less likely to happen.
- Another important shift is that innovation increasingly comes from academic labs and small biotech companies rather than Big Pharma. These small companies find it far harder to unable to absorb delays and regulatory barriers.
- Apart from cancer, China is the biggest winner from America's outdated medical regulations. China has a much faster trial system, with testing often starting a full year earlier. This allows Chinese pharmaceutical companies to experiment and improve medicines while American companies play with mice. Today, half of all drugs licensed by major pharmaceutical companies originate there, up from less than 5 percent only a decade ago.
- But we don't need to copy China. The best model is Australia: lots of on-site scientific and ethics reviews, and requirements that are proportionate to small, early-stage trials. Phase 1 studies there begin roughly 6–12 months faster, without any notable increases in adverse safety events.
- Operation TrialBlazer, a 2026 HHS initiative is a good start in this direction, but we need legislative action by Congress to truly make Phase I trials faster and more efficient!
I want to thank everyone who helped me with this article: everyone I interviewed and the amazing editors at the Times. This is the result of a months long journey of extensive interviews and research.
Special thanks go to those who came on the record. One of the features of the system is an atmosphere of fear, where practitioners are afraid to publicly come out and explain these issues. So anyone who does is a hero in my book!
I want to make sure we don't set a double standard for looking at mouse lifespan interventions.
Caloric Restriction is the OG way of extending lifespan in mice. GLP-1s in the paper published today mostly phenocopy CR - similar food intake decrease, similar lifespan change. All fine. Having excess adipose tissue is dangerous.
As we compare to other interventions (rapa is my favorite as a gold standard to compare to) is there a difference in kind between the GLP-1 data and rapa data?
Rapa also phenocopies CR in many ways, maybe a step downstream of food intake - more at the cell level of nutrient sensing. Rapa-treated animals don't gain weight and have less adiposity than vehicle controls. Sounds pretty "CR"-like on the surface if you wanted to explain the phenotype as "adipose tissue = shorter lifespan"
There are definitely differences in the two scenarios, but I think it highlights how tough it is to draw bright lines between anti-obesity and gerotherapeutic effects.
The killer evidence will be giving semaglutide to individuals with <27 BMI and seeing reduction in cancer/cardiac/dementia risk - but that's a high bar for a mouse study!
Today I am grateful for Feng et al to have published a thorough paper and start filling a gap about GLP + lifespan that had been missing in the literature.
Also grateful to @MartinBJensen @mkaeberlein and @BrackLab for day 1 public reflections
Replying to @BrackLab @MartinBJensen
That's a good point, and I agree it's a valuable observation that a drug that impacts multiple chronic diseases in middle-aged people can have health and longevity benefits when started during middle-age in mice. It's probably a good thing for the field, in terms of perceived legitimacy. Maybe it will even hasten big pharma jumping in. Having said that, it's also the expected result for a drug that induces CR, and there are numerous studies showing late-life extension from both CR and specific amino acid restriction paradigms. I guess I'm just not seeing where this advances our understanding of aging biology in any substantial way. Maybe I'm missing something.
Earlier this year I wrote an article for Nature Aging saying GLP-1s are great obesity drugs but we shouldn't be too quick to call them gerotherapeutics / longevity drugs - that we needed to run the experiments and see the data.
Here's a new paper that provides strong support to the notion that they may be able to target some of the core biology of aging.
They showed:
1) In ad libitum fed but not obese animals, median lifespan extended in females by about 12% when started late in life. Pretty impressive! Comparable to rapamycin in a similarly set up experiment.
2) They ran some experiments (not survival/lifespan) with ad lib vs semaglutide vs caloric restriction and saw some signs of the GLP-1 giving improvements over just CR - Barnes Maze and Glucose Tolerance Tests.
Kudos to Feng et al. for putting together an impressive study! I love seeing thoughtful papers like this one addressing key gaps in our collective knowledge.
Thoughts I walked away from:
- Does it work in male mice? So many mouse lifespan interventions work in only one sex
- Is the healthspan from CR just an anti-obesity effect since mice normally have unlimited access to food (even if that's not the high fat diets that lead to mouse obesity), and the majority of this effect would not have translational value to a human of lean weight?
- The anti-inflammation hypothesis for the weight independent effects of GLP-1s seems to be the dominant story here, but it's very hard to isolate. Here too but the group has made a good start at seeing some differences in activity patterns (which might just be differential food hunting)
nature.com/articles/s41586-0…
One of the most common Qs: "You can't run a trial for aging. What do?"
"Intrinsic Capacity" is the most important term to know for people who care about how we will be able to test new medicines for their ability to keep people living longer and healthier. This is a great intro by @SmithDanaG - featuring @BrackLab who is spearheading the first effort to test new drug candidates in IC as part of @ARPA_H PROSPR
nytimes.com/2026/08/26/well/…
Every year there's a new crop of these articles and the fact that people are covering this instead of real science is just depressing.
How many consecutive years do we release new results showing that humans without new technology max out at a bit over 100?
We’ve found the true limit on how long humans can live, say experts
sciencefocus.com/the-human-b…
I do! Here’s why:
While I agree that a good geroscience intervention is able to reverse, not just prevent, the underlying cellular pathology that comes with aging from a drug development and translational science perspective....
The hypothetical medicine that we are talking about - something that you would start taking before you're sick to ideally never get cancer or diabetes or frailty - is definitionally a preventative medicine. It allows us to talk intelligibly with regulators and people outside our field in terms of what we are trying to bring into existence.
What if every time SpaceX launched a new rocket prototype it had to be full of people? Welcome to drug development.
I find that even though interest in geroscience is at an all-time high. People flocking into the space have fundamental misconceptions about the process of drug development and the challenges in translating scientific discoveries to human medicines. Nothing in the world is more important than this field, so I'm going to try to offer some clarity where I can.
Give me your Qs where there is widespread confusion in the field and I'm going to try to do one of these each week or so.
James Peyer retweeted
Weight loss is not the only goal of weight-loss medication. Many patients also want to walk farther, move more, and stay physically independent.
In our latest blog, our team explores important questions that remain regarding the effects of GLP-1 therapies on physical activity, fitness, and functional ability, and why the field may need to look beyond the scale to define treatment success. Read more: cambrianbio.com/blogs/beyond…
One of the most pervasive misunderstandings in geroscience today starts from the beginning - why do we age at all?
if you haven't, read the @M_S_Ringel review from last year that walks through the evolutionary pressures that result in aging. onlinelibrary.wiley.com/doi/…
I gotta say it is fun to search for the name of the drug we're developing and find people I've never met geeking out over our preclinical data
Best version of googling oneself
James Peyer retweeted
Come join us
No safe bets. No incremental steps. Just high-risk, high-reward work that could change medicine forever.
ARPA-H is hiring Program Managers for the hardest problems in human health.
If you think from first principles, challenge assumptions, and want to accelerate breakthroughs for patients — this is your role.
Apply now ➡️ arpa-h.gov/careers/program-m…























