On February 24, 2026, ARPA-H announced the seven performer teams for its PROSPR program — the most ambitious federal initiative ever designed to treat aging itself, not just age-related diseases. Despite 90%+ of adults over 65 managing chronic conditions, no FDA-approved therapeutics target the biology of aging directly. PROSPR aims to change that by identifying early biomarkers, developing novel clinical trial designs measurable in 1–3 years instead of decades, and testing both repurposed and novel compounds in human participants.
"PROSPR represents a tectonic shift in how we study healthy aging. ARPA-H will push the envelope on new biomarkers, interventions, and clinical trial designs that bring us closer to therapies that can help all Americans stay healthier for longer."
— Alicia Jackson, Ph.D., ARPA-H DirectorPROSPR integrates three parallel tracks — biomarker discovery, therapeutic testing, and clinical infrastructure — into a unified framework designed to create a new "healthspan industry."
Identify physiological and biochemical markers responsive to aging interventions. Columbia FAST project + Stanford PROSPR-IC score development. Surrogate endpoints for 1–3 year trials.
4 biotech teams testing novel and repurposed compounds: next-gen rapalog (Cambrian), GPER agonist (Linnaeus), retrotransposon inhibitor (Brown/Rochester), stealth BBB compound (Apollo Alpha).
UT San Antonio VITAL-H hybrid/decentralized Phase 3 trial. WHOOP wearables + in-home assessment. Regulatory pathway for intrinsic capacity as FDA-grade endpoint.
"I built PROSPR because I kept seeing the same story play out: brilliant scientists uncover exciting ways to target the biology of aging in animal models, only to have those ideas sit on the shelf because there's no clear path to test them in humans. I wanted to change that."
— Andrew Brack, Ph.D., ARPA-H PROSPR Program ManagerEach team received milestone-contingent contracts (not grants) with varying funding amounts. Click any team to expand its profile.
Comparing all therapeutic compounds being tested across PROSPR, from next-gen rapalogs to repurposed HIV drugs.
| Compound | Team | Class | Target | Route | Key Advantage | Stage |
|---|---|---|---|---|---|---|
| Novel Rapalog | Cambrian | mTOR Inhibitor | Selective mTORC1 | Oral, daily | Next-gen selectivity; avoids mTORC2 side effects | Phase 1/2 |
| LNS8801 | Linnaeus | GPER Agonist | G protein-coupled estrogen receptor | Oral, once-daily | 100+ cancer pts safety data; cardiometabolic signals | Phase 1 (oncology) → aging |
| Censavudine (TPN-101) | Brown / Rochester | RT Inhibitor | LINE-1 reverse transcriptase | Oral | Decades of HIV drug safety; targets "dark genome" | Preclinical → RCT |
| Stealth Compound | Apollo Alpha | Metabolic | Energy homeostasis / lipid / inflammation | Oral, BBB-crossing | Brain-penetrant; multi-system metabolic | Undisclosed |
| Rapamycin | UT San Antonio | mTOR Inhibitor | mTORC1 (low-dose) | Oral | FDA-approved; most studied aging drug; ITP lifespan data | Phase 3 (VITAL-H) |
| Dapagliflozin | UT San Antonio | SGLT2 Inhibitor | Sodium-glucose cotransporter 2 | Oral | FDA-approved; CV + metabolic benefits proven | Phase 3 (VITAL-H) |
| Semaglutide | UT San Antonio | GLP-1 Agonist | GLP-1 receptor | Oral or injection | FDA-approved; weight loss + CV + diabetes; massive safety dataset | Phase 3 (VITAL-H) |
PROSPR strategically blends novel compounds (Cambrian's rapalog, Apollo's stealth agent) with repurposed FDA-approved drugs (rapamycin, dapagliflozin, semaglutide, censavudine). The repurposed drugs offer an accelerated path — decades of safety data allow focus on efficacy endpoints. Novel compounds push the frontier of what's targetable. Linnaeus' LNS8801 sits between: originally developed for oncology, now repurposed for aging. This dual strategy maximizes the odds of identifying at least one validated healthspan therapeutic within the 5-year window.
The core challenge PROSPR solves: aging takes decades, but clinical trials can't wait that long. These teams are building the surrogate endpoints that compress decades of aging into 1–3 year measurable signals.
Assessed across all PROSPR intervention trials — the composite that the FDA may recognize as a regulatory-grade endpoint.
"Older adults will soon visit clinics, learn their biological age, receive targeted interventions, and see themselves getting younger within months."
— Nir Barzilai, M.D., Albert Einstein College of Medicine (FAST co-PI)PROSPR's most radical innovation isn't the drugs — it's the clinical infrastructure. Decentralized trials, wearable-driven endpoints, and in-home data collection that could reshape how we test aging therapeutics forever.
- Wait for disease/disability to manifest
- 10–20+ year follow-up needed
- Disease-specific endpoints (e.g., cancer incidence)
- Centralized clinical sites only
- Annual or semi-annual check-ups
- High cost, slow accrual, massive dropout
- Detect earliest biomarker changes before disease
- 1–3 year surrogate endpoints
- Intrinsic Capacity composite (5 domains)
- Decentralized: in-home + multi-site hybrid
- Continuous wearable monitoring (WHOOP, rings)
- Lower burden, broader access, faster readouts
PROSPR compounds converge on a handful of core aging mechanisms — the "geroscience hypothesis" that a small number of biological drivers underlie most age-related diseases.
mTORC1 drives cell growth and suppresses autophagy (cellular cleanup). Dysregulated mTOR with age leads to senescent cell accumulation, metabolic decline, and immune dysfunction. Low-dose rapamycin and Cambrian's selective rapalog aim to rebalance mTORC1 without immunosuppressive mTORC2 effects. ITP mouse data: rapamycin extends lifespan 10–25% depending on sex and dose.
LINE-1 retrotransposons — virus-like sequences making up ~17% of the human genome — are normally silenced. With age, epigenetic control weakens, LINE-1 becomes active, and the innate immune system detects cytoplasmic DNA as a viral threat, triggering interferon signaling and chronic inflammation. Censavudine blocks the reverse transcriptase that LINE-1 needs to replicate, potentially silencing this false alarm at its source.
G protein-coupled estrogen receptor (GPER) mediates rapid, non-genomic estrogen signaling across multiple organ systems. Linnaeus' LNS8801 was developed as an oncology drug but showed unexpected cardiometabolic benefits in 100+ cancer patients. The "oncology-to-aging" repurposing is a novel pathway — leveraging an established safety profile to explore broad healthspan effects.
Dapagliflozin (SGLT2i) reduces glucose reabsorption, improving cardiovascular and metabolic outcomes. Semaglutide (GLP-1) promotes weight loss and CV risk reduction. Both are FDA-approved with massive safety datasets. VITAL-H tests them head-to-head against rapamycin and placebo, with aging-specific endpoints — the first time GLP-1/SGLT2i efficacy is measured through a geroscience lens.
Primary sources, press releases, and scientific literature underlying this tracker.
- ARPA-H. "Research teams to add more healthy years to Americans' lives as they age." Feb 24, 2026. arpa-h.gov
- ARPA-H. "PROSPR Program Page." arpa-h.gov/explore-funding/programs/prospr
- ARPA-H. "ARPA-H launches new program aimed at extending the healthspan of Americans." arpa-h.gov
- Longevity Technology. "ARPA-H pours millions into healthspan-focused human trials." Feb 2026. longevity.technology
- Longevity Technology. "WHOOP enters $34.5m ARPA-H-backed bid to quantify aging." Mar 2026. longevity.technology
- Forbes. "7 Research Teams Awarded $144 Million To Study Age-Related Illnesses." Nietzel, M. Feb 25, 2026. forbes.com
- Fight Aging! "A Fair Amount of ARPA-H Funding is Being Used for Clinical Trials Relevant to Aging." Mar 4, 2026. fightaging.org
- TIME. "Aging Is Medicine's Biggest Blind Spot." Feb 2026. time.com
- Brown University. "With federal award of up to $22 million, researchers to study treatment to slow the human aging process." Feb 24, 2026. brown.edu
- UT Health San Antonio. "UT San Antonio to lead $38 million national trial testing drugs to extend healthspan." Mar 2026. uthscsa.edu
- Columbia University Mailman School. "ARPA-H Contract to Advance Science of Healthy Aging." Mar 2026. publichealth.columbia.edu
- UConn Today. "Aging Research in U.S. Accelerated by Major ARPA-H Contract." Feb 2026. uconn.edu
- Bioengineer.org. "URochester Researchers Secure Up to $22M to Investigate a Key Hidden Factor in Aging." Feb 2026. bioengineer.org
- AllSci. "US ARPA-H throws USD 144m to tackle aging, universities and biotechs in support." Feb 2026. allsci.com
- Labiotech.eu. "11 anti-aging biotech companies leading longevity in 2026." Mar 2026. labiotech.eu
- De Cecco, M. et al. "L1 drives IFN in senescent cells and promotes age-associated inflammation." Nature 566, 73–78 (2019). doi:10.1038/s41586-018-0784-9
- Beard, J.R. et al. "The World report on ageing and health: a policy framework for healthy ageing." Lancet 387, 2145–2154 (2016). doi:10.1016/S0140-6736(15)00516-4
- Belsky, D.W. et al. "DunedinPACE, a DNA methylation biomarker of the pace of aging." eLife 11, e73420 (2022). doi:10.7554/eLife.73420
- CDC. "Chronic Disease Among Older Adults." Preventing Chronic Disease (2025). cdc.gov
- Harrison, D.E. et al. "Rapamycin fed late in life extends lifespan in genetically heterogeneous mice." Nature 460, 392–395 (2009). doi:10.1038/nature08221