Direction
Drugs against ageing
Cells constantly decide whether to grow, repair or recycle. Drugs can influence those decisions. Researchers test new molecules and revisit existing medicines to see whether they affect ageing itself.

Which benefits survive the journey from mice to people?
Inside the researchMouse experiment
In a 2009 study across three sites, mice receiving rapamycin late in life lived longer. The experiment made a powerful point: even an old mammal’s lifespan could respond to a drug targeting the mTOR pathway.
What this leaves open. The study tested mice. It did not establish a regimen that extends human lifespan.
Read the paperRapamycin fed late in life extends lifespan in genetically heterogeneous miceHarrison et al. · Nature · 2009Side by side
The rated projects, compared
| Project▲ | Promised effect▲ | Evidence▲ | Stage▲ | Strongest case against▲ |
|---|---|---|---|---|
| Aptah Bio | +2 years of life | The strongest evidence is a peer-reviewed Scientific Reports article with iPSC-derived AD neurons and SAMP8 mice, reporting molecular and electrophysiology changes but explicitly no cognitive change in mice. | Preclinical. | The failure case is that Aptah’s claimed breadth is mostly narrative, while the real effects are narrow, model-specific, or too small to translate. |
| Beijing Joekai Biotechnology | +0.7 years of life | The evidence base is stronger than a pure concept because it includes Joekai-assigned Alzheimer’s patents, a 2025 conference/news report of discovery and preclinical results for 50561, and a completed Phase IIa randomized placebo-controlled trial listing with 68 participants across 12 Chinese sites. | Historically, Joekai held Alzheimer’s-treatment patent filings and grants tied to synthetic compounds, though several records show ceased or fee-related expiry risks. | The evidence base is still dominated by patents, directory entries, and conference/trial metadata without published outcomes, so the project could easily be a case where a plausible mechanism and real clinical activity never translate into meaningful efficacy, differentiation, or durable IP advantage. |
| NYC-Vita | +1.5 years of life | The project has credible institutional and competition validation: Mount Sinai/NYC-Vita was named an XPRIZE Healthspan semifinalist and Milestone 1 awardee with funding for a New York City clinical trial. | Status is early and unproven. | NYC-Vita could fail because the intervention is a heterogeneous bundle with weak attribution, small sample size, and substantial forward-looking promotional framing; the most likely disappointing outcome is that exercise explains most of the effect, while rapamycin/lamivudine add safety risk, noise, or negligible incremental benefit without clear mechanistic readouts. |
| RIGHT Trial | +1.2 years of life | The evidence base is thin for the actual frailty indication. | Clinical-stage and actively structured as a mid-stage efficacy/safety test, with University of Pittsburgh as lead sponsor, Anne B. | Frailty is biologically heterogeneous and may not respond meaningfully to single-cytokine suppression; even if IL-6 is associated with frailty, blocking it may produce limited functional benefit, unacceptable tradeoffs, or effects too small to justify chronic biologic treatment in older adults. |
| Team GlyNAC | +2 years of life | There is more than pure preclinical speculation: evidence includes a randomized older-adult clinical trial, a pilot older-adult clinical trial, mouse lifespan and cognition studies, and smaller disease-context studies in type 2 diabetes and HIV. | Status is early clinical and preclinical, not validated. | The main failure case is that the project is over-extrapolating from small studies, institutional news coverage, and mouse data: biomarker improvements may not translate into durable clinical benefit, lifespan effects may be species-specific, sex-dependent responses may complicate generalization, and Baylor’s patent/licensing position creates conflict-of-interest pressure around interpretation. |
| Team Twilight | +1.2 years of life | The evidence base supports the broader HERV-K/HML-2 ALS hypothesis better than it supports Team Twilight’s therapeutic program. | The project appears to be a venture-stage therapeutic company in a preclinical or at least not yet clinically validated state based on the evidence here. | The main failure case is that the project is still resting on promotional claims plus field-context biology that does not yet prove intervention efficacy. |
Companies
Companies in this direction
Ambition is what a company claims. Independent replication is what others have confirmed. Read the two columns together: the gap between them is where a promise runs ahead of a result.
| Company▲ | Ambition▲ | Independent replication▲ | Stage▲ | Headquarters▲ |
|---|---|---|---|---|
| 5 Alarm Bio 5 Alarm Bio develops small-molecule therapeutics targeting an unexplored aging mechanism to delay or prevent age-related diseases. | 7 | 1 | seed | Cambridge, United Kingdom |
| 712 North Inc 712 North develops personalized mitochondrial medicines for age-related diseases. | 7 | 3 | – | San Francisco, California, United States |
| ADvantage Therapeutics ADvantage Therapeutics develops novel therapeutics for neurodegenerative conditions, with a major focus on Alzheimer’s disease. | 8 | 3 | – | Vienna, Austria |
| Aeovian Pharmaceuticals Clinical-stage biopharmaceutical company developing selective small molecules for rare genetic and age-related diseases. | 6 | 1 | – | 2930 Domingo Avenue #145, Berkeley, CA 94705 |
| AKL Therapeutics AKL Therapeutics develops APPA, an investigational oral therapy for osteoarthritis and other inflammatory diseases of ageing. | 6 | 4 | – | Stevenage, United Kingdom |
| Amplifier Therapeutics Amplifier Therapeutics develops AMPK activators to address metabolic disease and aging-related chronic diseases. | 6 | 2 | – | United States |
| Antoxis Antoxis conducted research and experimental development in biotechnology. | 4 | 2 | pre seed | Aberdeen, Scotland, United Kingdom |
| Atropos Therapeutics Atropos develops senescence-targeting drugs for aging-related diseases, cancer, and healthspan. | 7 | 3 | – | San Francisco, California, United States |
| Biophytis Biophytis develops transformative therapies impacting longevity, with BIO101 programs in sarcopenia and obesity. | 7 | 3 | public | Paris, France |
| Biosplice (was Samumed) Biosplice develops first-in-class therapies based on alternative splicing and small-molecule CLK/DYRK kinase inhibition. | 7 | 2 | – | San Diego, California, United States |
| Bolden Therapeutics Bolden Therapeutics develops first-in-class therapeutics to increase neurogenesis and improve outcomes in neurological disease. | 7 | 1 | pre seed | Boston, Massachusetts, United States |
| Cambrian Bio Clinical-stage drug development company developing therapeutics targeting metabolic pathways that decline with age. | 8 | 2 | series c plus | New York, New York |
| Cognition Therapeutics Cognition Therapeutics develops therapies for age-related neurodegenerative diseases including dementia with Lewy bodies and Alzheimer’s disease. | 7 | 3 | public | New York City, New York, United States; Pittsburgh, Pennsylvania, United States |
| Coya Therapeutics Clinical-stage biotechnology company developing multi-modality Treg therapies for neurodegenerative, autoimmune, and metabolic diseases. | 8 | 4 | public | Houston, Texas, United States |
| Cytonics Cytonics develops A2M-based biologic treatments intended to halt or reverse osteoarthritis progression. | 5 | 2 | – | Jupiter, Florida, United States |
| Epirium Bio Epirium Bio develops oral small-molecule therapies targeting PGE-2 signaling for neuromuscular, inflammatory, and fibrotic diseases. | 7 | 4 | series a | United States |
| Etheros Pharmaceuticals Etheros develops small molecule enzyme mimetics for neuroprotection and healthspan. | 7 | 1 | – | United States |
| Fission Pharma Fission Pharma is developing DRP1-FIS1 protein-protein interaction inhibitors for chronic inflammation, mitochondrial dysfunction, and age-related degenerative diseases. | 7 | 1 | pre seed | United States |
| Fountain Therapeutics Fountain develops first-in-class therapies for diseases and conditions caused by aging. | 7 | 1 | – | San Francisco, California, United States |
| Galilei Biosciences Galilei Biosciences develops small-molecule SIRT6 activators for neuroprotection in glaucoma and other age-related diseases. | 7 | 5 | – | Cambridge, Massachusetts, United States |
| Hayflick Partners Hayflick Therapeutics develops localized, micro-dose rapamycin therapies targeting mTOR for cellular aging interventions in skin. | 6 | 3 | – | Narberth, Pennsylvania, United States |
| HCW Biologics Clinical-stage biopharmaceutical company developing fusion immunotherapies for autoimmune diseases, cancer and senescence-associated dysplasia. | 8 | 3 | public | Miami, Florida, United States |
| Immunis Clinical-stage biotech developing stem cell-derived secretome biologics targeting age-related muscle and metabolic disease. | 8 | 3 | – | Irvine, California |
| Istesso Istesso develops first-in-class oral regenerative medicines focused on restoring the body’s natural capacity to repair tissue. | 8 | 2 | – | London, United Kingdom |
| Jocasta Neuroscience Jocasta develops Klotho-based therapeutics for cognitive vitality and age-related cognitive impairment. | 8 | 4 | series a | – |
| Jupiter Neurosciences A clinical-stage drug platform company focused on treating neuroinflammation. | 6 | 2 | – | Palm Beach Gardens, Florida, United States |
| Juvenescence Juvenescence develops innovative medicines targeting core aging mechanisms to extend healthy lifespan and prevent age-related diseases. | 7 | 2 | – | – |
| LinkGevity LinkGevity develops AI-driven longevity therapeutics, including first-in-class Anti-Necrotic necrosis inhibitors for kidney disease and other applications. | 8 | 2 | – | Babraham Research Campus, Cambridge, UK |
| Loyal Loyal develops longevity drugs for dogs that target age-associated disease and disability. | 7 | 3 | series c plus | SAN FRANCISCO |
| MetroBiotech MetroBiotech develops proprietary NAD+ precursors to enhance human healthspan and treat age-related diseases. | 6 | 3 | – | – |
| Mirscience Therapeutics Mirscience Therapeutics develops personalized microRNA therapies for longevity-associated diseases and challenging therapeutic targets. | 7 | 1 | – | Brazil |
| Mitochem Therapeutics MitoChem Therapeutics develops small molecules targeting mitochondrial dysfunction-driven loss of cellular metabolism in neurodegenerative disease. | 7 | 2 | – | Charleston, South Carolina, United States |
| Mitoconix Bio Mitoconix Bio develops disease-modifying therapeutics for neurodegenerative diseases by improving mitochondrial health. | 8 | 1 | – | Israel |
| Mitotech Mitotech develops orally bioavailable small molecules to protect mitochondria from oxidative stress and enhance energy expenditure. | 6 | 4 | – | Russia, Luxembourg |
| Mogling Bio Mogling Bio develops pharmacological therapies targeting Cdc42 overactivation to rejuvenate aged and exhausted cells, especially stem cells. | 8 | 3 | seed | 2900 Reading Road Suite #410 Cincinnati OH 45206 |
| Muna Therapeutics Muna Therapeutics develops therapies to slow or stop neurodegenerative diseases including Alzheimer’s and Parkinson’s. | 8 | 3 | – | Copenhagen, Denmark |
| Napa Therapeutics Napa Therapeutics develops small molecule drugs against a novel aging-related target linked to NAD metabolism. | 7 | 1 | – | San Francisco, California, United States |
| NeuroBio Neuro-Bio develops diagnostic and therapeutic strategies for Alzheimer's disease based on the toxic T14 peptide mechanism. | 8 | 2 | seed | Oxford, United Kingdom |
| NRG Therapeutics NRG Therapeutics develops disease-modifying medicines for neurodegenerative disorders by targeting mitochondrial function. | 8 | 2 | – | Stevenage, Hertfordshire United Kingdom |
| NuSirt NuSirt Sciences combines established pharmaceuticals and natural products to activate the sirtuin pathway for cardiometabolic diseases of aging and overnutrition. | 5 | 3 | – | Knoxville, Tennessee, United States |
| Olatec Olatec develops safe oral NLRP3 antagonist therapeutics for acute and chronic inflammatory diseases. | 7 | 5 | – | New York City, New York, United States; Boston, Massachusetts, United States |
| Pelage Pharmaceuticals Pelage develops regenerative medicines for hair loss grounded in stem cell biology. | 6 | 3 | series b | Los Angeles, California, United States |
| PharmatrophiX PharmatrophiX develops small-molecule disease-modifying therapies for neurodegenerative diseases. | 8 | 4 | – | San Francisco, California, United States |
| Praetego | 7 | 2 | – | Durham, North Carolina, United States |
| Pretzel Therapeutics Pretzel develops first-in-class medicines targeting mitochondrial biology and cellular energetics for rare, neurodegenerative, metabolic, and other diseases. | 8 | 4 | series a | Sweden; Boston, Massachusetts, United States |
| Refoxy Pharma Refoxy develops next-generation medicines targeting FOXO3 to treat age-related diseases and extend healthy lifespan. | 7 | 2 | – | Germany |
| ReGENE ReGENE develops small molecule therapies to prevent and treat aging-associated diseases by targeting mechanisms that drive aging. | 7 | 1 | – | Springfield, Massachusetts, United States |
| resTORbio Clinical-stage biopharmaceutical company developing medicines targeting the biology of aging to prevent or treat aging-related diseases. | 7 | 2 | – | Boston, Massachusetts, United States |
| Retrotope Retrotope develops proprietary therapeutics designed to treat degenerative disease by down-regulating lipid peroxidation. | 7 | 4 | series c plus | San Francisco, California, United States |
| Scripta Therapeutics Scripta Therapeutics modulates transcription factor activity using AI/ML-driven drug discovery to develop disease-modifying therapeutics. | 8 | 0 | – | Oxford, United Kingdom |
| Senisca Senisca develops RNA senotherapeutics to reverse cellular senescence and treat age-related disease. | 8 | 1 | seed | Exeter, United Kingdom |
| Sentcell Sentcell develops first-in-class human rejuvenating therapies targeting the sMAC pathway in ageing T cells. | 9 | 2 | series a | London, United Kingdom |
| Ship of Theseus A therapeutics company developing degradation-resistant Hox family biologics. | 7 | 4 | – | Philadelphia, Pennsylvania, United States |
| Sierra Sciences Sierra Sciences researches telomere science and telomerase activation to develop interventions intended to reverse cellular aging. | 8 | 0 | – | Reno, Nevada, United States |
| TNF Pharmaceuticals (was MyMD) Clinical-stage biopharma developing MYMD-1 and Supera-CBD for autoimmune, inflammatory, aging-related, pain, anxiety and seizure indications. | 6 | 2 | public | Baltimore, Maryland, United States |
| TOR Therapeutics TOR Therapeutics develops an oral fixed-dose combination of mTORC1 inhibitors for Alzheimer's disease and other mTORC1-driven disorders. | 7 | 0 | – | Jenkintown, Pennsylvania, United States |
| Tornado Therapeutics Tornado Therapeutics is developing safer, more effective rapalogs to treat disease and extend healthy lifespan. | 8 | 0 | – | United States |
| Trivium Vet TriviumVet develops animal health therapeutics for serious diseases in cats and dogs. | 6 | 4 | acquired | Ireland |
| Vasa Therapeutics Vasa develops therapeutics targeting cardiovascular aging, neuromuscular disease, and age-related disorders. | 7 | 2 | seed | Encinitas, California, United States |
| X-tosis X-tosis develops mitochondrial therapeutics to prevent neuronal loss in neurodegenerative diseases. | 8 | 2 | – | Gainesville, Florida, United States |
| YOXLO YOXLO builds science-based tools, products and research programs to help people understand and preserve functional reserve as they age. | 7 | 2 | pre seed | YOXLO B.V. Biopartner 5 Building De Limes 7 2343 DH Oegstgeest |
| Zoe Biosciences Zoe Biosciences is developing best-in-class therapies to treat cardiometabolic disease. | 6 | 0 | – | United States |
Projects
Projects in this direction
| Project▲ | Stage▲ | Strongest case against▲ |
|---|---|---|
| A NEW DIMENSION A NEW DIMENSION appears to be Aayam Therapeutics’ mitochondria-focused longevity effort: a drug-discovery and development project built around an undisclosed "LADR 4" platform and framed as delivering affordable, accessible therapeutics. | Early but real. | The project may fail because its public evidence is currently far weaker than its positioning: the mechanism is opaque, the platform is undefined, and mitochondria is a crowded, hype-prone area where patenting, competition recognition, and expert biography do not by themselves predict clinical efficacy. |
| Alpha Rejuvenation Alpha Rejuvenation appears to be a California-focused men’s health and wellness clinic marketing peptide therapies, testosterone replacement, erectile-dysfunction treatment, pelvic-floor therapy, NAD+, and semaglutide-based weight loss rather than a clearly documented R&D program. | Operational as a men’s rejuvenation clinic with named services, office details, and a stated licensing footprint limited to California and Arizona. | This may be mostly a marketing-driven men’s wellness clinic aggregating loosely supported interventions, with weak causal evidence, heavy reliance on testimonials and educational copy, unclear differentiation from standard cash-pay hormone/weight-loss practice, and a material evidence-quality problem around source attribution. |
| Aptah Bio Aptah Bio is a U.S.-based startup developing RNA therapeutics, centered on a U1 snRNP-modulating platform it calls RNA WiCo/RNA rejuvenation, for neurodegeneration, cancer, and other age-related diseases. | Preclinical. | The failure case is that Aptah’s claimed breadth is mostly narrative, while the real effects are narrow, model-specific, or too small to translate. |
| Beijing Joekai Biotechnology Beijing Joekai Biotechnology appears to be a Beijing-based small-molecule neurodegeneration company centered on Alzheimer’s disease. | Historically, Joekai held Alzheimer’s-treatment patent filings and grants tied to synthetic compounds, though several records show ceased or fee-related expiry risks. | The evidence base is still dominated by patents, directory entries, and conference/trial metadata without published outcomes, so the project could easily be a case where a plausible mechanism and real clinical activity never translate into meaningful efficacy, differentiation, or durable IP advantage. |
| Beiwe Beiwe appears to be an early therapeutic project centered on selective mTORC1 inhibition for longevity and cancer, with the core claim that it can preserve rapamycin-like benefits while avoiding mTORC2-related toxicity; however, the evidence here is mostly undated self-published website copy with no linked primary datasets, study details, patent record tied to the company, or disclosed clinical results. | Publicly presented as a company with a therapeutic thesis and named team members including Gino Cortopassi, PhD, and Zane Starkewolfe, PhD, but the supplied evidence does not show Beiwe-specific preclinical datasets, peer-reviewed papers, patents assigned to the project, trial registrations, or clinical-stage progress. | The current evidence does not substantiate the key claims. |
| BioArmor BioArmor appears to be an early-stage, student-led longevity concept from the QuestX Incubator in Kuala Lumpur that reached XPRIZE Healthspan semifinalist status, but the public evidence does not disclose a validated therapeutic program. | Status is best described as concept-stage with publicity and competition recognition but little disclosed validation. | The downside case is stronger on current evidence: BioArmor may be mostly a narrative bundle of popular longevity ingredients plus futuristic claims that are far ahead of any disclosed proof. |
| Cura Therapeutics and collaborators/ Cura Therapeutics appears to be a small, women-led biotech developing multifunctional fusion-protein therapeutics for metastatic cancer and age-related diseases, with recurring claims around multimodal immune activation plus anti-fibrotic and anti-senescence effects. | Status is best described as early translational with inconsistent but convergent signals of advancement. | The project may fail because most of the current support is still promotional, patent-based, or inherited from older academic fusokine work rather than direct proof that Cura's own candidates are effective, manufacturable, and safe in humans. |
| Klotho Longevity Klotho Longevity is a U.S. commercialization effort centered on Klotho-linked anti-aging products and procedures, led by Dr. | Current status appears to be an operating U.S. clinic-and-brand ecosystem with active commercialization, promotional conference visibility, and at least one granted Klotho-production patent linked to Gail Humble. | The downside case is that this is mostly a branding-and-patent story built on a biologically interesting target without adequate proof that project-specific products deliver meaningful human longevity benefits. |
| Lono Jaeyak Lono Jaeyak appears to be an anti-senescence composition program known only from a pending European patent application claiming formulations for rejuvenating senescent cells or delaying/preventing cellular aging. | Status is early and weakly validated. | The downside case is that this is only a broad patent filing with little evidentiary substance behind it. |
| Nishimura Lab Nishimura Lab appears, on the evidence provided, to be an EADERM-linked regenerative dermatology effort built around hair follicle and epidermal stem-cell biology, especially aging- and injury-related mechanisms involving COL17A1 and stem-cell motility. | Preclinical and early commercial. | This project could fail because the current evidence is still mostly a chain of academic titles, patents, and company positioning rather than hard translational proof. |
| NYC-Vita NYC-Vita is a Mount Sinai-led, New York City pilot longevity trial that appears to combine home-based exercise, daily spermidine, and low-dose rapamycin or lamivudine in adults roughly 65-80, with the stated goal of improving immune function, muscle strength, cognition, and overall healthspan. | Status is early and unproven. | NYC-Vita could fail because the intervention is a heterogeneous bundle with weak attribution, small sample size, and substantial forward-looking promotional framing; the most likely disappointing outcome is that exercise explains most of the effect, while rapamycin/lamivudine add safety risk, noise, or negligible incremental benefit without clear mechanistic readouts. |
| RIGHT Trial RIGHT Trial appears to be a University of Pittsburgh-led Phase 2, 24-week, placebo-controlled trial testing subcutaneous clazakizumab, an IL-6 blocker, in older adults with frailty and mobility limitation. | Clinical-stage and actively structured as a mid-stage efficacy/safety test, with University of Pittsburgh as lead sponsor, Anne B. | Frailty is biologically heterogeneous and may not respond meaningfully to single-cytokine suppression; even if IL-6 is associated with frailty, blocking it may produce limited functional benefit, unacceptable tradeoffs, or effects too small to justify chronic biologic treatment in older adults. |
| Team GlyNAC Team GlyNAC appears to be a Baylor College of Medicine-associated translational longevity project built around GlyNAC, a glycine plus N-acetylcysteine supplementation strategy intended to raise glutathione and improve mitochondrial and oxidative-stress-related aging defects. | Status is early clinical and preclinical, not validated. | The main failure case is that the project is over-extrapolating from small studies, institutional news coverage, and mouse data: biomarker improvements may not translate into durable clinical benefit, lifespan effects may be species-specific, sex-dependent responses may complicate generalization, and Baylor’s patent/licensing position creates conflict-of-interest pressure around interpretation. |
| Team Twilight Team Twilight is a U.S. biotech startup developing active immunotherapies against pathological proteins, especially HERV-K-linked targets in ALS, with broader stated ambitions in Alzheimer’s, Parkinson’s, and chronic pain. | The project appears to be a venture-stage therapeutic company in a preclinical or at least not yet clinically validated state based on the evidence here. | The main failure case is that the project is still resting on promotional claims plus field-context biology that does not yet prove intervention efficacy. |
| The Brigham Boston XPrize The Brigham-Boston XPRIZE Healthspan Team is a Mass General Brigham and Harvard-linked effort that became a Top 40 semifinalist in the seven-year, $101M XPRIZE Healthspan competition and received $250,000 in Milestone 1 funding in 2025. | As of May 12, 2025, the team was named a Top 40 semifinalist in XPRIZE Healthspan and awarded $250,000 in Milestone 1 funding. | The main failure mode is that the project remains high-profile but underspecified: the therapeutic is unnamed, the evidence is currently promotional rather than experimental, and the pilot may fail to produce endpoints or biomarkers that are persuasive enough to support a larger trial or any real conclusion about healthspan benefit. |
| TIME TRAVELER AND NUREKI TIME TRAVELER AND NUREKI presents as a University of Tokyo-linked startup pursuing healthy-aging products and therapeutics, especially plant-cell-derived exosomes and molecules said to inhibit aging-linked genes, with stated interests in cancer, frailty/sarcopenia, cachexia, supplements, and cosmetics. | Early-stage startup. | The main failure case is that the project is currently much stronger in narrative, patent-adjacent field context, and product marketing than in demonstrated science. |
| YOXLO YOXLO is a Dutch longevity startup building a proprietary healthspan intervention, Youniqor, around a centenarian-inspired thesis that mitochondrial function, cellular resilience, and inflammatory control, especially NLRP3-linked immune signaling, can be modulated to preserve strength, cognition, independence, and immune function with age. | YOXLO has a named founder and cofounding team, a live company website in 2025, SAFE fundraising, and XPRIZE Healthspan semifinalist recognition. | The strongest failure case is that YOXLO is currently much stronger on narrative, patents, and competition signaling than on disclosed evidence, and that its broad claims about mitochondria, oxidative stress, immune balance, and NLRP3 will not survive rigorous testing because the formulation effect size is small, nonspecific, or not mechanistically tied to the promised healthspan outcomes. |
People
People in this direction
- Aubrey de Greypopulariser · through Sierra Sciences
SENS Foundation founder and longevity advocacy pioneer.
- Alex Zhavoronkovpopulariser · through Napa Therapeutics
- João Pedro de Magalhãesscientist · through 5 Alarm Bio
Senescence.info founder and aging-database builder.
- Matt Kaeberleinscientist · through Hayflick Partners
- Laura Deminginvestor · through Loyal
Founded The Longevity Fund as an early dedicated VC vehicle for aging and life-extension companies, helping make longevity biotech a fundable startup category.
- Eric Verdinscientist · through BHB Therapeutics
- Celine Haliouaentrepreneur · through Loyal
Biotech founder pursuing the first approved lifespan-extension drugs for dogs
- Nir Barzilaiscientist · through SirtLab Corp
- Daisy Robintonentrepreneur · through Tornado Therapeutics
Biotech founder developing therapeutics for ovarian aging and women’s health
- Kristen Fortneyentrepreneur · through BioAge Labs
- Jim Mellonentrepreneur · through Napa Therapeutics
Co-founded Juvenescence and publicly framed longevity as an investable biotechnology thesis through the book Juvenescence and substantial company-building activity.
- James Peyerentrepreneur · through Amplifier Therapeutics
Biotech builder translating aging biology into a portfolio of medicines
- David Sinclairscientist · through MetroBiotech
- Joe Betts-LaCroixentrepreneur · through BioAge Labs
Biotech entrepreneur building therapies for age-driven disease
- Christian Angermayerentrepreneur · through Cambrian Bio
- Kelsey Moodyentrepreneur · through Ship of Theseus
Drug-development entrepreneur building an integrated longevity biotech platform
- Peter Diamandisentrepreneur · through Immunis
Chronology
What happened, and when
- Grant
X-tosis
The Michael J. Fox Foundation
- Debt financing
Biophytis
Hexagon Capital Fund
- Follow-on offering
HCW Biologics
$4M
- Follow-on offering
Jupiter Neurosciences
$2M
- Follow-on offering
Biophytis
- Grant
Cambrian Bio
$30.8M · ARPA-H PROSPR program
- Series C
Loyal
$100M · Age1
- Grant
Muna Therapeutics
$1M · Alzheimer's Association
- Series B
Aeovian Pharmaceuticals
$55M · Luma Group, CTI Life Sciences Fund
- Seed round
Scripta Therapeutics
$12M
- Series B
Pelage Pharmaceuticals
$120M · ARCH Venture Partners, GV
- Grant
ADvantage Therapeutics
$2.5M · NIH SBIR
- Series B
NRG Therapeutics
$67M · SV Health Investors’ Dementia Discovery Fund
- Grant
Ship of Theseus
- Series A
Jocasta Neuroscience
$35M
- Venture round
ADvantage Therapeutics
$3.5M
- Venture round
Pretzel Therapeutics
- Venture round
Etheros Pharmaceuticals
$600K
- Series B
Juvenescence
$76M · M42
- Acquisition
Trivium Vet
PBI-Gordon Companies
- Seed round
Refoxy Pharma
$9.8M · Boehringer Ingelheim Venture Fund (BIVF)
- Venture round
Aeovian Pharmaceuticals
$50M · Hevolution Foundation
- Series B
Loyal
$45M · Bain Capital Ventures
- Debt financing
Loyal
$12.5M · Bridge Bank
Hypotheses
Hypotheses under test in this direction
Published by the Omega Point engine and tagged to this direction by a classifier; the gap each one attacks is named under it
- Skin lipid receptors may trigger internal signals that reduce damage in distant tissuesOct 10, 2026In paired older-human skin explants linked to human endothelial cells, a topical lipid may trigger a skin-made mediator that reduces remote damage. Selective mediator blockade must remove its protection and add-back restore it; failure would challenge this mechanism under adequately tested conditions.
- Training may raise kidney filtration and sodium transport costs enough to cause oxygen deficitsOct 10, 2026In a prospectively characterized subgroup of older humans, maintained training could improve mobility while raising kidney filtration, sodium transport costs and lasting renal harm during ordinary warm activity. Precise absence of acquisition, excess oxygen cost, oxygen imbalance or sustained dysfunction would reject that link
- Blocking interleukin-11 may shift genome repair toward error-prone end joiningOct 10, 2026In prospectively specified cycling epithelial progenitors from aging humans, blocking interleukin-11 may increase structural repair errors despite reduced inflammatory injury and preserved early function. Bounded equivalence in repair accuracy for comparable initial lesions would constrain this claim
- Interleukin-11 blockade may change displayed self-peptides and trigger immune injuryOct 10, 2026In susceptible aging-human epithelia, blocking interleukin-11 may alter protein processing and displayed self-peptide identities, allowing pre-existing memory T cells to cause persistent injury. Injury independent of the specified peptide-recognition interaction would argue against this mechanism.
- Blocking interleukin-11 may free shared receptors to sustain harmful competing signalsOct 10, 2026In older-human epithelial cells, blocking interleukin-11 may release the shared receptor component gp130 to competing receptors and sustain harm. Testing must establish exchange within a limiting surface pool and sustained functional harm; neutral, beneficial or transient allocation would not confirm this harmful mechanism.
- Connected mitochondria may protect ageing heart cells when muscle glutamine supply fallsOct 6, 2026An early-fasting mimic may protect ageing heart muscle cells by keeping their mitochondria connected, reducing reliance on muscle glutamine. The hypothesis would be rejected if independent changes in connectivity fail to shift the threshold for loss of heart function when glutaminase activity is reduced.
- Muscle glutamine may protect the heart by supporting glutathione-dependent lipid peroxide removalOct 6, 2026An early-fasting mimetic may protect the heart by using muscle glutamine to make glutathione. The claim would be challenged if restoring energy supply alone restored protection, or if blocking lipid damage failed to restore function while glutamine oxidation remained low.
- Muscle glutamine may protect the heart by supplying nitrogen for protein glycosylationOct 6, 2026During delayed feeding, muscle glutamine may preserve heart protein quality through nitrogen-dependent sugar production. The proposal predicts that blocking this pathway removes protection despite preserved energy and glutathione; protection persisting under that blockade would reject its claimed necessity.
- Early-fasting mimetics may protect the heart by burning glutamine supplied by muscleOct 6, 2026In old mice with delayed feeding, a fasting mimetic may sustain heart energy using muscle-derived glutamine, potentially depleting muscle over repeated cycles. Failure of alternative fuel to restore protection despite verified recovery of energy flow in an isolated heart would reject this explanation.
- Mismatched ribosome assembly may make muscle recovery limit fasting-mimetic lifespan gainsOct 6, 2026In old mice, muscle protein production between fasting-mimetic cycles may outpace ribosome assembly, causing toxic protein buildup and limiting lifespan gains. Shorter life after blocking this recovery, despite normal ribosome assembly, would count against the hypothesis.
- Incomplete sarcomere repair may erase a fasting mimetic's lifespan benefitOct 6, 2026Blocking muscle rebuilding between cycles could erase a fasting mimetic's lifespan benefit by preventing filamin C replacement in Z-discs. Losing that benefit with intact Z-discs and no dependence on mechanical load would refute the mechanism.
- Suppressing fatal disease outside muscle may preserve a mimetic’s lifespan benefitOct 6, 2026A substance that mimics fasting may extend animal lifespan by suppressing fatal disease outside muscle despite blocked muscle recovery. The hypothesis fails if restoring muscle recovery restores a lost survival benefit while disease in other tissues remains comparable
Forecasts
What the forecasts expect here
- When will the first NEDD8-pathway drug with a longevity indication reach Phase 2b trials?17% yesby Nov 1, 2026
- When will a Phase 2/3 trial show an aging-biology target improving a hard functional endpoint beyond molecular markers?17% yesby Nov 1, 2026
- When will therapeutic plasmapheresis confirm a reduction in biological age or mortality in a randomized trial?17% yesby Nov 1, 2026
- In what year will Loyal get FDA conditional approval for a daily dog-longevity pill?17% yesby Nov 1, 2026
- Will canagliflozin (SGLT2 inhibitor) plus low-dose rapamycin show synergy in old marmosets — HSC rejuvenation without high-dose immunosuppression?17% yesby Nov 1, 2026
- Will TRIAD (rapamycin in aging dogs, 580 animals, 3-year design) show a survival or disease-onset benefit by 30 Jun 2028?20% yesby Nov 1, 2026
- Will a large rapamycin/rapalog trial in older adults show a convincing signal on immune resilience, frailty, or functional endpoints before 2028?20% yesby Nov 1, 2026
- Will Retro Biosciences publish first human safety/PK/biomarker data on RTR242 and move to Phase 2 by 30 Jun 2028?20% yesby Nov 1, 2026
This month
Reported recently
- Life extension has spawned two industries: clinics sell scans and procedures of sometimes questionable benefit to patients paying out of pocket, while biotech and pharmaceutical companies pursue drugs to treat aging, The Economist reportsNov 5, 2026Longevity has split into clinics selling costly, unproven services and drug developers attracting billions while navigating regulatory barriers.
- In mice with Duchenne muscular dystrophy, immune cells with an engineered receptor cleared most uPAR-bearing cells that sustained muscle inflammation and scarring: tissue regeneration resumed, and lower-leg muscle strength reached 1,8 times that of controlsNov 5, 2026uPAR-targeted CAR-T cells reduced muscle inflammation and scarring in mice with Duchenne muscular dystrophy, restoring regeneration and improving strength.
- Liver biopsy ten weeks after a single gene therapy infusion showed correction of the faulty DNA “letter” in 54–57% of gene copies in a patient with alpha-1 antitrypsin deficiency, with no unintended edits detectedNov 4, 2026A single low-dose YOLT-202 infusion corrected 54–57% of faulty gene copies in liver tissue, restored functional protein production and caused no detectable unintended edits.
- Dog aging researchers identify LINE-1 “jumping” DNA as a potential drug target, while the relative effects of IGF-1 on aging during development and adulthood remain uncertainNov 4, 2026Dog aging data implicate LINE-1 activation as a potential therapeutic target, while whether IGF-1 shapes aging mainly during development or adulthood remains unresolved.
- A review from Wrocław proposes testing the hypothesis that aging is a wound that never begins to heal by measuring the speed and completeness of tissue recovery after a defined injuryNov 4, 2026A review proposes testing whether aging reflects stalled tissue repair by measuring response magnitude, resolution speed, and functional recovery after injury.
- Three claims about the first ER-100 gene therapy results require different evidence: better vision, tissue rejuvenation and a longer healthspan, says biologist George MurphyNov 4, 2026Early ER-100 vision results warrant further study, but clinical benefit, retinal rejuvenation and longer healthspan each require distinct evidence.
- Revel Pharmaceuticals co-founder chose enzymes to repair aging proteins over cell reprogramming, using differences between old and young tissue to identify repair targetsNov 4, 2026Revel engineers enzymes such as CMLase to reverse age-related protein damage, aiming to restore tissue function without cell reprogramming.
- Maternal mitochondria that “three-parent IVF” was intended to replace have been found in some children, prompting debate over whether to suspend its use for mitochondrial disease or test it first for infertilityNov 4, 2026Maternal mitochondrial DNA can rebound after three-parent IVF, renewing debate over its safety for mitochondrial disease and its experimental use in infertility.