Living dossier · Competitive landscape

Cellular senescence in Age-related functional decline

Primary identifiers: 13
Sponsors tracked: 12
Evidence types: 2 of 3
Last refreshed: 2026-07-28 · monthly

MightyRayn panel synthesis

OmniRayn’s reading of this landscape — our interpretation, not a registry fact

Read the sponsor column before the mechanism column. Every interventional programme here is run by a university, a hospital or a small diagnostics company — there is no large pharmaceutical sponsor anywhere on this page. That is not an oversight in our enumeration; it is the finding. The agents being tested are off-patent natural compounds (fisetin, quercetin, a vitamin-E fraction) or repurposed generics (dasatinib, digoxin), so there is no composition of matter for a sponsor to own, and the trials are sized accordingly: n=25 to n=220, mostly single centre, several explicitly labelled pilots. Set that against our Lp(a) landscape, where Amgen, Novartis and Lilly are each running outcome trials on the order of ten thousand participants. Same year, same registry, opposite capital. The difference is not the strength of the biology — it is ownability. Two caveats that the trial records alone will not tell you, and both come from the most authoritative venues available. The JAMA geroscience review states that greater senescent-cell abundance tracks with physical impairment and mortality, and that clearing these cells extends lifespan in animals, yet concludes the benefit of reducing them in humans remains unclear. And a Science perspective argues senescent cells can PROMOTE health and serve physiological roles — so indiscriminate clearance carries a mechanistic downside, not merely an efficacy risk. Anyone reading this field as a proven biology merely starved of capital has the funding half right and the biology half backwards. What would change our reading: a trial powered on a hard functional endpoint rather than a molecular clock or a biomarker, and a senescent-cell biomarker specific enough to confirm the drug did what it was meant to do.

Programs and primary evidence

Sponsor	Asset	Phase	Mechanism	Primary source
Sundeep Khosla, M.D. (Mayo Clinic)	Dasatinib + quercetin / fisetin (skeletal health)	2	intermittent senolytic clearance of senescent cells	NCT04313634 — Completed 20-week open-label randomised trial in older humans, n=74 — titled for targeting cellular senescence directly. CAVEAT: open-label, single-centre, and a bone-turnover rather than a fracture endpoint
Mayo Clinic	Fisetin (AFFIRM, frailty)	2	flavonoid senolytic	NCT03430037 — Placebo-controlled study of frailty and inflammation in older women. CAVEAT: n=40, single-centre, still enrolling by invitation eight years after start — a slow read, not a definitive one
TruDiagnostic	Dasatinib + quercetin (epigenetic age)	2	senolytic effect measured against epigenetic-clock readouts	NCT04946383 — Effect on epigenetic aging rates in healthy individuals. CAVEAT: n=25, single site, and registry status is UNKNOWN — no verified result; the endpoint is a molecular clock, not a clinical outcome
Cedars-Sinai Medical Center	Dasatinib + quercetin (adipose senescence)	2/3	senolytic plus lifestyle intervention, read out by single-nuclei RNA sequencing of adipose	NCT05653258 — Maps senescent cells in adipose tissue of older subjects, n=160 — one of the few trials measuring the cells the drug is meant to remove, rather than a downstream proxy
Cedars-Sinai Medical Center	Fisetin (OLD AIR, lung function)	2	flavonoid senolytic against age-related lung decline	NCT07676435 — Double-blind placebo-controlled study of age-related lung function decline. CAVEAT: n=40, single-centre pilot scale
Northwestern University	Fisetin (FIRST, peripheral artery disease)	2	senolytic targeting senescence-driven mobility loss	NCT06399809 — Pilot randomised trial of senescence and mobility impairment in peripheral artery disease. CAVEAT: explicitly a pilot at n=34 — sized to inform a later trial, not to decide the question
Ohio State University	Dasatinib + quercetin (multiple sclerosis)	1	senolytic applied to accelerated ageing in a neurological population	NCT07270120 — Physical and cognitive function in older adults with secondary progressive MS, n=30. CAVEAT: Phase 1 — safety and feasibility, not efficacy
University of Leeds	Digoxin (repurposed senolytic)	2	cardiac glycoside repurposed to clear senescent cells from adipose tissue	NCT06240403 — Titled as a NEW senolytic for dysfunctional adipose tissue in heart failure with type 2 diabetes, n=100 — an off-patent generic entering the field on repurposing grounds
National University of Malaysia	Tocotrienol-rich fraction	N/A	vitamin-E fraction evaluated as a senolytic agent	NCT07637487 — Placebo-controlled study in middle-aged adults, n=220 — the largest trial on this page, and it tests a nutraceutical rather than a drug
Wake Forest University School of Medicine	review (JAMA)	—	geroscience — modifying ageing biology rather than one disease	10.1001/jama.2025.11289 — States that greater abundance of senescent cells is associated with more physical impairment and increased mortality, and that clearing them extends lifespan in animal models — but concludes the potential health benefits of reducing senescent cells IN HUMANS remain unclear
University of Birmingham	perspective (Science)	—	senescence as normal physiology, not only pathology	10.1126/science.adj7050 — Argues that senescent cells can PROMOTE health and have physiological roles — the direct counterweight to the thesis that clearing them is straightforwardly beneficial
MRC Laboratory of Medical Sciences	review (Nat Rev Drug Discov)	—	senolytics, senomorphics, senescence mitigation, immune clearance	10.1038/s41573-024-01074-4 — Notes senescence has a crucial role in development, tissue maintenance and cancer prevention, and reviews the challenges in moving senotherapies into clinical practice
S.D. Asfendiyarov Kazakh National Medical University	review (Biomolecules)	—	senolytics that kill senescent cells vs senomorphics that mute their secretome	10.3390/biom15060860 — Draws the senolytic/senomorphic distinction and flags the biological heterogeneity of senescent cells and the absence of specific biomarkers as core obstacles

Method and limits

Programs are enumerated from primary registries (ClinicalTrials.gov, PubMed). A program appears here only if a primary record links this target to this indication as a therapeutic hypothesis — associations and risk markers are excluded by design.
Every claim above carries the identifier it rests on. We report what the record states; we do not assert efficacy, and computational findings are pending wet-lab confirmation.
Absence is not evidence of absence: unregistered, non-US and stealth-stage programs are not visible to these sources.
This page refreshes monthly (no net-new primary entity in 41 days). Mechanism classifications are our reading of the public record and may be revised.

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