Long game
Is there any evidence it makes people live longer?
Read this one carefully. Almost everything sold for longevity has never been tested against death in a human being, and this page will say so plainly when that is the case.
1,483,885
people in trials
60
human studies
57
compounds, animal or cell only
11
trials found nothing
Measured in people
Ranked by how many people, which is a fact about the evidence and not a judgement about the compound. The one at the top is the most studied, which is not the same as the best. Counts are never added across compounds, because the same person can appear in more than one trial.
- 1,206,174 people1 human study
Two separate pieces of work in one short paper. An observational weighted regression across 18 neighbouring Japanese municipalities totalling 1,206,174 individuals found an inverse correlation between tap water lithium concentration and all-cause mortality (beta -0.661, p = 0.003). Separately, exposing Caenorhabditis elegans to a comparably low lithium chloride concentration extended lifespan (p = 0.047). The human half is an ecological correlation between places, not an intervention in people, and the lifespan half is a worm.
European Journal of Nutrition, 2011 · 1,206,174 people
- 199,698 people1 human study
The epidemiology that any page about giving people more IGF-1 has to state. 199,698 men in UK Biobank followed a mean of 6.9 years, 5,402 diagnosed with and 295 dying from prostate cancer. Higher circulating IGF-1 was associated with prostate cancer diagnosis (hazard ratio 1.09 per 5 nmol/L increment, 95 percent CI 1.05 to 1.12) and with prostate cancer mortality (1.15, 1.02 to 1.29), with hazard ratios corrected for regression dilution using repeat measurements. A two-sample Mendelian randomisation analysis using genetic instruments and outcome data from 79,148 cases and 61,106 controls supported a causal role (cis-MR odds ratio 1.34 per 5 nmol/L, 1.07 to 1.68). This is an association study in men with naturally varying IGF-1, not a study of mecasermin, and it does not establish that treating a deficient child raises cancer risk.
International Journal of Cancer, 2021 · 199,698 people
- 24,980 people2 human studies
20,536 UK adults aged 40 to 80 with coronary, other occlusive arterial disease or diabetes, randomised to 40 mg simvastatin daily or placebo. All-cause mortality 12.9 percent versus 14.7 percent (p equals 0.0003). Major vascular events fell 24 percent, from 25.2 percent to 19.8 percent. Benefit held even in participants entering with LDL cholesterol below 3.0 mmol/L. The annual excess risk of myopathy was about 0.01 percent.
Lancet, 2002 · 20,536 people
4,444 people with angina or previous myocardial infarction, randomised double-blind, median follow-up 5.4 years. 256 placebo patients (12 percent) died against 182 on simvastatin (8 percent), relative risk of death 0.70 (95 percent CI 0.58 to 0.85, p equals 0.0003). Coronary deaths fell from 189 to 111. Major coronary events occurred in 28 percent on placebo and 19 percent on simvastatin.
Lancet, 1994 · 4,444 people
Also measured, in animals or cells
found nothingInterventions Testing Program. Simvastatin at 12 and 120 ppm in the diet had no significant effect on survival in male or female mice. Resveratrol at 300 and 1200 ppm also had none. In the same cohort rapamycin, started at 9 months, extended median survival by an average of 10 percent in males and 18 percent in females, including maximum life span, at each of three test sites.
- 12,597 people2 human studies
EMPA-KIDNEY. 6,609 people with chronic kidney disease, median 2.0 years. Kidney disease progression or cardiovascular death occurred in 13.1 percent against 16.9 percent (hazard ratio 0.72). Notably for anyone reading the drug as a mortality intervention, death from any cause was 4.5 percent against 5.1 percent and was not a significant difference in this trial.
New England Journal of Medicine, 2023 · 6,609 people
EMPEROR-Preserved. 5,988 people with class II to IV heart failure and an ejection fraction above 40 percent, median 26.2 months. Cardiovascular death or heart failure hospitalisation occurred in 13.8 percent against 17.1 percent (hazard ratio 0.79). The authors state the effect was mainly driven by fewer heart failure hospitalisations rather than fewer deaths.
New England Journal of Medicine, 2021 · 5,988 people
Also measured, in animals or cells
The entire mouse lifespan case, from one laboratory. Empagliflozin extended the median survival of male mice by 5.9 percent, improved learning, memory and motor balance, lowered body weight, reduced hepatic P21 and P16, altered gut flora composition and raised short-chain fatty acids. A single-site study, not part of any multi-site replication programme.
GeroScience, 2024 · animal
This is the Interventions Testing Program SGLT2 result, and it is canagliflozin, not empagliflozin. Canagliflozin at 180 ppm in chow from 7 months of age extended median male survival by 14 percent and raised the 90th percentile survival age by 9 percent, with parallel effects at all three test sites. No lifespan benefit in females. Attributing this result to empagliflozin is a factual error that circulates widely.
JCI Insight, 2020 · animal
- 8,341 people1 human study1 found nothing
found nothingThe historical result that kept niacin in the guidelines for thirty years, and it is weaker than its reputation. In the Coronary Drug Project, 8,341 men aged 30 to 64 with a previous myocardial infarction were treated between 1966 and 1975. Niacin modestly reduced definite non-fatal recurrent myocardial infarction but did not reduce total mortality during the trial. At a mean follow-up of 15 years, nearly 9 years after the drug was stopped, all-cause mortality was 52.0 percent on niacin versus 58.2 percent on placebo, 11 percent lower, P=0.0004. This is a post-trial observational mortality difference in a pre-statin population, not a result obtained on top of modern therapy, and both AIM-HIGH and HPS2-THRIVE tested niacin on top of modern therapy and found nothing.
Journal of the American College of Cardiology, 1986 · 8,341 people
- 7,050 people3 human studies1 found nothing
found nothing4,228 asymptomatic people with ejection fraction 0.35 or below, mean follow-up 37.4 months. Total mortality 313 versus 334 deaths, risk reduction 8 percent (95 percent CI -8 to 21, p = 0.30), not significant. Death or development of heart failure 630 versus 818 (29 percent reduction, p < 0.001). The null mortality result in people without symptoms is the relevant one for anyone reading enalapril as a longevity drug.
New England Journal of Medicine, 1992 · 4,228 people
2,569 patients with symptomatic heart failure and ejection fraction 0.35 or below, enalapril 2.5 to 20 mg a day or placebo, mean follow-up 41.4 months. Deaths 452 (35.2 percent) versus 510 (39.7 percent), risk reduction 16 percent (95 percent CI 5 to 26, p = 0.0036); death or heart failure hospitalisation 613 versus 736 (26 percent reduction). Run by the US National Heart, Lung, and Blood Institute.
New England Journal of Medicine, 1991 · 2,569 people
253 patients with NYHA class IV heart failure, double-blind, enalapril 2.5 to 40 mg a day or placebo on top of conventional therapy. Six-month mortality 26 versus 44 percent (40 percent reduction, p = 0.002); one-year 31 percent reduction; 50 versus 68 deaths overall (27 percent). Entire benefit in progressive heart failure deaths, none in sudden death. Hypotension withdrawals 7 versus 0. Funding not stated in the abstract retrieved.
New England Journal of Medicine, 1987 · 253 people
Also measured, in animals or cells
found nothingReanalysis of 132 ITP comparisons from 2004 to 2022. Enalapril 120 ppm from 4 months, 170 treated males against 357 controls: median lifespan +7 percent, log-rank p = 0.22 (not significant), Gehan p = 0.046, proportional hazards assumption violated. No female effect. No multiplicity correction reported. The authors describe the benefit as limited to midlife. NIA funded.
GeroScience, 2024 · animal
The ITP report whose cohort included enalapril and CAPE as agents that did not significantly extend lifespan by log-rank test in either sex, alongside the landmark rapamycin result. NIA funded.
Nature, 2009 · animal
- 6,800 people1 human study1 found nothing
found nothing6,800 patients with heart failure and ejection fraction 0.45 or less randomised to digoxin or placebo, average follow-up 37 months. Mortality unchanged: 1,181 deaths (34.8 percent) versus 1,194 (35.1 percent), risk ratio 0.99, 95 percent confidence interval 0.91 to 1.07. Hospitalisation for worsening heart failure fell from 34.7 to 26.8 percent, risk ratio 0.72. This is cardiology evidence and says nothing about senescence.
New England Journal of Medicine, 1997 · 6,800 people
- 3,236 people1 human study
3,236 adults followed 21 years: higher plasma ergothioneine independently predicted lower coronary disease, cardiovascular and overall mortality.
Heart, 2020 · 3,236 people
- 2,435 people3 human studies1 found nothing
Pooled analysis of two Japanese cohorts, 2,435 patients with acute decompensated heart failure split by carperitide dose. Cardiovascular and all-cause mortality within 1 year were lower in the low-dose group (at or above 0.02 micrograms per kilogram per minute) than in the no-carperitide and very-low-dose groups. This observational result points in the opposite direction to the propensity-matched in-hospital analyses and is reported here alongside them, not instead of them.
ESC Heart Failure, 2022 · 2,435 people
found nothing9 studies, 4 randomised and 5 propensity score-matched. Pooled in-hospital mortality was higher with carperitide, odds ratio 1.38, 95 percent confidence interval 1.07 to 1.78, with high heterogeneity (I squared 77 percent). The 4 randomised trials alone gave odds ratio 0.85 with a 95 percent confidence interval of 0.07 to 10.49, which is uninformative. No significant difference in long-term mortality, rehospitalisation, hypotension or length of stay.
BMC Cardiovascular Disorders, 2025 · no headcount in the line
Retrospective multicentre cohort, 402 of the patients treated with carperitide, 367 matched pairs analysed. Carperitide was associated with in-hospital mortality, odds ratio 2.13, 95 percent confidence interval 1.17 to 3.85, with a larger association in older patients (odds ratio 2.93, 1.54 to 5.91). Observational, so treatment choice and severity cannot be separated.
Journal of Cardiac Failure, 2015 · no headcount in the line
- 2,000 people2 human studies
2,000 New Zealand women aged 65 or older with osteopenia, randomised to four infusions of 5 mg zoledronate or saline at 18-month intervals over six years. Fragility fracture occurred in 190 on placebo and 122 on zoledronate, hazard ratio 0.63 (95 percent CI 0.50 to 0.79). Number needed to treat 15. This is the large trial in older women, and its primary endpoint was fracture, not mortality.
New England Journal of Medicine, 2018 · 2,000 people
HORIZON Recurrent Fracture Trial, NCT00046254. 1,065 assigned to yearly 5 mg intravenous zoledronic acid and 1,062 to placebo within 90 days of hip fracture repair, mean age 74.5, median follow-up 1.9 years. Primary endpoint new clinical fracture: 8.6 percent against 13.9 percent, a 35 percent reduction. In the safety analysis 101 of 1,054 (9.6 percent) on drug and 141 of 1,057 (13.3 percent) on placebo died, a 28 percent reduction in all-cause death, p equals 0.01. Mortality was not the primary endpoint. Commonest adverse events were pyrexia, myalgia and bone and musculoskeletal pain; no osteonecrosis of the jaw was reported.
New England Journal of Medicine, 2007 · no headcount in the line
Also measured, in animals or cells
Mayo Clinic. In human lung fibroblasts and DNA-repair-deficient mouse embryonic fibroblasts, zoledronic acid killed senescent cells with minimal effect on non-senescent cells. In aged mice treated for eight weeks it significantly reduced circulating SASP factors including CCL7, IL-1 beta, TNFRSF1A and TGF beta 1, and improved grip strength. Cell and mouse work proposing a senolytic or senomorphic mechanism for the non-skeletal effects; it does not test the mortality question in people.
Aging (Albany NY), 2023 · animal
- 1,161 people2 human studies1 found nothing
found nothing1,161 patients hospitalised with acute heart failure randomised 1:1 to a 48 hour infusion of serelaxin at 30 micrograms per kilogram per day or placebo within 16 hours of presentation. Serelaxin improved the visual analogue scale dyspnoea endpoint by 448 mm times hours (95 percent CI 120 to 775, p = 0.007) but had no effect on the co-primary Likert endpoint (27 percent against 26 percent, p = 0.70). There was no effect on cardiovascular death or readmission at 60 days (hazard ratio 1.02, 0.74 to 1.41) or on days alive out of hospital. Among prespecified additional endpoints, 42 deaths occurred by day 180 on serelaxin against 65 on placebo, hazard ratio 0.63 (0.42 to 0.93, p = 0.019). Funded by Corthera, a Novartis affiliate company. Registered as NCT00520806.
The Lancet, 2013 · 1,161 people
An adjudicated analysis of every death in RELAX-AHF-2, run specifically to understand why the two trials disagreed. By 180 days 11.5 percent of patients had died, 38 percent of those deaths from heart failure. Unlike in RELAX-AHF, there was no apparent effect of serelaxin on any category of cause of death. Patients aged 75 or over died more often (14.2 percent against 8.8 percent) and more often from non-cardiovascular causes. Patients with preserved ejection fraction had less heart failure mortality (30 percent against 40 percent) and more non-cardiovascular mortality (36 percent against 20 percent).
JACC: Heart Failure, 2020 · no headcount in the line
- 1,106 people2 human studies1 found nothing
found nothing1,106 adults with sepsis, 22 centres, double blinded and placebo controlled. 28 day all cause mortality was 23.4% on thymosin alpha-1 and 24.1% on placebo, hazard ratio 0.99, p = 0.93. Included here as the contrast: this is what a defined thymic peptide looks like when tested under modern conditions, and the result was null.
BMJ, 2025 · 1,106 people
266 elderly and older persons assessed over six to eight years, with thymalin and epithalamin applied during the first two to three years. Acute respiratory disease incidence fell 2.0 to 2.4-fold, with reduced clinical ischaemic heart disease, hypertension, deforming osteoarthrosis and osteoporosis against control. Mortality fell 2.0 to 2.1-fold with thymalin, 1.6 to 1.8-fold with epithalamin and 2.5-fold with both, and a separate group treated with both annually for six years had a 4.1-fold lower mortality rate. Single group, no described blinding or randomisation, never replicated.
Neuro Endocrinology Letters, 2003 · no headcount in the line
- 1,106 people1 human study
1,106 adults with sepsis at 22 Chinese centres: 28-day mortality 23.4% with thymosin alpha-1 vs 24.1% with placebo (HR 0.99), so no clear mortality benefit.
BMJ, 2025 · 1,106 people
- 1,106 people1 human study
1,106 adults with sepsis across 22 centres in China, randomised 1 to 1 to subcutaneous thymosin alpha-1 or placebo every 12 hours for seven days. 28 day all cause mortality was 23.4% on thymosin alpha-1 and 24.1% on placebo, hazard ratio 0.99, 95% CI 0.77 to 1.27, p = 0.93. No secondary or safety outcome differed significantly. The trial found no clear evidence that thymosin alpha-1 decreases 28 day mortality in sepsis. Several authors received grants from the manufacturer, disclosed in the paper.
BMJ, 2025 · 1,106 people
- 876 people1 human study
876 Swedish men aged 35 to 80 followed up to 14 years: serum GDF15 at entry predicted all-cause mortality with an adjusted odds ratio of 3.38 (95 percent CI 1.38 to 8.26), validated in 324 same-sex twins and independent of telomere length, IL-6 and CRP. An association in a cohort, not an intervention.
Aging Cell, 2010 · 876 people
- 778 people1 human study
778 patients: 28-day mortality 35.4% with low-dose vasopressin versus 39.3% with norepinephrine, not significantly different.
New England Journal of Medicine, 2008 · 778 people
- 513 people2 human studies
The only randomised human data on glutaminase inhibition. 444 patients with metastatic renal cell carcinoma. Median progression-free survival 9.2 months with telaglenastat plus cabozantinib versus 9.3 months with placebo plus cabozantinib, hazard ratio 0.94, P = 0.65. Manufacturer funded. Oncology, not senescence.
JAMA Oncology, 2022 · 444 people
69 patients randomised 2:1. Median progression-free survival 3.8 months versus 1.9 months, hazard ratio 0.64, one-sided P = 0.079 against a pre-specified one-sided alpha below 0.2. Grade 3 to 4 events in 74 percent versus 61 percent. Manufacturer funded.
Clinical Cancer Research, 2022 · 69 people
Also measured, in animals or cells
Human cells and mice. GLS1 was identified as essential for the survival of human senescent cells: lysosomal damage lowers intracellular pH, inducing kidney-type glutaminase, whose ammonia production neutralises the acidity. Inhibiting it in aged mice eliminated senescent cells specifically and ameliorated age-associated organ dysfunction.
Science, 2021 · animal
- 513 people2 human studies1 found nothing
found nothing444 patients randomised, double blind, placebo controlled. Median progression-free survival 9.2 versus 9.3 months, hazard ratio 0.94, 95 percent confidence interval 0.74 to 1.21, P = 0.65. Overall response 31 versus 28 percent. Grade 3 to 4 adverse events in 71 versus 79 percent. Manufacturer funded. The primary endpoint was missed.
JAMA Oncology, 2022 · 444 people
69 patients randomised 2:1 after a median of three prior lines. Median progression-free survival 3.8 versus 1.9 months, hazard ratio 0.64, 95 percent confidence interval 0.34 to 1.20, one-sided P = 0.079 against a pre-specified one-sided alpha below 0.2. One partial response on telaglenastat. Grade 3 to 4 events 74 versus 61 percent. Manufacturer funded.
Clinical Cancer Research, 2022 · 69 people
Also measured, in animals or cells
Mouse and human cells. The senolytic rationale for this drug class: glutaminase 1 is required for senescent cell survival, and inhibiting it in aged mice eliminated senescent cells and improved age-associated organ dysfunction. This is why telaglenastat appears on senolytic lists. It is a mouse result.
Science, 2021 · animal
- 480 people2 human studies
480 patients randomised to 250 mg azithromycin three times weekly or placebo for two years after allogeneic transplant. Stopped early in December 2016 after the safety board detected an imbalance in haematological relapses. Two-year airflow decline-free survival 32.8 percent on azithromycin against 41.3 percent on placebo (hazard ratio 1.3). Two-year survival 56.6 percent against 70.1 percent (hazard ratio 1.5, 95 percent CI 1.1 to 2.0). Two-year cumulative haematological relapse 33.5 percent against 22.3 percent. Long-term low-dose azithromycin produced worse outcomes than placebo.
JAMA, 2017 · 480 people
Tennessee Medicaid cohort. During five days of azithromycin, compared with no antibiotics, risk of cardiovascular death rose (hazard ratio 2.88, 95 percent CI 1.79 to 4.63) and of death from any cause (1.85, 1.25 to 2.75). Amoxicillin showed no such increase. Estimated 47 additional cardiovascular deaths per million courses, and 245 per million in the highest cardiovascular risk decile. An observational cohort, not a randomised trial, and the absolute risk is small.
New England Journal of Medicine, 2012 · no headcount in the line
- 420 people1 human study
420 patients with moderate to severe chronic heart failure, 100 mg three times daily, two years. Major adverse cardiovascular events 15% against 26%, hazard ratio 0.50 (95% CI 0.32 to 0.80, p = 0.003). Cardiovascular mortality 9% against 16% (p = 0.026) and all-cause mortality 10% against 18% (p = 0.018). The short-term 16-week endpoints were null.
JACC Heart Failure, 2014 · 420 people
- 412 people1 human study
412 patients randomised to placebo or escalating minocycline up to 400 mg per day for nine months. ALSFRS-R deterioration was faster on minocycline, -1.30 against -1.04 units per month (p equals 0.005), with non-significant trends toward faster decline in forced vital capacity and muscle testing and greater mortality (hazard ratio 1.32). The authors concluded minocycline had a harmful effect with implications for its trials in other neurological disorders.
Lancet Neurology, 2007 · 412 people
Also measured, in animals or cells
Interventions Testing Program cohort comparing three late-life rapamycin regimens started at 20 months. Rapamycin at 42 ppm increased survival in both sexes. The same experimental design tested four other drugs, minocycline, beta-guanidinopropionic acid, MitoQ and 17-DMAG, and none of these led to a change in survival in either sex.
Aging Cell, 2020 · animal
- 407 people1 human study
Open label phase 3, 407 patients with untreated advanced melanoma randomised 1:1 to IO102-IO103 (85 mcg each) plus pembrolizumab or pembrolizumab alone for up to 2 years. Median progression free survival 19.4 versus 11.0 months, HR 0.77 (95% CI 0.58 to 1.00), p = 0.0558; the prespecified threshold of p at most 0.045 was missed. Grade 3 or worse treatment related adverse events 14.5 versus 15.6 percent; injection site reactions in 56 percent. Sponsored by IO Biotech; the authors declare extensive industry relationships.
Annals of Oncology, 2026 · 407 people
- 356 people2 human studies
Gargano Heart Study, 356 patients with type 2 diabetes, mean follow-up 5.4 years, 58 cardiovascular deaths. The ADIPOQ variant rs822354 raised adiponectin and was associated with cardiovascular mortality (incidence rate ratio 1.94, 95 percent CI 1.23 to 3.07), with a genetic effect larger than the observational one, interpreted by the authors as evidence that the paradoxical association is causal. Non-US government funded.
Cardiovascular Diabetology, 2016 · 356 people
Population-based cohort of older adults. In those free of cardiovascular disease, the association with all-cause mortality was U-shaped: hazard ratio 0.81 per SD up to 12.4 mg/L, then 1.19 per SD (95 percent CI 1.12 to 1.27) above it. No association in those with cardiovascular disease alone; in heart failure or atrial fibrillation, higher adiponectin meant higher mortality, hazard ratio 1.31 (1.15 to 1.50) after adjustment. Results were similar for high molecular weight adiponectin and cardiovascular death. NIH funded.
Circulation, 2012 · no headcount in the line
- 309 people1 human study
COMFORT-I, NCT00952289, 309 patients with intermediate-2 or high-risk myelofibrosis. Spleen volume reduction of at least 35 percent at 24 weeks: 41.9 percent on ruxolitinib against 0.7 percent on placebo. Total symptom score improved by at least 50 percent in 45.9 percent against 5.3 percent. Thirteen deaths on ruxolitinib against 24 on placebo (hazard ratio 0.50, 95 percent CI 0.25 to 0.98). Anaemia and thrombocytopenia were the commonest adverse events; both transformations to acute myeloid leukaemia were in the ruxolitinib arm. This is a cancer trial, not an ageing trial.
New England Journal of Medicine, 2012 · 309 people
- 308 people3 human studies
266 elderly people in Russia and Ukraine followed 6 to 8 years, treated during the first 2 to 3 years: in the Thymalin arm acute respiratory illness fell 2.0 to 2.4-fold and mortality was 2.0 to 2.1-fold lower than control; combined with Epithalamin the reported reduction was 2.5-fold, and 4.1-fold in a subgroup dosed annually for 6 years. Open-label, single research lineage.
Neuro Endocrinology Letters, 2003 · 266 people
Single-centre, open-label, prospective randomized controlled trial, April to July 2020: 42 patients received thymalin 10 mg intramuscularly daily for 5 days plus standard care, 50 received standard care. No deaths in either group. Radiological progression in 2 of 42 treated against 5 of 50 controls, with faster falls in IL-6, C-reactive protein and D-dimer.
Stem Cell Reviews and Reports, 2021 · 42 people
Three-arm comparison in severe COVID-19 in middle-aged and elderly patients: hospital mortality 40.9% on standard therapy, 28.4% with tocilizumab and 20.6% with thymalin, per the English abstract. Group sizes are not reported, and the paper's own Russian abstract gives different figures for two arms (28.8% and 16.2%).
Advances in Gerontology, 2022 · no headcount in the line
- 266 people3 human studies
266 elderly people in Russia and Ukraine followed 6 to 8 years, treated during the first 2 to 3 years: mortality 1.6 to 1.8-fold lower with Epithalamin, 2.0 to 2.1-fold lower with Thymalin, 2.5-fold lower with both, and 4.1-fold lower in a subgroup given both annually for 6 years; acute respiratory illness fell 2.0 to 2.4-fold. Open-label, single research lineage.
Neuro Endocrinology Letters, 2003 · 266 people
12-year randomized study in elderly coronary patients with accelerated cardiovascular aging: total deaths 28% lower and cardiovascular mortality 2-fold lower than control on the same basic therapy, with lower functional age and higher exercise tolerance. Not blinded, not placebo-controlled.
Bulletin of Experimental Biology and Medicine, 2006 · no headcount in the line
The same Kiev cohort at 15 years: 39 coronary patients given 6 courses of Epithalamin over 3 years plus basic therapy versus 40 on basic therapy alone, reporting slower cardiovascular aging, preserved physical endurance, normalized melatonin rhythm and significantly lower mortality. The title says pituitary; the text is about the pineal preparation Epithalamin.
Bulletin of Experimental Biology and Medicine, 2011 · no headcount in the line
- 196 people1 human study
196 patients: primary endpoint (alive and free of respiratory failure at day 60) not met; survival odds favored aviptadil in secondary analysis.
Critical Care Medicine, 2022 · 196 people
- 147 people2 human studies1 found nothing
found nothingRetrospective single-centre cohort of 147 patients needing 3 or more vasopressors, 56 given angiotensin II. After propensity score weighting mortality was 86.0 percent with angiotensin II and 71.0 percent without, a difference that was not statistically significant (p = 0.16), and more angiotensin II patients still required 5 or more vasopressors (45.9 versus 12.5 percent, p < 0.01). Observational, and the sicker patients were the ones given the drug.
Critical Care Explorations, 2022 · 147 people
Analysis of the ATHOS-3 population examining baseline and follow-up renin concentrations against survival, testing whether renin identifies which patients respond.
American Journal of Respiratory and Critical Care Medicine, 2020 · no headcount in the line
- 46 people1 human study
46 women with platinum-resistant high-grade serous ovarian cancer, median four prior lines, single-arm. Three-month progression-free survival 22.7 percent, median progression-free survival 1.64 months, one partial response and 15 stable diseases. Grade 3 or 4 thrombocytopenia in 12 of 46, causing dose reduction in 8 and discontinuation in 3. The authors concluded activity was poor.
Gynecologic Oncology, 2022 · 46 people
- 28 people1 human study
Two double blind placebo controlled phase 1 trials in adults aged 19 to 69 with Friedreich ataxia: single ascending dose 25 to 100 mg (28 participants) and multiple ascending dose up to 100 mg daily for 13 days (27 participants). Mostly mild adverse events, no serious adverse events or deaths; peak plasma levels at 15 minutes; frataxin rose in buccal cells, skin and platelets with higher and more frequent dosing. Funded by Larimar Therapeutics; most authors are or were Larimar employees.
Annals of Clinical and Translational Neurology, 2024 · 28 people
- 20 people1 human study
20 patients, median age 60.5, 60 percent female, dose escalation 0.04 to 0.4 mg/kg intravenously twice weekly. One dose-limiting toxicity, a grade 4 thrombocytopenia resolving within 48 hours; lowest first-cycle platelet count 24,000 to 297,000, recovery above 50,000 within four days in all cases. Stable disease in 20 percent, median overall survival 7.9 months. Recommended phase 2 dose 0.4 mg/kg. National Institutes of Health supported.
Journal of Hematology and Oncology, 2025 · 20 people
- 20 people1 human study
20 people with metastatic sarcoma received 20 mg subcutaneously daily. Median progression-free survival 2.7 months (95 percent confidence interval 1.4 to 4.1) and median overall survival 10.2 months (5.3 to 18.3). The placental growth factor biomarker effect seen in phase 1 was not confirmed. Two people with vascular sarcomas had prolonged disease stabilisation at 10 and 19 months.
Sarcoma, 2016 · 20 people
- no headcount stated1 human study
Adding 3 years of goserelin to radiotherapy raised 10-year disease-free survival from 22.7% to 47.7% and improved overall survival.
The Lancet Oncology, 2010 · no headcount in the line
- no headcount stated1 human study
Case report: a 92-year-old woman with atrial fibrillation, taking over-the-counter nattokinase and no prescribed anticoagulant or antiplatelet drug, developed spontaneous bleeding into the abdominal cavity and died. The authors warn against consumption of herbal supplements, especially nattokinase, in this kind of patient.
Cureus, 2021 · no headcount in the line
- no headcount stated1 human study1 found nothing
found nothingFrom the National Institute on Aging intramural programme. Measured longitudinally across three human cohorts, nonhuman primates and mice, taurine increased or stayed unchanged with age, contradicting the decline premise the 2023 lifespan paper rests on.
Science, 2025 · no headcount in the line
- no headcount stated1 human study
Human observational. Glycosylation features of alpha-2-macroglobulin vary with age. A measurement of how the protein changes across the lifespan, not a test of any intervention.
Cell Biochemistry and Biophysics, 2019 · no headcount in the line
- no headcount stated1 human study
The CLARINET randomised phase 3 in metastatic enteropancreatic neuroendocrine tumours, showing prolonged progression-free survival on lanreotide. A hard clinical endpoint in a randomised trial, which very few peptides documented on this site can claim.
New England Journal of Medicine, 2014 · no headcount in the line
- no headcount stated1 human study
The metabolomic screen that identified alpha-hydroxybutyrate, the reduction product of alpha-ketobutyrate, as an early marker of insulin resistance and glucose intolerance in non-diabetic people. This is the human context that the lifespan claim sits inside: in people, this branch of metabolism is elevated in the direction of metabolic disease rather than health.
PLoS One, 2010 · no headcount in the line
- no headcount stated1 human study
A 12-year study in elderly patients with coronary disease and accelerated cardiovascular aging. Deaths in the epithalamine group were 28 percent lower than control, cardiovascular mortality was 2-fold lower, and the incidence of cardiovascular failure and respiratory disease was 2-fold lower. Reported as randomised by its authors. Again the institute's own work, again the injectable extract, again no outside replication.
Bulletin of Experimental Biology and Medicine, 2006 · no headcount in the line
Also measured, in animals or cells
found nothingEpithalamin, the bovine pineal extract, raised mean lifespan by 11 to 31 percent in female Drosophila, SHR mice, C3H/Sn mice and LIO rats. Ninety percent mortality and maximum lifespan rose in flies, C3H/Sn mice and rats. Mortality rate fell 52 percent in flies, 52 percent in rats and 27 percent in C3H/Sn mice, and did not change at all in SHR mice. Note the split: the effect was absent in one of the four mouse and rat groups tested.
- no headcount stated1 human study1 found nothing
found nothing73 inpatients with COVID-19 pneumonia randomised to icatibant plus standard care or standard care alone. The primary endpoint, clinical response at day 10 or discharge, was 73.0 versus 55.6 percent and did not reach significance (p = 0.115). The secondary endpoint at 28 days favoured icatibant (100 versus 83.3 percent, p = 0.011) and no deaths occurred on icatibant versus 6 on control. Open-label and small, with the primary endpoint missed.
Clinical Infectious Diseases, 2023 · no headcount in the line
- no headcount stated1 human study1 found nothing
found nothingMonthly high-dose vitamin D in older Australian adults. All-cause mortality hazard ratio 1.04. No benefit, again in a population whose placebo group averaged about 31 ng/mL.
Lancet Diabetes and Endocrinology, 2022 · no headcount in the line
- no headcount stated1 human study
Pooled across 17 prospective cohorts. The highest blood omega-3 quintile carried roughly 15 to 18% lower mortality than the lowest. Observational, and the exposure is a measured blood level rather than a supplement taken.
Nature Communications, 2021 · no headcount in the line
Measured in animals or cells, not yet in people
These are separated from the trials above rather than ranked against them, because they answer a different question. A result in a rat is a real result and a reason somebody ran the study; it is not a measurement of what happens in you. Where the human work is missing, the reason is usually money rather than failure, and that is set out at the bottom of this page.
- 2 preclinical studies
Measured in animals or cells
Most potent senolytic among 10 flavonoids; late-life fisetin reduced senescence markers and extended median and maximum lifespan in mice.
EBioMedicine, 2018 · animal
NIA Interventions Testing Program: fisetin did not significantly affect lifespan in either sex at the doses used.
GeroScience, 2024 · animal
- 2 preclinical studies
Measured in animals or cells
found nothingNIA Interventions Testing Program: alpha-ketoglutarate did not increase lifespan in male or female mice at either starting age tested.
GeroScience, 2026 · animal
Dietary calcium AKG extended lifespan and compressed frailty in C57BL/6 mice, with lower systemic inflammatory cytokines.
Cell Metabolism, 2020 · animal
- 2 preclinical studies
Measured in animals or cells
Overexpression extended lifespan by about 20 to 30%.
Science, 2005 · animal
19.7% lifespan extension in males with bone, muscle and brain benefits.
Molecular Therapy, 2025 · animal
- 2 preclinical studies
Measured in animals or cells
Mouse, physiologically ageing wild-type rather than progeroid. Long-term partial reprogramming regimens produced duration-dependent effects in kidney and skin, with reversion of epigenetic clock measures and reduced inflammation, senescence and stress-response gene expression. The authors make no lifespan extension claim for wild-type mice.
Nature Aging, 2022 · animal
Mouse. Systemically delivered AAV encoding an inducible OSK system, given to 124-week-old male mice, extended median remaining lifespan by 109 percent over wild-type controls and improved frailty scores. Read the number carefully: this is remaining lifespan from very late life in male mice only, from one group, in a specialty journal, and it has not been replicated by the NIA Interventions Testing Program or any independent laboratory.
Cellular Reprogramming, 2024 · animal
- 2 preclinical studies
Measured in animals or cells
Mouse. In a PROGEROID model of premature ageing, short-term cyclic expression of Oct4, Sox2, Klf4 and c-Myc ameliorated cellular and physiological hallmarks of ageing and prolonged lifespan. In older WILD-TYPE mice the same treatment improved recovery from metabolic disease and muscle injury, with no lifespan claim made for those animals.
Cell, 2016 · animal
Mouse. The authors open by naming the gap directly: partial reprogramming extends the lifespan of a premature ageing mouse model, but the effects of longer-term partial reprogramming in physiologically ageing wild-type mice were unknown. Their result is molecular and tissue-level rejuvenation plus protocol safety, not lifespan.
Nature Aging, 2022 · animal
- 2 preclinical studies
Measured in animals or cells
Mouse and cultured cells. Low concentrations suppressed the senescence-associated secretory phenotype; higher concentrations killed senescent cells. Intermittent dosing of old mice alleviated physical dysfunction and prolonged survival. This paper is subject to an Editorial Expression of Concern issued in March 2026.
Nature Metabolism, 2021 · animal
Naturally aged mice. Long-term procyanidin C1 treatment reduced retinal senescent cell burden and ameliorated age-related structural and functional decline in the retina, characterised by single-cell RNA sequencing. Mouse, no lifespan endpoint.
Proceedings of the National Academy of Sciences, 2024 · animal
- 2 preclinical studies
Measured in animals or cells
CAPE 300 ppm from 4 months, 147 treated females against 289 controls: median lifespan +5 percent, log-rank p = 0.0665, Gehan p = 0.0481, proportional hazards assumption not violated. No male effect at 30 or 300 ppm. One of 132 comparisons reanalysed with no multiplicity correction reported. NIA funded.
GeroScience, 2024 · animal
found nothingThe ITP report whose cohort tested CAPE at two doses and found no significant lifespan effect in either sex by the protocol log-rank test. NIA funded.
Nature, 2009 · animal
- 2 preclinical studies
Measured in animals or cells
Green tea extract 2,000 ppm from 4 months, 129 treated females against 275 controls: median lifespan +7 percent, log-rank p = 0.37, Gehan p = 0.034, proportional hazards assumption violated. No male effect. One of 132 comparisons reanalysed without a reported multiplicity correction; the authors describe the effect as limited to midlife. NIA funded.
GeroScience, 2024 · animal
ITP report: none of the five agents, including green tea extract from 4 months, had a statistically significant effect on lifespan in either sex by log-rank test; a secondary analysis suggested the extract might reduce midlife deaths in females only. NIA funded.
- 2 preclinical studies
Measured in animals or cells
17-DMAG 30 ppm from 6 months, 152 treated males against 264 controls: median +7 percent, log-rank p = 0.12, Gehan p = 0.032, proportional hazards assumption not violated. No female effect. Effect on mortality appears diminished at later ages. One of 132 comparisons reanalysed with no multiplicity correction reported. NIA funded.
GeroScience, 2024 · animal
Screen of autophagy-regulating compounds in senescent Ercc1-deficient mouse fibroblasts identified HSP90 inhibitors as senolytic in mouse and human cells. In Ercc1-deficient progeroid mice, 17-DMAG extended healthspan, delayed onset of several age-related symptoms and reduced p16INK4a expression. Progeroid model, not normal ageing; no lifespan endpoint.
Nature Communications, 2017 · animal
- 2 preclinical studies
Measured in animals or cells
The ITP's own later summary: the metformin plus rapamycin survival results "were not significantly higher than those noted in earlier experiments using the same dose (14.7 ppm) of rapamycin by itself". Also reports rapamycin at 42 ppm from 20 months extending lifespan in both sexes. NIA funded.
Aging Cell, 2020 · animal
Rapamycin alone at 42 ppm extended median lifespan 23 percent in males and 26 percent in females, with maximal lifespan increased in both sexes, and females gained more at every dose. The benchmark showing rapamycin alone can match the combination's 23 percent when its dose is tripled. NIA funded.
Aging Cell, 2014 · animal
- 2 preclinical studies
Measured in animals or cells
Interventions Testing Program. 17-alpha-estradiol at a threefold higher dose than previously tested robustly extended both median and maximal lifespan, still only in males. The same paper reports nordihydroguaiaretic acid replicated in males at the original dose and at threefold lower and higher doses, dose-dependently and without an effect on maximal lifespan, and that Protandim extended median lifespan in males only. It also reports that neither fish oil nor ursodeoxycholic acid extended lifespan, and that metformin alone at 0.1 percent of diet did not significantly extend lifespan while metformin combined with rapamycin robustly did.
Aging Cell, 2016 · animal
found nothingThe late-start result, which is the property that makes this compound unusual: benefit when treatment began late in life, in males. The same cohort reports that nicotinamide riboside and three other compounds did not affect lifespan in either sex, which is the relevant null for anyone taking an NAD precursor.
Aging Cell, 2021 · animal
- 2 preclinical studies
Measured in animals or cells
found nothingInterventions Testing Program. The male-specific extension of median lifespan by NDGA was replicated at the original dose and at doses threefold lower and threefold higher. Effects were dose dependent and male specific, and there was no effect on maximal lifespan. Replication across three doses in the same programme is unusual and is the strongest thing about this compound.
Aging Cell, 2016 · animal
The original report of the male-preferential lifespan effect, alongside acarbose and 17-alpha-estradiol.
Aging Cell, 2014 · animal
- 2 preclinical studies
Measured in animals or cells
The positive. Astaxanthin extended lifespan in male mice, started at 12 months of age. The 90th percentile lifespan was extended in absolute value by 6 percent in males, though not significantly by the Wang-Allison test. Late-life weights were lower in females fed astaxanthin without a significant lifespan effect in them. Disclosed conflict: two authors run the company that supplies the astaxanthin used in the study.
GeroScience, 2024 · animal
The retest. Astaxanthin showed no lifespan benefit when administered at a different dose or starting at a later age. In females, pooling all three sites, astaxanthin was associated with significantly reduced lifespan; site-specific reanalysis excluding one site with unusually long-lived control females left a negative effect only for mitoglitazone and pioglitazone. The authors conclude that timing and dosage are critical variables.
GeroScience, 2026 · animal
- 2 preclinical studies
Measured in animals or cells
Interventions Testing Program. Meclizine, fed at 544 plus or minus 48 ppm and started at 12 months of age, extended lifespan in male mice. The 90th percentile lifespan was extended in absolute value by 6 percent in males but not significantly by the Wang-Allison test. Late-life weights were lower in treated females without a significant lifespan effect in them.
GeroScience, 2024 · animal
The retest. Meclizine showed no lifespan benefit at a different dose or a later starting age. One of eleven compounds in that cohort, none of which increased lifespan in either sex.
GeroScience, 2026 · animal
- 2 preclinical studies
Measured in animals or cells
The paper that put rilmenidine into geroscience. Identified by searching for compounds with a caloric-restriction-like expression signature. Increased lifespan in C. elegans when given at young and older ages, with the stress resilience, healthspan and lifespan benefits all dependent on the I1-imidazoline receptor nish-1, on DAF-16 and SKN-1, and on autophagy but not AMPK. Adding it to calorically restricted worms, reduced TORC1 function or rapamycin produced no further gain. Mice treated with rilmenidine showed caloric-restriction-like transcriptional changes in liver and kidney, which is a gene expression finding and not a lifespan finding. Two authors disclose commercial longevity interests.
Aging Cell, 2023 · animal
The second and harder negative. In TDP-43WTxQ331K double transgenic mice, rilmenidine induced robust spinal cord autophagy and exacerbated the phenotype: truncated lifespan, accelerated motor neuron loss and pronounced clearance of TDP-43 from nuclei. A lifespan result in mice pointing the wrong way.
Neurobiology of Disease, 2021 · animal
- 2 preclinical studies
Measured in animals or cells
The founding paper. LINE-1 elements become transcriptionally derepressed during cellular senescence and activate a type I interferon response, triggered by cytoplasmic LINE-1 complementary DNA and blocked by LINE-1 reverse transcriptase inhibitors. Treating aged mice with lamivudine downregulated interferon activation and age-associated inflammation in several tissues. Inflammation endpoints, not survival. The paper carries a published author correction in Nature in 2019, which is a correction and not a retraction.
Nature, 2019 · animal
The lifespan-shaped result, and it is in a progeroid model. SIRT6-deficient mice, which are severely short lived, accumulate cytoplasmic LINE-1 complementary DNA that triggers a type I interferon response via cGAS. Nucleoside reverse transcriptase inhibitors significantly improved the health and lifespan of these knockout mice and completely rescued the interferon response. The same paper reports elevated LINE-1 transcription, cytoplasmic complementary DNA and type I interferon in normally aged wild-type mice, without a lifespan experiment in those animals.
Cell Metabolism, 2019 · animal
- 2 preclinical studies
Measured in animals or cells
Mouse. Identified GPNMB as a seno-antigen enriched in senescent cells. Genetic ablation of Gpnmb-positive cells attenuated adipose senescence and improved systemic metabolic abnormalities in high-fat-diet mice and reduced atherosclerotic burden in ApoE knockout mice. Immunisation against Gpnmb reduced Gpnmb-positive cells, improved age-related phenotypes, and extended the male lifespan of progeroid mice.
Nature Aging, 2021 · animal
The same group's mechanistic follow-up, in human endothelial cells and mice. Depleting GPNMB shortened the replicative lifespan of human vascular endothelial cells, and depleting Gpnmb in mice impaired vascular function and enhanced atherogenesis, while overexpression protected against stress-induced senescence and attenuated vascular dysfunction. GPNMB is a survival factor maintaining lysosomal integrity in senescent cells, not a neutral surface tag.
Scientific Reports, 2022 · animal
- 2 preclinical studies
Measured in animals or cells
Transgenic overexpression of FGF21 markedly extended lifespan in mice without reducing food intake, apparently by blunting hepatic growth hormone and IGF-1 signalling. The same paper records that FGF21 blocks somatic growth and causes bone loss in mice. There is no human lifespan data.
eLife, 2012 · animal
In mice with diet-induced obesity, FGF21 extended lifespan through metabolic effects that did not depend on suppressing growth. Mouse only.
Cell Metabolism, 2025 · animal
- 1 preclinical study
Measured in animals or cells
The NIA Interventions Testing Program, three sites, treatment from four months of age, with Sinclair and Baur among the authors. Resveratrol had no statistically significant effect on lifespan in male or female mice at the concentrations tested. The 2006 Nature result of improved survival applied to mice on a high-calorie diet, and a 2008 paper from the same collaboration found no lifespan extension on a normal diet.
What people using it report
- Not everyone in the same audience is convinced it is worth taking at all: longevity physician Peter Attia has said publicly and repeatedly that he does not take resveratrol and considers it to have shown no meaningful human benefit, pointing to the null lifespan result in the NIA Interventions Testing Program mouse study.
- 1 preclinical study
Measured in animals or cells
After coronary artery ligation in mice, thymosin beta-4 upregulated ILK/Akt, enhanced early myocyte survival and improved cardiac function.
Nature, 2004 · animal
- 1 preclinical study
Measured in animals or cells
Humanin overexpression extended lifespan in C. elegans and an analogue improved metabolic healthspan in mice. In a human Ashkenazi Jewish cohort, circulating humanin was significantly higher in the 18 adult offspring of centenarians than in 19 age-matched controls (p<.05); in a 4-person CSF sample, humanin was lower in Alzheimer's patients than 3 controls (p<.05, very small n).
Aging (Albany NY), 2020 · animal
- 1 preclinical study
Measured in animals or cells
After coronary ligation in mice, Tbeta4 activated ILK/Akt, improved early cardiomyocyte survival and cardiac function.
Nature, 2004 · animal
- 1 preclinical study
Measured in animals or cells
Lys-Glu from month 6 of life increased physical activity and endurance, prolonged lifespan and reduced spontaneous tumors in female CBA mice.
Bulletin of Experimental Biology and Medicine, 2000 · animal
- 1 preclinical study
Measured in animals or cells
found nothingNIA Interventions Testing Program: nicotinamide riboside at 1000 ppm from 8 months did not increase lifespan in either sex. The authors note this came despite data suggesting it would be effective.
Aging Cell, 2021 · animal
- 1 preclinical study
Measured in animals or cells
Oral spermidine extended mouse lifespan and preserved cardiac function through enhanced cardiac autophagy and mitophagy.
Nature Medicine, 2016 · animal
- 1 preclinical study
Measured in animals or cells
Intermittent D+Q in old mice improved physical function and extended remaining lifespan by about 36%.
Nature Medicine, 2018 · animal
- 1 preclinical study
Measured in animals or cells
Started at 600 days of age, rapamycin extended lifespan at three sites: 14% in females and 9% in males at the 90th percentile.
Nature, 2009 · animal
- 1 preclinical study
Measured in animals or cells
Better muscle function in old mice; 17.9% lifespan extension in C. elegans; low levels in human sarcopenia.
Nature Metabolism, 2024 · animal
- 1 preclinical study
Measured in animals or cells
The positive mouse result that launched metformin's longevity reputation, in C57BL/6 mice. The multi-site Interventions Testing Program, using genetically heterogeneous mice specifically to catch results that do not travel, did not reproduce a significant lifespan effect in either sex.
Nature Communications, 2013 · animal
- 1 preclinical study
Measured in animals or cells
Aged human cells in culture plus Caenorhabditis elegans. Chemical-induced partial reprogramming improved genomic instability and epigenetic alterations in aged human cells. An optimised two-molecule combination also reduced cellular senescence and oxidative stress, and extended lifespan and healthspan in C. elegans. The lifespan result is in a nematode, not a mammal.
EMBO Molecular Medicine, 2025 · animal
- 1 preclinical study
Measured in animals or cells
Animal. FGF17 acted on neuronal survival and oligodendrogenesis together to restore deficits in a stroke model, extending the oligodendrocyte finding beyond normal ageing into injury.
Neurotherapeutics, 2026 · animal
- 1 preclinical study
Measured in animals or cells
Mouse. Genetic or senolytic ablation of senescent cells, or macrophage depletion, reduced tumour burden and increased survival in KRAS-driven lung cancer models. Macrophages with senescent features were also found in human pre-malignant lung lesions, an observation rather than an intervention.
Cancer Cell, 2023 · animal
- 1 preclinical study
Measured in animals or cells
Interventions Testing Program 2021 cohort, treatment from 7 months. Male median lifespan 836 versus 794 days (+5.3 percent, log-rank p = 0.037), 90th percentile survival +6.2 percent (p = 0.01); 141 treated males against 298 controls. Females: median -2.2 percent, p = 0.6. NIA funded.
GeroScience, 2026 · animal
- 1 preclinical study
Measured in animals or cells
Interventions Testing Program 2021 cohort, treatment from 7 months. Male median lifespan 864 versus 794 days (+8.8 percent, log-rank p = 0.002), 90th percentile survival +6.9 percent (p = 0.01); 154 treated males against 298 controls. Females: median +0.2 percent, p = 0.75. NIA funded.
GeroScience, 2026 · animal
- 1 preclinical study
Measured in animals or cells
found nothingInterventions Testing Program 2021 cohort, treatment from 7 months. Male median lifespan 863 versus 794 days (+8.7 percent, log-rank p = 0.015); 90th percentile survival +2.9 percent, not significant (p = 0.19); 149 treated males against 298 controls. Treated males were heavier at 12, 18 and 24 months. Females: median -2.3 percent, p = 0.07. NIA funded.
GeroScience, 2026 · animal
- 1 preclinical study
Measured in animals or cells
Mice lacking the ketogenesis enzyme HMGCS2 died early, which a 1,3-butanediol diet prevented. In normal mice the same diet started early in life increased midlife mortality, while started in aged mice it extended lifespan and prevented atherosclerosis deaths in ApoE-deficient mice. An ad libitum ketogenic diet markedly increased mortality. Independent Japanese group.
Aging Cell, 2023 · animal
- 1 preclinical study
Measured in animals or cells
Rapamycin alone from 600 days of age: 90th percentile survival +14 percent in females and +9 percent in males at three sites. The founding rapamycin result the combination is measured against. NIA funded.
Nature, 2009 · animal
- 1 preclinical study
Measured in animals or cells
Interventions Testing Program, eleven compounds in UM-HET3 mice across three sites. None significantly increased lifespan in male or female mice. In females, pooling all sites, astaxanthin, late-start mitoglitazone and pioglitazone were associated with significantly reduced lifespan. After excluding one site whose control females lived unusually long, the negative effect remained for mitoglitazone and pioglitazone only.
GeroScience, 2026 · animal
- 1 preclinical study
Measured in animals or cells
Interventions Testing Program, eleven compounds in genetically heterogeneous UM-HET3 mice at three sites. Mifepristone did not significantly increase lifespan in male or female mice.
GeroScience, 2026 · animal
- 1 preclinical study
Measured in animals or cells
Interventions Testing Program, eleven compounds in UM-HET3 mice at three sites. Methotrexate did not significantly increase lifespan in male or female mice.
GeroScience, 2026 · animal
- 1 preclinical study
Measured in animals or cells
found nothingInterventions Testing Program. Dimethyl fumarate did not increase lifespan significantly in either sex at the dose and method of administration tested. The authors report that the amount in the diet averaged 35 percent of the target dose, which they state may explain the absence of lifespan effects. Note the disclosed conflicts in this paper: two authors run a company supplying the astaxanthin used, and others hold senolytic patents or company interests.
GeroScience, 2024 · animal
- 1 preclinical study
Measured in animals or cells
found nothingInterventions Testing Program. Mycophenolic acid did not increase lifespan significantly at the dose and method of administration tested, in either sex.
GeroScience, 2024 · animal
- 1 preclinical study
Measured in animals or cells
found nothingInterventions Testing Program. 4-phenylbutyrate did not increase lifespan significantly at the dose and method of administration tested, in either sex.
GeroScience, 2024 · animal
- 1 preclinical study
Measured in animals or cells
found nothingInterventions Testing Program. SG1002, described as a hydrogen sulfide donor, did not increase lifespan significantly at the dose and method of administration tested, in either sex.
GeroScience, 2024 · animal
- 1 preclinical study
Measured in animals or cells
found nothingInterventions Testing Program. An 8 percent glycine diet produced a 4 to 6 percent lifespan increase, with an increase in maximum lifespan, in both males (p equals 0.002) and females (p less than 0.001). In parallel analyses of the same cohort the authors report no benefit from TM5441, from inulin described as a source of soluble fibre, or from aspirin at either of two doses.
Aging Cell, 2019 · animal
- 1 preclinical study
Measured in animals or cells
Interventions Testing Program C2017 cohort, testing (R/S)-1,3-butanediol, captopril, leucine, the Nrf2-activating botanical mixture PB125, sulindac, syringaresinol, and rapamycin plus acarbose started at 9 or 16 months. The rapamycin and acarbose combination started at 9 months produced longer male lifespan than either drug alone in prior cohorts. Captopril gave a small 4 to 5 percent female increase. The authors state that none of the other four tested agents, which includes leucine, led to any lifespan benefit.
Aging Cell, 2022 · animal
- 1 preclinical study
Measured in animals or cells
Interventions Testing Program, three test sites, treatment beginning at 4 months of age. None of the five agents, oxaloacetic acid included, had a statistically significant effect on lifespan of male or female mice by log-rank test at the concentrations tested. A secondary analysis suggested green tea extract might diminish the risk of midlife deaths in females only.
- 1 preclinical study
Measured in animals or cells
Interventions Testing Program. Acarbose at 400, 1,000 and 2,500 ppm produced significant survival changes in both sexes, with the two higher doses giving 16 to 17 percent increases in male median longevity against 4 to 5 percent in females. In the same report, three other interventions were tested, ursolic acid, 2-(2-hydroxyphenyl) benzothiazole and INT-767, and none of these affected lifespan at the doses tested.
Aging Cell, 2019 · animal
- 1 preclinical study
Measured in animals or cells
Interventions Testing Program, three test sites, treatment beginning at 4 months of age. None of the five agents, medium-chain triglyceride oil included, had a statistically significant effect on lifespan of male or female mice by log-rank test at the concentrations tested.
- 1 preclinical study
Measured in animals or cells
Interventions Testing Program, mice bred in 2021, all agents fed in the diet from 7 months of age. The cohort tested 2BAct, dichloroacetate, epicatechin, forskolin, halofuginone and mitoglitazone. In males, epicatechin increased median lifespan by about 5 percent and halofuginone and mitoglitazone by about 9 percent each, with epicatechin and halofuginone also increasing 90 percent survival. Forskolin was not among the agents reported to extend lifespan. The authors note the report continues the strong male bias among the programme's positive findings.
GeroScience, 2026 · animal
- 1 preclinical study
Measured in animals or cells
19 month old Fischer 344 rats fed diets containing 0.004 or 0.016 percent pterostilbene, selected as the most effective of seven stilbenes in a cell screen. Pterostilbene reversed cognitive behavioural deficits and dopamine release deficits, and working memory correlated with pterostilbene levels in the hippocampus. Aged rats, not people, and a cognition endpoint rather than a lifespan one.
- 1 preclinical study
Measured in animals or cells
The ageing result, and the only one. ISRIB reversed integrated stress response activation in the aged mouse brain, reversed spatial memory deficits and improved working memory in old mice, and in hippocampus restored intrinsic neuronal electrophysiological properties and spine density while reducing interferon and T cell mediated immune profiles. Memory endpoints, not lifespan or healthspan. Several authors disclose commercial interests in the compound class.
eLife, 2020 · animal
- 1 preclinical study
Measured in animals or cells
Purified enzyme and yeast work. Physiological concentrations of nicotinamide non-competitively inhibited both yeast Sir2 and human SIRT1 in vitro, with an IC50 below 50 micromolar, which the authors describe as equal to or better than the best synthetic inhibitors of the class. In yeast, nicotinamide abolished silencing, increased rDNA recombination and shortened replicative lifespan to that of a sir2 mutant. This is yeast and test-tube data. It has never been shown to occur in a person taking a supplement, and it has never been shown not to.
Journal of Biological Chemistry, 2002 · in vitro
- 1 preclinical study
Measured in animals or cells
found nothingThe relevant lifespan null for the nicotinamide riboside half of this product. In the National Institute on Aging Interventions Testing Program, genetically heterogeneous UM-HET3 mice fed nicotinamide riboside from 8 months of age showed no significant effect on lifespan in either sex in the pooled three-site dataset, the programme's primary endpoint. In the same cohort and the same three sites, 17-alpha-estradiol extended median male lifespan by 19 percent, demonstrating the experiment could detect a large effect. Funded by the National Institute on Aging, conflicts declared as none.
Aging Cell, 2021 · animal
- 1 preclinical study
Measured in animals or cells
Mouse and in vitro. Identified uPAR as a cell-surface protein broadly induced during senescence, and showed that uPAR-specific CAR T cells ablated senescent cells in vitro and in vivo, extended survival of mice with lung adenocarcinoma treated with a senescence-inducing drug combination, and restored tissue homeostasis in mice with chemically or diet-induced liver fibrosis. This paper carries a published Author Correction, cited below.
Nature, 2020 · animal
- 1 preclinical study
Measured in animals or cells
Human cells and intact degenerating human discs maintained ex vivo. RG-7112 selectively killed senescent disc cells by apoptosis; both it and o-vanillin decreased the SASP and affected a shared cell death and survival gene network, with o-vanillin additionally affecting cell cycle and connective tissue networks. A single dose improved disc matrix homeostasis in the ex vivo discs, correlating with fewer senescent cells and less SASP.
eLife, 2020 · in vitro
- 1 preclinical study
Measured in animals or cells
The best-documented animal result in the whole bioregulator family, for a different organ preparation entirely. Mean lifespan rose 11 to 31 percent in female Drosophila, SHR mice, C3H/Sn mice and LIO rats. It is cited on this page as the class benchmark: this is what a bioregulator result looks like when one exists, and Ovagen has nothing comparable.
What people using these actually report
Uncontrolled self-reports, gathered from clinic write-ups, regulatory complaint records and public forums, and reproduced here as written. They are the best guide on this page to what people actually do, what they expect, and what goes wrong, and they cannot show that anything works, because nobody was measured against a placebo and the people who saw no effect mostly stopped posting. Both halves of that are true at once. The negative reports are kept in for the same reason.
- Not everyone in the same audience is convinced it is worth taking at all: longevity physician Peter Attia has said publicly and repeatedly that he does not take resveratrol and considers it to have shown no meaningful human benefit, pointing to the null lifespan result in the NIA Interventions Testing Program mouse study.
Sources: LONGECITY's Resveratrol subforum (including a long-running 'Positive, Negative, ZERO, effect noticed?' poll thread and a dedicated side-effects thread), general web search of longevity-community and vendor commentary on dosing, form and piperine practice, and Peter Attia's public podcast and written statements. Direct access to r/longevity, r/Supplements and r/Biohackers on Reddit was not available in this research pass (Reddit pages could not be fetched and did not surface in general web search here), so those specific subreddits could not be independently checked and any overlap with the sentiment described above is inferred, not confirmed firsthand.
- Allergic sensitisation with repeated exposure is documented in trials: 4 of 40 Parkinson patients developed positive skin tests during monthly injections and had to stop. The Toxicon review records anaphylaxis and several deaths in people who had previously tolerated the therapy.
Sources: The published apitherapy and bee venom acupuncture literature, including the Toxicon 2018 review, the Korean safety trial of filtered versus unfiltered venom, the recruitment rationale stated in the MS and Parkinson trials, and the registered Apitox trials. No forum or social media content was retrieved for this entry and nothing here is attributed to a specific post.
Why the trial record looks like this
A missing trial is usually a missing sponsor. Nobody runs a nine-figure programme on a molecule they cannot own, so the compounds with the thinnest human records are often the oldest and most freely available ones rather than the weakest. Taking OSK Partial Reprogramming as the example, because it states the problem most clearly:
Partial reprogramming is the most heavily funded area in longevity biotechnology and the one with the least human data. Altos Labs launched in 2022 with about three billion dollars and has no registered human trial. YouthBio Therapeutics, Turn Biotechnologies and Retro Biosciences likewise return no genuine reprogramming trial on ClinicalTrials.gov. The single registered study in the world is Life Biosciences' ER-100, which this site also covers under its own entry. The gap between the money and the registry is the most informative fact on this page.
The reason for the gap is the safety problem, and it is not speculative. Two high-profile mouse papers, in Nature in 2013 and Cell in 2014, showed that transient induction of reprogramming factors in living animals produces teratomas across multiple organs and, when reprogramming is started and then stopped, tumours resembling paediatric Wilms tumour. The therapeutic window sits between not enough expression to rejuvenate and enough to dedifferentiate into cancer, it is defined by duration and dose, and it has only been characterised in mice. Dropping c-Myc to give OSK, and injecting into one eye with an oral switch that can be turned off, are both engineering responses to that problem. Neither has been shown to solve it in a person.
One further distinction is worth holding on to, because popular coverage collapses it constantly. The 2016 result that partial reprogramming extends lifespan is in a progeroid mouse, an animal engineered to age prematurely from a specific lesion. Reversing that lesion extends that animal's life without demonstrating anything about normal ageing. The one report of lifespan extension in normal mice is a 2024 paper in 124-week-old males from a single group, measuring remaining rather than total lifespan, and it has not been replicated.
A compound appears here only when a citation on its own page states this outcome and reports a result for it; naming it is not enough. Human, animal and cell work are counted separately and never merged. Participant counts are read from the study lines and deliberately undercount. Nothing here is advice, and nothing here is a recommendation to take or to avoid anything.