The finder
Pick what you want to change. See who actually measured it.
Every other tool like this gives you a compound and a match score. Those scores are not measured. Ours does not exist. What you get instead is what was actually measured and where: trials in people first with the participant count, then the animal and cell work kept separate, then what people using it report, and the trials that found nothing, counted rather than dropped.
82 of the 444 compounds here have never been through a trial in people. That is worth knowing and it is not a verdict: a molecule nobody can patent has no sponsor to pay for a trial, so a thin human record is usually a fact about money rather than about the compound. Where that is the case, this says so and shows you what does exist.
What are you trying to change?
Pick as many as you like. The number on each one is how many people it has been measured in across the whole archive, so you can see where the evidence is before you choose.
Or start from the compounds
Somebody handed you a stack. What is actually known about it?
Add what you are looking at and you get every outcome those compounds have been measured for in people, and then the longer list of the ones they have not.
Inflammation
Does it bring inflammation down?
Almost always measured as a marker in blood rather than as something a person notices. Worth knowing which one a trial actually moved.
54,269 people · 9 human studies · 7 compounds
- 53,902 people2 studies
UK Biobank proteomics, 53,026 participants, 13.3 years of follow-up: GDF15 was positively associated with 20 to 24 incident chronic diseases (hazard ratios 1.21 to 3.77) and with multimorbidity, with levels largely explained by renal function, liver function, inflammation and obesity.
Metabolism, 2025 · 53,026 people
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
- 203 people2 studies1 found nothing
found nothingThe largest and longest diabetes trial here: 192 patients, 40 or 500 mg per day for six months. CRP fell 5.6% and 15.9% versus placebo but not significantly, and there was no significant change in weight, BMI, waist, blood pressure, fasting glucose, HbA1c, insulin, C-peptide, free fatty acids, liver enzymes, uric...
Pharmacological Research, 2016 · 192 people
Eleven healthy obese men, randomised double-blind crossover, 150 mg per day for 30 days. Sleeping and resting metabolic rate fell; muscle AMPK was activated with higher SIRT1 and PGC-1alpha protein and improved mitochondrial respiration on a fatty-acid substrate; intrahepatic lipid, circulating glucose, triglycerides,...
Cell Metabolism, 2011 · 11 people
- 60 people1 study
60 hypopituitary adults on GH for a mean of 10 years were crossed over to four months of placebo. IGF-1 fell from 168 to 98 micrograms per litre, two quality-of-life domains deteriorated, waist circumference and visceral fat rose, and lipids and C-reactive protein worsened, while insulin sensitivity improved.
Journal of Clinical Endocrinology and Metabolism, 2012 · 60 people
- 42 people1 study
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...
Stem Cell Reviews and Reports, 2021 · 42 people
- 42 people1 study1 found nothing
found nothingNCT05038488. 42 adults hospitalised with COVID-19 and acute kidney injury randomised 3:2 to MIB-626 1.0 g or placebo tablets twice daily for 14 days. Blood NAD rose gradually from 16.0 to 25.5 to 42.6 micrograms per millilitre at baseline, day 5 and day 14, and NAD metabolites rose rapidly by day 3. Serum creatinine,...
FASEB BioAdvances, 2025 · 42 people
- 20 people1 study
Phase 1b, 20 patients with post-surgical or post-traumatic intraocular inflammation, single subconjunctival dose of 45, 90, 450 or 900 mcg (5 per group). 17 non-serious adverse events judged unrelated to treatment; plasma peptide undetectable in the three lower dose groups. No control group, so the observed fall in...
Journal of Ocular Pharmacology and Therapeutics, 2015 · 20 people
- no headcount stated1 study
30 participants, sponsor AgelessRx (a telehealth prescriber), active not recruiting. Arms combine rapamycin 2 to 6 mg weekly, metformin 500 mg daily, low-dose naltrexone, intranasal NAD+, topical glutathione and a proprietary supplement; primary endpoints VO2 max, a cognitive composite and an inflammation index....
ClinicalTrials.gov, 2025 · no headcount in the line
- no headcount stated0 studies
Nanoparticle-delivered KPV accelerated mucosal healing and lowered TNF-alpha in a mouse colitis model.
Molecular Therapy, 2017 · no headcount in the line
- no headcount stated0 studies
A thymulin analogue (PAT) dose-dependently reduced endotoxin-induced hyperalgesia and inflammation in rats.
British Journal of Pharmacology, 2002 · no headcount in the line
- no headcount stated0 studies
In two mouse colitis models KPV led to earlier recovery, greater body-weight regain, fewer inflammatory infiltrates and lower myeloperoxidase activity in colon tissue. Mouse gut inflammation with KPV given alone; nothing here tests KPV in a blend or in people.
Inflammatory Bowel Diseases, 2008 · no headcount in the line
- no headcount stated0 studies
In THP-1 human monocytes, the Chonluten tripeptide cut TNF release from LPS-stimulated cells and, with the four other Khavinson peptides tested, reduced TNF and IL-6 expression and adhesion to activated endothelium. Cell culture only; the study was run with the Khavinson institute, so it is not independent of the...
International Journal of Molecular Sciences, 2022 · no headcount in the line
- no headcount stated0 studies
Reduced inflammation after injury in rats.
Journal of Neurosurgery, 2017 · no headcount in the line
- no headcount stated0 studies
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...
Nature Aging, 2022 · no headcount in the line
- no headcount stated0 studies
Rat. Six epigenetic clocks were developed and validated for rat tissues from 613 tissue samples, with two clocks trained on an additional 1,366 human tissue samples to work across both species. A young porcine plasma fraction treatment more than halved the epigenetic ages of blood, heart and liver tissue in old rats,...
GeroScience, 2024 · no headcount in the line
- no headcount stated0 studies
Mouse, with a human observational component. Plasma from voluntarily running mice infused into sedentary mice reduced baseline neuroinflammatory gene expression and experimentally induced brain inflammation. Proteomics showed a coordinated increase in complement cascade inhibitors including clusterin. Intravenous...
Nature, 2021 · no headcount in the line
- no headcount stated0 studies
Mouse atherosclerosis models, with 25-hydroxycholesterol and CH25H expression also measured in human lesions. Macrophage-derived 25-hydroxycholesterol promoted vascular inflammation and lesion remodelling, a harm direction in the same organ system as the aortic stiffness study.
Circulation, 2023 · no headcount in the line
- no headcount stated0 studies
Retinal pigment epithelial cybrid cell lines carrying mitochondria from 5 AMD and 3 normal donors treated with clinical dose equivalents of each drug for 48 hours. AMD cybrids had higher baseline caspase activity; the two drugs produced different patterns of apoptosis, oxidative stress and inflammation gene...
Experimental Eye Research, 2021 · no headcount in the line
- no headcount stated0 studies
A mechanistic follow-up asking why these effects are sex-specific, reporting that the reduction in hypothalamic inflammation itself differs by sex. A partial answer rather than a resolution.
Aging Cell, 2017 · no headcount in the line
- no headcount stated0 studies
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...
Nature, 2019 · no headcount in the line
- no headcount stated0 studies
Human cells in culture plus aged mice. Senescent human preadipocytes and HUVECs developed a SASP that was suppressed by JAK-pathway RNAi or JAK inhibitors, and conditioned medium from JAK-inhibitor-treated senescent cells was much less proinflammatory. Giving a JAK inhibitor to aged mice for 10 weeks alleviated...
Proceedings of the National Academy of Sciences, 2015 · no headcount in the line
- no headcount stated0 studies
Cell culture. The senescence-associated secretory phenotype of chondrocytes was characterised by raised p16, p21 and p53, raised TNF-alpha and IL-1-alpha, and lowered Sirt1. Both the AED peptide and a cartilage polypeptide complex normalised the synthesis of those molecules. Chondrocytes in culture, not joints, and no...
Advances in Gerontology, 2023 · no headcount in the line
- no headcount stated0 studies
Apelin production by contracting muscle falls with age in humans and rodents and associates with exercise benefit in older people (observational). Mice lacking apelin or its receptor showed marked age-related muscle deterioration, and restoring apelin signalling improved muscle function via mitochondrial biogenesis,...
Nature Medicine, 2018 · no headcount in the line
- no headcount stated0 studies
- no headcount stated0 studies
How this is counted
Human studies only. Animal and test-tube work never enters this ranking, because the question you asked was about a person.
A compound is listed for an outcome only when a citation on its own page states that outcome and reports a result for it. Naming it is not enough: a paper that measures testosterone and reports a result about something else does not count as testosterone evidence, which is a mistake this tool made on its first run and no longer makes.
People counts are read out of the study lines themselves and are deliberate undercounts. Where a line states no number, the study still counts as a study and adds nothing to the headcount. Counts are never added across compounds, because the same person can appear in more than one trial.
Ranking is by people measured. That is a fact about the evidence, not a judgement about the compound, and it is the only ordering this site will defend. A compound at the top of a list is the most studied, which is not the same as the best.
Nothing here is advice, and nothing here is a recommendation to take anything.