What does it do to the kidneys?

What this archive is for. Trials of the compound come first, ranked by how many people were actually given it. Studies that only observed people are below them and labelled.

1. 01SemaglutidePeptideStrong. At least two finished studies in people, and at least 1,000 people who took it. 12 completed trials, 42,363 people given it.10 reported

   9,650 people given it1 trial, 1 watch-only1 found nothing

   • found nothingThe pill form of semaglutide also cut heart attacks and strokes, by a modest amount. 9,650 people with type 2 diabetes at high risk took a daily 14 mg tablet or a dummy tablet for about four years. Heart attacks, strokes and cardiac deaths hit 12.0% on the drug and 13.8% on the dummy, about 18 fewer such events for every 1,000 people. The kidney and other follow-up measures came out the same in both groups, so this result rests on the heart numbers alone.

     The numbers SOUL, 9,650 participants over a mean 47.5 months: major adverse cardiovascular events in 12.0% versus 13.8% (HR 0.86). The confirmatory secondary outcomes, including the kidney composite, did not differ significantly.

     New England Journal of Medicine, 2025· 9,650 people

   • Semaglutide protected the kidneys well enough that the trial was stopped early. 3,533 people with type 2 diabetes and kidney disease got the drug or a dummy shot, and nobody involved knew which. Major kidney events, meaning kidney failure, a large drop in kidney function or death from kidney or heart causes, hit 331 on the drug and 410 on the dummy. Fewer people died of any cause as well. Independent monitors halted it because the benefit was already clear.

     The numbers FLOW, 3,533 participants, stopped early at interim analysis: major kidney disease events 331 versus 410 (HR 0.76, 95% CI 0.66 to 0.88) and all-cause death HR 0.80 over a median 3.4 years.

     New England Journal of Medicine, 2024· 3,533 peopleobserved only, nobody was given it

2. 02InsulinPeptideStrong. At least two finished studies in people, and at least 1,000 people who took it. 5 completed trials, 29,691 people given it.4 reported

   7,637 people given it1 trial

   • Two long-acting insulins protected the heart equally, and one caused fewer dangerous lows. 7,637 people with type 2 diabetes, most already with heart or kidney disease, got degludec or glargine without knowing which. Major heart events happened in 8.5 percent against 9.3 percent, close enough to call equal. Severe low blood sugar hit 4.9 percent against 6.6 percent, about 17 fewer people in every thousand. Novo Nordisk, which sells degludec, paid for it.

     The numbers DEVOTE: 7,637 people with type 2 diabetes, 85.2 percent with established cardiovascular or kidney disease, randomised double-blind to insulin degludec or glargine U100. Major cardiovascular events occurred in 8.5 versus 9.3 percent (hazard ratio 0.91, 95 percent confidence interval 0.78 to 1.06, non-inferior). Severe hypoglycaemia occurred in 4.9 versus 6.6 percent, an absolute difference of 1.7 percentage points (rate ratio 0.60, p < 0.001 for superiority). Sponsor Novo Nordisk.

     New England Journal of Medicine, 2017· 7,637 people

3. 03BNP and nesiritidePeptideStrong. At least two finished studies in people, and at least 1,000 people who took it. 3 completed trials, 7,149 people given it.4 reported

   7,146 people given it2 trials1 found nothing

   • This is the study that settled it, and the drug failed. 7,141 people in hospital with heart failure got nesiritide or a dummy drip on top of usual care. Breathlessness improved a shade more on the drug, not enough to count. Death or return to hospital within 30 days came out the same. Kidneys were no worse, but low blood pressure was more common. The maker paid for the study that ended its own product. A study this size would have found a real benefit.

     The numbers ASCEND-HF: 7,141 people hospitalised with acute heart failure randomised to nesiritide or placebo for 24 to 168 hours on top of standard care. Dyspnoea improvement 44.5 versus 42.1 percent at 6 hours and 68.2 versus 66.1 percent at 24 hours, neither meeting the prespecified threshold. Rehospitalisation or death within 30 days 9.4 versus 10.1 percent (difference -0.7 percentage points, 95 percent confidence interval -2.1 to 0.7). No excess worsening renal function; more hypotension. Funded by Scios, the manufacturer.

     New England Journal of Medicine, 2011· 7,141 peoplepoints the wrong way

   • found nothingSmall studies said the drug damaged kidneys, and the large one later said it did not. Five small studies covering 1,269 patients were pooled. Kidney function got worse about half as often again on nesiritide as on other treatment. Nobody needed dialysis more often. The 7,141 person study that followed found no extra kidney harm at all. When a big study and a pool of small ones disagree, the big study is the better evidence.

     The numbers Meta-analysis of 5 randomised studies, 1,269 patients. FDA-approved doses of nesiritide increased worsening renal function against non-inotrope control, relative risk 1.52, 95 percent confidence interval 1.16 to 2.00, p = 0.003. There was no difference in the need for dialysis. ASCEND-HF later found no excess renal harm in 7,141 people.

     Circulation, 2005· 5 people

4. 04CotadutidePeptideStrong. At least two finished studies in people, and at least 1,000 people who took it. 6 completed trials, 1,221 people given it.

   248 people given it1 trial

   • Cotadutide sharply cut protein leaking into the urine in diabetic kidney disease. 248 people with type 2 diabetes and kidney damage were split by chance across three doses, a dummy, or semaglutide, for about six months. Protein in the urine fell by roughly half at the two higher doses, and the fall held. Serious side effects were balanced across groups. Protein in the urine is a marker, not a kidney that has been saved. Nobody was followed long enough to see kidney failure. The sponsor paid.

     The numbers 248 people with type 2 diabetes and chronic kidney disease (mean eGFR 55, 47 percent on SGLT2 inhibitors), 26 weeks, randomised to cotadutide 100, 300 or 600 mcg, placebo, or open-label semaglutide 1 mg weekly. Urine albumin to creatinine ratio fell 43.9 percent at 300 mcg (95 percent CI 30.6 to 54.7) and 49.9 percent at 600 mcg (38.4 to 59.3) against placebo at week 14, sustained to week 26. Serious adverse events balanced; tolerability at 600 mcg described as comparable to semaglutide. Sponsor funded (NCT04515849, results posted January 2025).

     Kidney International, 2024· 248 people

5. 05PEG-loxenatidePeptideModerate. At least one finished study in people, and at least 100 people who took it. 4 completed trials, 590 people given it.

   106 people given it1 trial1 found nothing

   • found nothingIt matched the comparison drug on a urine marker, and no actual kidney outcome was measured. 106 people at one centre were assigned by chance and everybody knew what they were taking. 80 finished. Over 24 weeks, protein leaking into the urine fell 29.3 percent on PEG-loxenatide and 31.8 percent on dapagliflozin, a gap too small to call. Average blood sugar fell almost identically. Stomach side effects were more common on PEG-loxenatide. Protein in the urine is a marker. Nobody counted dialysis, transplants or failing kidneys.

     The numbers Single-centre open-label trial against dapagliflozin. 106 randomised, 80 completed. Urine albumin to creatinine ratio fell 29.3 percent on PEG-loxenatide against 31.8 percent on dapagliflozin over 24 weeks, a difference that was not significant. Glycated haemoglobin fell almost identically in both arms. Triglycerides fell more on PEG-loxenatide. Gastrointestinal adverse events were more common on PEG-loxenatide. Albuminuria is a surrogate marker; no kidney outcome such as dialysis, transplantation or doubling of creatinine was measured.

     Frontiers in Endocrinology, 2024· 106 people

6. 06ANPPeptideModerate. At least one finished study in people, and at least 100 people who took it. 4 completed trials, 188 people given it.4 reported

   75 people given it1 trial

   • This looked for who passes more water on the drug, and found two blood tests that predict it. 75 people in hospital with heart failure got a low dose of carperitide through a drip for six hours. Those who started with lower levels of their own natriuretic hormone, and lower vasopressin, produced the most urine. Blood pressure, kidney function and previous water tablets predicted nothing. Everyone here got the drug, so there is no comparison group and no way to know what would have happened anyway.

     The numbers 75 patients with acute heart failure given 0.0125 micrograms per kilogram per minute of carperitide for 6 hours. Lower baseline plasma ANP (r = -0.35, p = 0.002) and lower vasopressin (r = -0.54, p < 0.001) predicted a larger diuretic response; baseline blood pressure, renal function and prior loop diuretic use did not.

     ESC Heart Failure, 2022· 75 people

7. 07BPC-157PeptideLimited. People have taken it in a published study, but fewer than 100 of them. 3 completed trials, 31 people given it.10 reported

   2 people given it1 trial1 found nothing

   • found nothingA study this small cannot show that anything is safe. Two healthy adults were given BPC-157 into a vein, 10 mg on the first day and 20 mg on the second. Neither reported side effects, and blood tests covering the heart, liver, kidneys, thyroid and blood sugar did not shift. That is worth knowing, and it is all it is. Two people cannot reveal a side effect that strikes one person in fifty, let alone one in a thousand.

     The numbers Two adults received 10 mg intravenously on day 1 and 20 mg on day 2. No adverse effects were reported and cardiac, liver, kidney, thyroid and glucose laboratory values did not change meaningfully. Two subjects cannot characterise safety.

     Alternative Therapies in Health and Medicine, 2025· 2 people

8. 08RetatrutidePeptideStrong. At least two finished studies in people, and at least 1,000 people who took it. 5 completed trials, 1,345 people given it.8 reported

   nobody was given it1 watch-only study

   • Nothing is known about what retatrutide does to heart attacks, strokes or kidney failure. This is the only trial built to find out, and it is still running. 10,000 people with extra weight and either heart or kidney disease are enrolled, and the first results are not due until February 2029. Everything published so far measures weight and blood sugar, which are not the events people take these drugs to avoid.

     The numbers The only retatrutide trial with hard clinical endpoints: 10,000 participants, event-driven, primary completion listed for February 2029. Until it reports, nothing is known about retatrutide and cardiovascular or kidney outcomes.

     ClinicalTrials.gov NCT06383390 (TRIUMPH-Outcomes), Eli Lilly, 2026· 10,000 peopleobserved only, nobody was given it

9. 09VasopressinPeptideModerate. At least one finished study in people, and at least 100 people who took it. 1 completed trial, 778 people given it.3 reported

   nobody was given it1 watch-only study1 found nothing

   • found nothingStarting vasopressin early did not protect the kidneys. Four hundred and nine people in septic shock were given it first, instead of the usual drug. The number of days they spent free of kidney failure was no better. Fewer of them ended up on dialysis, which is a real difference but a lesser one, and it was not what the trial was built to answer. Two trials now point the same way. Vasopressin is an option in septic shock, not a step forward.

     The numbers 409 patients: early vasopressin did not improve kidney-failure-free days, though renal replacement therapy use was lower.

     JAMA, 2016· 409 peopleobserved only, nobody was given it

Vitamins, minerals, amino acids and botanicals sold over the counter, held to the same standard.

1. 01NicotinamideSupplementModerate. At least one finished study in people, and at least 100 people who took it. 4 completed trials, 591 people given it.2 reported

   205 people given it1 trial1 found nothing

   • found nothingNicotinamide did not do what this kidney trial asked of it. 205 people with fairly advanced kidney disease took nicotinamide, a phosphate binder, both, or two dummy pills for a year. Neither drug meaningfully lowered blood phosphate or the hormone that tracks with it, which were the two things the trial was built to move. Side effects were similar across groups, but stomach upset made it hard for people to keep taking the pills. The funding was independent of any manufacturer.

     The numbers 205 people with stage 3b or 4 chronic kidney disease randomised to nicotinamide 750 mg twice daily, lanthanum carbonate, both, or double placebo for 12 months. Neither drug significantly lowered serum phosphate or intact FGF23, the dual primary endpoints. Adverse event rates were similar across arms but gastrointestinal symptoms limited adherence. Another well-run, independently funded, multi-year nicotinamide trial that missed its primary endpoint.

     Journal of the American Society of Nephrology, 2019· 205 people

2. 02MIB-626SupplementModerate. At least one finished study in people, and at least 100 people who took it. 4 completed trials, 107 people given it.1 reported

   42 people given it1 trial1 found nothing

   • found nothingThe tablet raised NAD in very sick patients and made no difference to them. 42 adults in hospital with COVID-19 and sudden kidney injury took MIB-626 or dummy tablets twice a day for two weeks. NAD in the blood roughly doubled by the end. Kidney blood tests came out the same in both groups. So did inflammation markers and how ill people were. The authors want the drug tried as a drip instead. Two authors work for the manufacturer and a third consults for it.

     The numbers NCT05038488. 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, cystatin C and serum markers of acute kidney injury did not differ between groups. Serum CRP, IL-6 and TNF alpha and indices of disease severity also did not differ. The authors attribute the absence of clinical effect to the slow rise in NAD and call for studies of parenteral administration. Two authors are employees of Metro International Biotech and a third is a consultant to the company.

     FASEB BioAdvances, 2025· 42 people

3. 03NRPTSupplementModerate. At least one finished study in people, and at least 100 people who took it. 3 completed trials, 176 people given it.3 reported

   24 people given it1 trial1 found nothing

   • found nothingThe pills raised NAD in patients with sudden kidney injury, and nothing about their kidneys changed. 24 hospital patients took rising doses of the combination or a dummy for two days. The kidney injury itself halved NAD in the untreated patients, which is a finding in its own right. Pooled across doses the supplement lifted NAD by about a third, though results jumped around between individuals and only one dose step stood out alone. Kidney and liver blood tests were unchanged. Two authors work for Elysium Health.

     The numbers NCT03176628. 24 hospitalised patients with acute kidney injury received escalating doses of NRPT or placebo twice daily for 2 days across four dose steps up to 1000 mg NR with 200 mg pterostilbene. Acute kidney injury itself reduced whole blood NAD by 50 percent at 48 hours in placebo patients (P=0.05). Pooling all steps, NRPT increased NAD by 37 percent at 48 hours (P=0.002), but only one individual step reached significance and interindividual variability was considerable. Creatinine, eGFR, electrolytes, liver function tests and blood counts were unchanged. Three of 20 patients on NRPT reported minor gastrointestinal effects. Two authors are Elysium Health employees.

     BMC Nephrology, 2020· 24 people

4. 04EcdysteroneSupplementModerate. At least one finished study in people, and at least 100 people who took it. 3 completed trials, 233 people given it.5 reported

   0 people given it1 trial

   • In a study in people, those taking ecdysterone gained more muscle than the comparison group and lifted more on the bench press. Blood tests for liver and kidney damage did not rise. The researchers checked everyone for banned drugs and tested the supplement for hidden steroids first. They said it should go on the banned list in sport. That is how strong they judged the effect. In a dish, the same growth showed up in muscle cells.

     The numbers A controlled clinical trial in humans. Significantly higher increases in muscle mass in participants dosed with ecdysterone, and significantly more pronounced increases in one-repetition bench press performance. The same hypertrophic effect appeared in C2C12 myotubes in vitro. No increase in liver or kidney toxicity biomarkers. Participants were screened for prohibited performance-enhancing substances and the supplement was tested for anabolic steroid contamination before administration. The authors conclude their results strongly suggest including ecdysterone on the prohibited list in class S1.2, other anabolic agents.

     Archives of Toxicology, 2019· number of people not given

5. 05PterostilbeneSupplementLimited. People have taken it in a published study, but fewer than 100 of them. 1 completed trial, 80 people given it.4 reported

   nobody was given it1 watch-only study

   • This is a safety report and it makes no claim that the compound works. It covers the same 80 patients, of whom 91.3 percent finished, averaging 54 years old and 71 percent women. Liver, kidney and blood sugar markers showed no drug reactions, and no meaningful self-reported or major reactions turned up. The authors conclude pterostilbene is generally safe up to 250 mg a day. Read it beside the trial it came from. Safe is not the same as useful, and that same trial found bad cholesterol rising.

     The numbers The safety report from the same 80-patient trial, 91.3 percent completion, average age 54, 71 percent female. No adverse drug reactions on hepatic, renal or glucose markers and no statistically significant self-reported or major adverse reactions. The stated conclusion is that pterostilbene is generally safe for use in humans up to 250 mg a day. It reports safety only and makes no efficacy claim.

     Journal of Toxicology, 2013· 80 peopleobserved only, nobody was given it

Approved drugs, biologics and hormones that have been measured for this. They are here because leaving them out would misrepresent the evidence, and they are below the peptides because that is not what most people come here to read.

1. 01ErythropoietinBiologicStrong. At least two finished studies in people, and at least 1,000 people who took it. 3 completed trials, 4,641 people given it.6 reported

   4,641 people given it2 trials

   • This drug did not extend life or save kidneys, and it doubled the risk of stroke. 4,038 people with type 2 diabetes, kidney disease and anaemia got darbepoetin alfa or a dummy shot, with rescue treatment if counts dropped too low. Death and heart events came out the same. Kidney failure came out the same. Strokes hit 101 people on the drug against 53 on the dummy. Fewer needed transfusions, and tiredness improved a little. Amgen, which sells it, paid for the study.

     The numbers TREAT: 4,038 people with type 2 diabetes, chronic kidney disease and anaemia randomised to darbepoetin alfa targeting 13 g/dL or to placebo with rescue below 9 g/dL. Death or a cardiovascular event, hazard ratio 1.05 (0.94 to 1.17); death or end-stage renal disease, hazard ratio 1.06 (0.95 to 1.19). Fatal or non-fatal stroke 101 versus 53, hazard ratio 1.92, 95 percent confidence interval 1.38 to 2.68, p < 0.001. Fewer transfusions (297 versus 496) and only a modest improvement in fatigue. Sponsor Amgen.

     New England Journal of Medicine, 2009· 4,038 people

   • Aiming for a normal blood count did not help, and more of those patients ended up on dialysis. 603 people with failing kidneys were treated towards a normal or a lower blood count target and followed for three years. Heart events came out about the same, 58 against 47, a gap that could be chance. More people in the normal target group needed dialysis, 127 against 111. General health and physical function scores did improve. Roche, which sells the drug, ran it.

     The numbers CREATE: 603 people with estimated GFR 15 to 35 randomised to a normal (13.0 to 15.0 g/dL) or subnormal (10.5 to 11.5 g/dL) haemoglobin target using epoetin beta, 3 years. First cardiovascular events 58 versus 47, hazard ratio 0.78, 95 percent confidence interval 0.53 to 1.14, p = 0.20. More people in the normalisation group needed dialysis, 127 versus 111, p = 0.03. General health and physical function scores improved. Sponsor Hoffmann-La Roche.

     New England Journal of Medicine, 2006· 603 people

2. 02EfpeglenatideBiologicStrong. At least two finished studies in people, and at least 1,000 people who took it. 2 completed trials, 4,076 people given it.3 reported

   4,076 people given it1 trial

   • This one did protect the heart. Just over four thousand people with type 2 diabetes and a high risk of heart trouble took efpeglenatide or a dummy injection. Heart attacks, strokes and deaths from heart disease happened about a quarter less often on the drug. Kidney problems were down by roughly a third. Two results pointing the same way are harder to dismiss than one. Everybody here was picked for being at high risk, so healthier people should not expect the same size of gain.

     The numbers 4,076 high-risk patients: MACE hazard ratio 0.73 and composite renal outcome hazard ratio 0.68 versus placebo.

     New England Journal of Medicine, 2021· 4,076 people

3. 03BPTESSmall moleculeModerate. At least one finished study in people, and at least 100 people who took it. 2 completed trials, 513 people given it.1 reported

   444 people given it1 trial

   • The only proper test of blocking this enzyme in people found nothing. 444 adults with advanced kidney cancer got telaglenastat plus the cancer drug cabozantinib, or a dummy pill plus cabozantinib. Both groups went about 9.2 and 9.3 months before their cancer grew again. That is the same result twice. Telaglenastat is a different drug from BPTES, but it hits the same target, and this is cancer medicine, not ageing. The maker paid for the study.

     The numbers 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

   Also measured in animals or in the lab

   • In mice and in human cells in a dish. Worn-out human cells needed the glutaminase enzyme to survive. Leaky internal compartments make them acidic inside, and the enzyme makes ammonia that cancels the acid out. Blocking it in old mice killed worn-out cells and eased age-related organ problems.

     The numbers 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 study

4. 04NattokinaseBiologicStrong. At least two finished studies in people, and at least 1,000 people who took it. 9 completed trials, 1,795 people given it.6 reported

   45 people given it1 trial1 found nothing

   • found nothingThree clotting proteins fell, and there was nothing to compare them against. 45 people, some healthy, some at risk of heart disease and some on dialysis, took a high daily dose for two months. Two of the proteins fell by up to about a tenth, and the third by nearly a fifth. Everyone got the supplement and knew it, so time, season or chance could explain some of that. Cholesterol did not move.

     The numbers Open-label, self-controlled trial, 45 subjects across healthy, cardiovascular-risk and dialysis groups, 4,000 FU/day for 2 months: fibrinogen fell 7 to 10%, factor VII 7 to 14%, factor VIII 17 to 19% (all p<0.001 for the time effect) across groups; no placebo or control arm, and blood lipids did not change.

     Nutrition Research, 2009· 45 people

5. 05Nandrolone decanoateHormoneLimited. People have taken it in a published study, but fewer than 100 of them. 3 completed trials, none stating how many people.6 reported

   0 people given it1 trial

   • Nandrolone built real muscle in people on dialysis, in a small but well-run study. 29 adults on long-term dialysis got the drug or a dummy shot for six months. Lean body mass rose about 4.5 kg on nandrolone against 1.9 kg on the dummy shot. Treated patients also walked and climbed stairs faster, while the dummy group got slower. Grip strength did not change in either group. 29 people is a small study.

     The numbers A randomised controlled trial in dialysis patients, published in JAMA, reporting anabolic effects. One of the few randomised trials of an anabolic steroid in a major general medical journal, and the basis of the drug's renal indication.

     JAMA, 1999· number of people not given

6. 06GDF15BiologicModerate. At least one finished study in people, and at least 100 people who took it. 2 completed trials, 313 people given it.3 reported

   nobody was given it1 watch-only study

   • GDF15 tracks with getting sick in general, not with any one disease. Researchers measured thousands of blood proteins in 53,026 UK adults and followed them for over 13 years. Higher GDF15 went with later diagnosis of more than twenty different long-term illnesses, and with having several at once. Much of the level was explained by kidney function, liver function, inflammation and body fat. Nobody was given anything here. This is a marker of trouble, not a proven cause of it.

     The numbers 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 peopleobserved only, nobody was given it

7. 07EmpagliflozinSmall moleculeStrong. At least two finished studies in people, and at least 1,000 people who took it. 3 completed trials, 16,738 people given it.4 reported

   nobody was given it1 watch-only study

   • It slowed kidney disease down, and it did not stop people dying. 6,609 people with chronic kidney disease were followed for two years. Their kidney disease got worse, or they died of heart disease, in 16.9 percent of the dummy group against 13.1 percent on empagliflozin. Deaths from any cause were 5.1 percent against 4.5 percent, a gap too small to separate from chance. Anyone treating this drug as something that makes people live longer should stop at that last sentence.

     The numbers 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 peopleobserved only, nobody was given it

8. 08TIMP2BiologicPreliminary. Studied in people, but no published study has had people take it. 1 human study where nobody was given it.4 reported

   nobody was given it1 watch-only study

   • This is the biggest body of human TIMP-2 data, and none of it is about ageing. Two observational studies followed critically ill adults: 522 people in the first, with over 300 markers checked, and 728 in a second group to confirm the result. A urine test combining TIMP-2 with another marker spotted serious kidney injury within 12 hours better than any marker tried before. Nobody was given TIMP-2. This is a test that reads the body, not a treatment.

     The numbers Human, and the largest body of TIMP-2 data in people, though it is not about ageing. Two multicentre observational studies in critically ill adults: 522 in discovery across sepsis, shock, major surgery and trauma cohorts with over 300 markers examined, and 728 in the Sapphire validation cohort. Urinary TIMP-2 combined with IGFBP7 gave an area under the curve of 0.80 for moderate to severe acute kidney injury within 12 hours, significantly better than all previously described markers (p < 0.002), none of which exceeded 0.72.

     Critical Care, 2013· number of people not givenobserved only, nobody was given it

Peptides and blends

1. 01AdipotidePeptideAnimal or lab only. Only animal or lab studies on this page. No study in people yet. 2 animal studies, no human study.6 reported

   1 animal or lab study

   What people using it report

   • The specific problem raised is the kidney. An account circulated in these threads of someone whose creatinine rose several fold while using it, into a range the discussion treated as the kidneys failing.
   • The more technical posters say the kidney damage comes from the drug doing what it is meant to do, not from bad luck. The contents of the destroyed fat cells all hit the blood at once. The comparison they reach for is tumour lysis.
   • Weight loss is not generally disputed in these threads. The argument is entirely about whether the cost in kidney function is acceptable, and the position described as consensus is that it is not.

   Measured in animals or in the lab

   • In obese rhesus monkeys, adipotide killed off blood vessels in white fat. They lost 7.4 to 14.7% of their weight in four weeks and handled insulin better. Kidney changes grew with the dose and went away after stopping.

     The numbers Adipotide induced apoptosis in white-fat blood vessels of obese rhesus monkeys, producing 7.4 to 14.7% weight loss in four weeks with improved insulin resistance; renal proximal tubule changes were dose-dependent and reversible.

     Science Translational Medicine, 2011· animal study

2. 02FOXO4-DRIPeptideLimited. People have taken it in a published study, but fewer than 100 of them. 1 completed trial, 74 people given it.8 reported

   1 animal or lab study

   Measured in animals or in the lab

   • In mice. The peptide made worn-out cells die. It brought back fitness, fur and kidney function in mice that age fast and in naturally old mice.

     The numbers A designed FOXO4 peptide that blocks the FOXO4-p53 interaction selectively triggered apoptosis in senescent cells and restored fitness, fur density and renal function in fast-aging XpdTTD/TTD and naturally aged mice.

     Cell, 2017· animal study

3. 03SS-20PeptideAnimal or lab only. Only animal or lab studies on this page. No study in people yet. 4 animal studies, 1 lab study, no human study.6 reported

   1 animal or lab study

   Measured in animals or in the lab

   • In rats. A dose of SS-20 before blood flow was cut let the kidney cope longer without it. It kept kidney cells and their mitochondria in better shape, and cut scarring later on. This is about a surgery window in rats. It is not a treatment for kidney disease in people.

     The numbers Rats. Pretreatment with SS-20 thirty minutes before warm ischaemia raised tolerated ischaemia time from 30 to 45 minutes. It reduced cytoskeletal breakdown, cell swelling and mitochondrial matrix swelling, preserved cristae, improved state 3 respiration and respiratory control ratio in isolated kidney mitochondria, and reduced later interstitial fibrosis when given after ischaemia. A surgical-window result in rats, not a chronic kidney disease treatment in people.

     American Journal of Physiology, Renal Physiology, 2015· animal study

Supplements

1. 01Procyanidin C1SupplementAnimal or lab only. Only animal or lab studies on this page. No study in people yet. 2 animal studies, no human study.2 reported

   1 animal or lab study

   Measured in animals or in the lab

   • In mice. After a blocked kidney, procyanidin C1 cut worn-out kidney cells and kidney scarring. Worn-out kidney cells were also seen in blocked human kidneys, but only looked at, not treated.

     The numbers Mouse ureteral obstruction model, with senescent tubular cells also observed in obstructed human kidney tissue. Procyanidin C1 reduced senescent tubular cells and renal fibrosis in the mice. The human component is tissue observation, not treatment.

     FASEB Journal, 2025· animal study

2. 02NMNHSupplementLimited. People have taken it in a published study, but fewer than 100 of them. 1 completed trial, none stating how many people.1 reported

   1 animal or lab study

   Measured in animals or in the lab

   • In a dish and in mice. This paper first made and tested NMNH. It raised NAD more and faster than NMN or NR in cells, by a route that skips two slow enzyme steps. It cut damage and sped up repair in kidney cells starved of oxygen. In mice, it caused a fast, lasting rise of NAD in the blood, and in the liver, kidney, muscle, brain, brown fat and heart, but not in white fat.

     The numbers Synthesis and first characterisation. NMNH raised NAD to a much higher extent and faster than NMN or NR in mammalian cells, through an NRK-independent and NAMPT-independent pathway. It reduced damage and accelerated repair in renal tubular epithelial cells after hypoxia and reoxygenation injury. In mice, administration caused a rapid and sustained NAD surge in whole blood, with increases in liver, kidney, muscle, brain, brown adipose tissue and heart, but not in white adipose tissue.

     FASEB Journal, 2021· animal study

Other compounds

1. 01OSK Partial ReprogrammingBiologicPreliminary. Studied in people, but no published study has had people take it. 1 registered with no result.5 reported

   1 animal or lab study

   Measured in animals or in the lab

   • In normally ageing mice, not ones bred to age fast, long stretches of partial reprogramming changed the kidney and skin. The longer the treatment ran, the bigger the change. Ageing clocks read younger. Genes for inflammation, worn-out cells and stress were turned down. The authors did not claim these mice lived longer.

     The numbers 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 study

2. 02OSKM Cyclic Partial ReprogrammingBiologicAnimal or lab only. Only animal or lab studies on this page. No study in people yet. 6 animal studies, no human study.5 reported

   1 animal or lab study

   Measured in animals or in the lab

   • In mice, from the Yamada and Yamanaka labs. Switching the reprogramming genes on and then taking the doxycycline switch away caused tumours in several tissues. The tumour cells were unformed and abnormal, with big changes to the chemical tags across their DNA. The kidney tumours looked like Wilms tumour, a childhood cancer. Stem cells taken from those tumours grew into normal kidney cells, which proves the tumours came from the tags, not from damaged genes.

     The numbers Mouse, from the Yamada and Yamanaka laboratories. Transient expression of reprogramming factors followed by doxycycline withdrawal produced tumours in various tissues, consisting of undifferentiated dysplastic cells with global DNA methylation changes. Kidney tumours shared characteristics with Wilms tumour. Stem cells derived from those tumour cells gave rise to non-neoplastic kidney cells, proving the tumours were epigenetically rather than genetically driven.

     Cell, 2014· animal study

3. 03RilmenidineSmall moleculePreliminary. Studied in people, but no published study has had people take it. 1 human study where nobody was given it.1 reported

   1 animal or lab study

   Measured in animals or in the lab

   • In worms. Rilmenidine made tiny worms live longer and handle stress better, whether they started young or old. It only worked through one specific receptor and the cell's clean-up system. It added nothing for worms already eating less or on rapamycin. In mice, it changed genes in the liver and kidney to look like eating less, but the mice's lifespan was not measured. Two authors have business interests in longevity.

     The numbers 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 study