30 compounds were read against these 2 conditions; 8 produced a graded row. The other 22 are named further down.

The ranking, and the key it uses

Ordered by the best rung the compound holds anywhere in this goal; then by what that study measured; then by how many graded rows it holds here, as a tie-break only; then by name. There is no blended score — one number mixing the rung and what was measured would invent a third scale nothing was graded against. Every rung links to the rubric that assigned it.

1. 01

   NAD+ Boosting / Precursor Peptides

   human RCT · direct outcome · 2 graded rows across 2 of 2 conditions

   Age related mitochondrial dysfunction · Epigenetic age acceleration

   2 graded rows, 2 sources

   1. Age related mitochondrial dysfunction

      human RCT Direct outcome Not approved for this condition

      Who was studied

      men aged 70-80, median 75, n=12, oral nicotinamide riboside 1 g/day for 21 days with a 21-day washout, randomised double-blind placebo-controlled crossover

      Nicotinamide riboside raised the aged skeletal-muscle NAD+ metabolome as intended and then changed nothing downstream that was measured: complex I- and complex II-supported respiration, maximal respiratory capacity, citrate synthase activity, mitochondrial DNA copy number, mitochondrial resident protein levels and hand-grip strength were all unchanged against placebo. Twelve men for three weeks is small and short, and no longer trial of a NAD+ precursor has measured muscle mitochondrial respiration in older people. A separate 12-week randomised trial of nicotinamide mononucleotide 250 mg/day in men aged 65 and over reported nominal gains in gait speed (p=0.033) and left-hand grip (p=0.019) with no correction for multiple comparisons, and took no respirometry, ATPmax or phosphocreatine measurement at all.

      Source PubMed Central 2 primary sources read for this row

   2. Epigenetic age acceleration

      human RCT Direct outcome Not approved for this condition

      Who was studied

      adults with mild cognitive impairment, n=20 randomised 1:1 (nicotinamide riboside arm 5 men and 5 women, mean age 77.1, range 71-83; placebo arm 2 men and 8 women, mean age 75.2, range 67-86), oral nicotinamide riboside 1 g/day for 10 weeks

      DNA methylation in peripheral blood mononuclear cells was an exploratory outcome of a safety-focused pilot, and the four clocks disagreed with each other: PhenoAge and GrimAge showed a subtle decrease in paired mean difference on nicotinamide riboside, the Hannum-based extrinsic measure showed markers of accelerated ageing on treatment and not on placebo, and the Horvath-based intrinsic measure showed no difference between groups. The authors state the analysis was not corrected for multiple comparisons and that the study was not powered to detect methylation changes. Blood NAD+ rose 2.6-fold, confirming the dose was delivered; the primary endpoint was the Montreal Cognitive Assessment, which did not change, and no trial has been designed with an epigenetic clock as its primary outcome.

      Source PubMed Central 1 primary source read for this row

2. 02

   N-Acetylcysteine (NAC)

   human RCT · direct outcome · 1 graded row across 1 of 2 conditions

   Age related mitochondrial dysfunction

   1 graded row, 1 source

   1. Age related mitochondrial dysfunction

      human RCT Direct outcome Not approved for this condition

      Who was studied

      older adults aged 61-80, n=24 randomised (12 to GlyNAC, 8 men and 4 women; 12 to isonitrogenous alanine placebo, 4 men and 8 women), 16 weeks; a separate non-randomised group of 12 young adults aged 21-40 was given the same supplement for 2 weeks

      A 16-week randomised placebo-controlled trial of GlyNAC, meaning glycine and N-acetylcysteine at 100 mg/kg/day each, measured mitochondrial fatty-acid oxidation directly: it rose 78% against placebo (p<0.001), with gait speed up from 1.13 to 1.34 m/s (p=0.032), grip strength improved in both hands (p=0.004) and 6-minute walk distance short of significance (p=0.053). Every arm received the combination and none received N-acetylcysteine alone, so this compound's own contribution cannot be separated from glycine's, and the whole randomised sample is 24 people at one centre. N-acetylcysteine is approved as a mucolytic and as the antidote for paracetamol overdose; neither approval covers ageing or mitochondrial function.

      Source PubMed Central 1 primary source read for this row

3. 03

   SS-31

   human RCT · direct outcome · 1 graded row across 1 of 2 conditions

   Age related mitochondrial dysfunction

   1 graded row, 1 source

   1. Age related mitochondrial dysfunction

      human RCT Direct outcome Not approved for this condition

      Who was studied

      healthy community-dwelling older adults aged 60-85, n=39 randomised (19 elamipretide, 20 placebo), 46% female, screened in on muscle ATPmax below 0.7 mM/sec; a single 2-hour intravenous infusion

      A randomised, double-blind, placebo-controlled parallel-group trial infused 0.25 mg/kg/hour for two hours and measured in-vivo muscle mitochondrial capacity (ATPmax) by 31-phosphorus magnetic resonance spectroscopy: ATPmax rose about 27% against 12% on placebo immediately after the infusion (p=0.045 for percent change), and the difference was gone by day 7, while resting mitochondrial coupling (P/O) and fatigue resistance both showed no significant change. This is one dose in one session rather than a treatment course, and no trial of repeated dosing in older adults is on file. The phase 3 programme was in genetic primary mitochondrial myopathy, not ageing: MMPOWER-3 (NCT03323749) randomised 218 people to 40 mg daily subcutaneously for 24 weeks and missed both primary endpoints, and the FDA's September 2025 accelerated approval of elamipretide as Forzinity covers muscle strength in Barth syndrome weighing at least 30 kg, which is a different condition from this one.

      Source PubMed Central 3 primary sources read for this row

4. 04

   Humanin

   human observational · mechanistic only · 1 graded row across 1 of 2 conditions

   Age related mitochondrial dysfunction

   1 graded row, 1 source

   1. Age related mitochondrial dysfunction

      human observational Mechanistic only Not approved for this condition

      Who was studied

      18 offspring of centenarians against 19 age-matched controls (circulating humanin); 3 people with Alzheimer's disease against 4 controls aged 60-80 (cerebrospinal fluid humanin); 73 newborn cord-blood samples; nobody in any cohort received humanin

      Recorded, and not evidence for this condition

      Every human finding in this paper is an association involving an endogenous humanin concentration: higher circulating humanin in centenarians' offspring, lower cerebrospinal-fluid humanin in Alzheimer's disease, and lower cord-blood humanin where mitochondrial DNA copy number was lower. No study measured mitochondrial function in a person given humanin, because no person has been given it, and a natural blood level tracking age says nothing about what administering the peptide would do. The animal work used HNG, the S14G-humanin analogue rather than humanin itself, and in 18-month-old mice it reduced visceral fat and raised lean mass without extending lifespan.

      Source PubMed Central 1 primary source read for this row

5. 05

   DHEA

   human case series · direct outcome · 1 graded row across 1 of 2 conditions

   Epigenetic age acceleration

   1 graded row, 1 source

   1. Epigenetic age acceleration

      human case series Direct outcome Not approved for this condition

      Who was studied

      men aged 51-65, n=10 enrolled and 9 completed, DHEA 50 mg three to four times weekly from week 2 as one part of a five-agent combination, open-label with no control group, 12 months

      DHEA appears in this literature only as one component of the TRIIM combination, taken with recombinant human growth hormone, metformin 500 mg, vitamin D3 and zinc for a year. Mean epigenetic age across the Horvath, Hannum, PhenoAge and GrimAge clocks fell about 2.5 years against the expected chronological trajectory, but the study was open-label with no control arm, and DHEA was never administered by itself, so nothing here separates its effect from growth hormone's or metformin's. No trial of DHEA alone has measured any named epigenetic clock in this population.

      Source PubMed Central 1 primary source read for this row

6. 06

   hGH

   human case series · direct outcome · 1 graded row across 1 of 2 conditions

   Epigenetic age acceleration

   1 graded row, 1 source

   1. Epigenetic age acceleration

      human case series Direct outcome Not approved for this condition

      Who was studied

      men aged 51-65, n=10 enrolled and 9 completed, open-label with no control group and no randomisation, 12 months of treatment with measurements to 18 months

      The TRIIM study is the only human work on file in which any compound in this corpus was measured against named epigenetic clocks. Nine men completed a year of recombinant human growth hormone, starting at 0.015 mg/kg three to four times weekly, given alongside DHEA 50 mg, metformin 500 mg, vitamin D3 3,000 IU and zinc 50 mg; mean epigenetic age across the Horvath, Hannum, PhenoAge and GrimAge clocks fell about 2.5 years against the expected chronological trajectory, and the GrimAge decrease of roughly 2 years was still present six months after treatment stopped. There was no control arm, no randomisation and no blinding, the comparison is against expected ageing rather than against untreated people, growth hormone was never given alone beyond a three-week sequencing period so its own contribution cannot be separated, and several authors held shares or share options in the sponsoring company.

      Source PubMed Central 1 primary source read for this row

7. 07

   MOTS-c

   animal in vivo · mechanistic only · 1 graded row across 1 of 2 conditions

   Age related mitochondrial dysfunction

   1 graded row, 1 source

   1. Age related mitochondrial dysfunction

      animal in vivo Mechanistic only Not approved for this condition

      Who was studied

      mice aged 2, 12 and 22 months given MOTS-c 5 or 15 mg/kg/day intraperitoneally for about two weeks, plus a late-life cohort started at 23.5 months and dosed three times weekly; the human part of the same paper was 10 sedentary healthy men aged 24.5 +/- 3.7 who were given nothing

      Recorded, and not evidence for this condition

      In mice, injected MOTS-c improved treadmill running, rotarod performance and grip at every age tested, with old treated animals running roughly twice as long as controls. No human has been administered MOTS-c in any study on file, so no study measured mitochondrial capacity, exercise tolerance or any other endpoint in a person given this peptide; the human evidence is an association between endogenous levels and something else, which is a mechanistic argument rather than a result. A cross-sectional study of 104 healthy men found plasma MOTS-c about 21% lower in the 70-81 group than the 18-30 group, but muscle MOTS-c was higher in the older men, not lower, which runs opposite to the decline the peptide is sold to correct.

      Source PubMed Central 2 primary sources read for this row

8. 08

   Epitalon

   in vitro · mechanistic only · 1 graded row across 1 of 2 conditions

   Age related mitochondrial dysfunction

   1 graded row, 1 source

   1. Age related mitochondrial dysfunction

      in vitro Mechanistic only Not approved for this condition

      Who was studied

      cultured human pineal gland cells taken through replicative senescence; no living human or animal subject

      Recorded, and not evidence for this condition

      Confocal laser scanning microscopy of senescing human pinealocyte cultures found that AEDG, the tetrapeptide sold as epitalon, increased the stained area of MitoTracker Red by about 1.5-fold and lowered ribosomal protein L7A expression by 22%. A dye-stained area in a cell culture is not mitochondrial capacity, and no study measured mitochondrial function, exercise tolerance or any other ageing endpoint in a living person given epitalon. The long-running Russian geroprotection reports that are usually cited for this peptide, including the 15-year follow-up in 79 coronary patients and the melatonin-rhythm work in elderly subjects, both used epithalamin, a bovine pineal gland extract, and not the synthetic AEDG tetrapeptide.

      Source PubMed 3 primary sources read for this row

Checked, and nothing on file

22 compounds were read against these conditions and produced no gradeable row. They are named here rather than left off, because a list of 8 reads identically whether 8 survived 30 or 8 were all anyone thought of.

1. Anserine

   No rung — nothing on file to grade

   Checked against age related mitochondrial dysfunction, epigenetic age acceleration. No study meeting the rubric was found for any of them.

2. Balenine

   No rung — nothing on file to grade

   Checked against age related mitochondrial dysfunction, epigenetic age acceleration. No study meeting the rubric was found for any of them.

3. Carnosine

   No rung — nothing on file to grade

   Checked against age related mitochondrial dysfunction, epigenetic age acceleration. No study meeting the rubric was found for any of them.

4. Elastin Peptides

   No rung — nothing on file to grade

   Checked against age related mitochondrial dysfunction. No study meeting the rubric was found for any of them.

5. FOXO4-DRI on age related mitochondrial dysfunction

   No rung — nothing on file to grade Not approved for this condition

   The record is one 2017 paper in Cell. A designed FOXO4 peptide disrupted the FOXO4-p53 interaction, selectively killed senescent cells, and in naturally aged and XpdTTD/TTD fast-ageing mice restored running-wheel fitness, fur density and renal function. Nothing mitochondrial was measured in it, no ageing endpoint has been measured in any human given FOXO4-DRI, and a healthspan result in a mouse is not a human claim, so this row records an absence rather than a rung.

6. GHK-Cu

   No rung — nothing on file to grade

   Checked against age related mitochondrial dysfunction, epigenetic age acceleration. No study meeting the rubric was found for any of them.

7. GHRH (Growth Hormone-Releasing Hormone) on age related mitochondrial dysfunction

   No rung — nothing on file to grade Not approved for this condition

   No trial has used this compound against this condition; no mitochondrial endpoint was measured in any retrieved GHRH study.

8. GHRP-1 on age related mitochondrial dysfunction

   No rung — nothing on file to grade Not approved for this condition

   No trial has used this compound against this condition; no mitochondrial or ageing endpoint was measured.

9. Glutathione on age related mitochondrial dysfunction

   No rung — nothing on file to grade Not approved for this condition

   Glutathione is the deficiency these ageing studies report, not the substance they administer. In the 16-week GlyNAC trial in adults aged 61-80, red-cell glutathione was an outcome and glycine plus N-acetylcysteine were the intervention; a glutathione level corrected by giving its precursors is not evidence about giving glutathione. No trial located here administered glutathione itself, by any route, and then measured mitochondrial function in older adults, so this row records an absence rather than a rung.

10. Hexapeptide-11

    No rung — nothing on file to grade

    Checked against age related mitochondrial dysfunction. No study meeting the rubric was found for any of them.

11. Hexapeptide-9

    No rung — nothing on file to grade

    Checked against age related mitochondrial dysfunction. No study meeting the rubric was found for any of them.

12. L-Carnitine

    No rung — nothing on file to grade

    Checked against age related mitochondrial dysfunction. No study meeting the rubric was found for any of them.

13. NAD+ on age related mitochondrial dysfunction

    No rung — nothing on file to grade Not approved for this condition

    NAD+ is the molecule these ageing studies measure, not usually the one they administer; the muscle and function trials give precursors such as nicotinamide riboside or nicotinamide mononucleotide instead. The only located human study of NAD+ given directly is a pilot 6-hour intravenous infusion of 750 mg in 11 men aged 30-55, which tracked plasma and urine NAD+ metabolites and took no mitochondrial, muscle or functional measurement whatever, and enrolled nobody old. No controlled trial of intravenous NAD+ with a mitochondrial endpoint in older adults is on file, so this row records an absence rather than a rung.

14. Palmitoyl Hexapeptide-12

    No rung — nothing on file to grade

    Checked against age related mitochondrial dysfunction. No study meeting the rubric was found for any of them.

15. Palmitoyl Tetrapeptide-7

    No rung — nothing on file to grade

    Checked against age related mitochondrial dysfunction. No study meeting the rubric was found for any of them.

16. Palmitoyl Tripeptide-38

    No rung — nothing on file to grade

    Checked against age related mitochondrial dysfunction. No study meeting the rubric was found for any of them.

17. Pinealon

    No rung — nothing on file to grade

    Checked against age related mitochondrial dysfunction. No study meeting the rubric was found for any of them.

18. Silk Peptides

    No rung — nothing on file to grade

    Checked against age related mitochondrial dysfunction. No study meeting the rubric was found for any of them.

19. Soy Peptides

    No rung — nothing on file to grade

    Checked against age related mitochondrial dysfunction. No study meeting the rubric was found for any of them.

20. Tetrapeptide-30

    No rung — nothing on file to grade

    Checked against age related mitochondrial dysfunction. No study meeting the rubric was found for any of them.

21. Thymalin

    No rung — nothing on file to grade

    Checked against age related mitochondrial dysfunction, epigenetic age acceleration. No study meeting the rubric was found for any of them.

22. Thymulin

    No rung — nothing on file to grade

    Checked against age related mitochondrial dysfunction, epigenetic age acceleration. No study meeting the rubric was found for any of them.

Browse by goal

• Weight loss — 29 compounds with a graded row, from 48 checked
• Anti-ageing & metabolic — 16 compounds with a graded row, from 30 checked
• Muscle growth — 9 compounds with a graded row, from 20 checked
• Infection & immunity — 23 compounds with a graded row, from 30 checked
• Cardiovascular — 29 compounds with a graded row, from 33 checked
• Healing & recovery — 16 compounds with a graded row, from 29 checked
• Sexual health & fertility — 13 compounds with a graded row, from 28 checked
• Pain — 8 compounds with a graded row, from 19 checked
• Skin & hair — 9 compounds with a graded row, from 33 checked
• Brain & nerve recovery — 7 compounds with a graded row, from 15 checked
• Mood & anxiety — 3 compounds with a graded row, from 12 checked
• Sleep — 9 compounds with a graded row, from 30 checked
• Cognition — 8 compounds with a graded row, from 43 checked
• Inflammation — 5 compounds with a graded row, from 23 checked
• Gut health — 12 compounds with a graded row, from 27 checked