Peptides for longevity.
The category where the claims are largest, the timelines are longest, and the evidence is hardest to ever actually produce.
Longevity peptides face a structural problem that no amount of enthusiasm resolves: the outcome they claim to affect takes decades to measure. A trial that genuinely demonstrates extended human healthspan would need to run for a large part of a lifetime, which is why almost nothing in this category has evidence of the kind that would settle the question.
What exists instead is a chain of inference. A compound affects a pathway associated with aging in cells. That pathway is conserved in mice, where lifespan can actually be measured, and the compound extends it there. Therefore, the argument goes, it should help humans. Each link in that chain is plausible and each is also where the argument commonly breaks, because mouse lifespan studies have a long history of not translating.
A specific caution applies to a subset of this category. Several longevity peptides originate from a single research group in Russia, working on what they call peptide bioregulators. That literature is real, internally consistent, and spans decades, but it is also overwhelmingly produced by the same laboratory, published largely in Russian-language journals, and has not been independently replicated in Western randomized trials. Confidence in a body of work should scale with independent replication, and that replication has not happened here.
The mitochondrial compounds are on somewhat firmer ground mechanistically, and at least one has reached genuine clinical development for a rare mitochondrial disease. That is a meaningful distinction: a compound with a real trial program for a defined condition is a different proposition from one marketed directly for slowing aging, even when they share a mechanism.
Interesting biology, enormous claims, and an outcome that is nearly impossible to demonstrate. Treat confident longevity claims as hypotheses, and be especially careful where an entire evidence base comes from one group.
It extended lifespan in mice, so it will in humans.
Mouse lifespan extension has a poor translation record. It justifies further study, not a conclusion.
Biological age tests prove it is working.
Those tests measure correlates of aging, and shifting a correlate is not the same as changing the underlying trajectory.
Every compound in this category.
Graded on what has actually been published, with the regulatory reality on each one.
5-Amino-1MQ (5-amino-1-methylquinolinium) is a small-molecule, substrate-site inhibitor of the enzyme nicotinamide N-methyltransferase (NNMT).
Epitalon (also spelled Epithalon or Epithalone; sequence Ala-Glu-Asp-Gly, abbreviated AEDG) is a synthetic tetrapeptide developed in the 1980s by the Russian gerontologist Vladimir Khavinson and colleagues at the St.
FOXO4-DRI is a synthetic senolytic peptide derived from the transcription factor FOXO4 (Forkhead box O4).
Glutathione (GSH) is a tripeptide of glutamate, cysteine, and glycine that serves as the body's principal intracellular antioxidant and a key cofactor in detoxification.
Humanin is a 24-amino-acid mitochondrial-derived peptide (MDP), one of the first members of a class of small peptides encoded by short open reading frames within the mitochondrial genome rather than the nuclear genome.
MOTS-c is a 16-amino-acid mitochondrial-derived peptide encoded within the 12S rRNA region of the mitochondrial genome, first described around 2015.
SS-31, known generically as elamipretide and chemically as the tetrapeptide D-Arg-Dmt-Lys-Phe-NH₂ (Dmt = 2',6'-dimethyltyrosine), is a synthetic, cell-permeable, mitochondria-targeting peptide of the "Szeto-Schiller" (SS) aromatic-cationic class, originally discovered by Hazel Szeto and Peter Schiller at Cornell during opioid-peptide work.
Vilon is a synthetic dipeptide, L-lysyl-L-glutamate (Lys-Glu), one of the short peptide bioregulators developed by Vladimir Khavinson's St.
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