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Research HubReference LibraryEducationCompareBlogCOAsContactAboutFAQCalculatorGlossaryShort reads on one research compound at a time: where it came from, what its name means, what has been tested, and what its regulatory status says.
For the full, cited evidence on each compound, see the Research Hub; for its chemistry and handling, the Reference Library; for the basics every peptide shares, Education.
Every registered human trial using follistatin itself delivers the gene, by viral vector or plasmid, rather than injecting the protein. The closest injected relative to reach people is an engineered fusion.
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One compound per post, written for researchers.
GDF-8 is myostatin, a protein that restrains muscle growth. Deleting or mutating its gene points the same way in mice, cattle, dogs and one child, though in mice the larger muscle was not the stronger one.
GHRP-6 was reported in 1984, its receptor found in 1996 and the body's own hormone for it in 1999. The hormone that came last reclassified the whole family.
A primate weight-loss result drew a published objection: maybe it was just reduced eating. A separate study, built specifically to test that, found the effect held up anyway.
AICAR is usually described as an AMPK activator. Two experiments, each blocking a different step of the same pathway, point instead to a different molecule doing the work.
Kisspeptin-10's human studies come from at least four independent research groups on three continents. Its 54-residue relative's record is close to a single group's program.
Orexin-A was found by two research groups in the same year, each with its own name for it. Both names are still in use, even inside the same body of work.
Livagen was tested head to head against Epitalon in the same study. The paper's own conclusion named Epitalon as the more protective agent.
A clinical trial really does show up when you search Testagen's name. It belongs to an unrelated testosterone patch, not the peptide sold here.
Sermorelin held two full US approvals. Both are gone. A 2013 FDA finding states plainly that neither left the market for safety or efficacy reasons.
Pal-GHK's mechanism is usually explained by borrowing Matrixyl's story. The two molecules fold completely differently in solution, and that matters.
SS-31 holds a genuine US drug approval granted last September. What "accelerated" actually means, and what the approval does and doesn't cover.
Oxytocin has held a US approval for over forty years, for a physical obstetric use. The behavioral research everyone talks about is a separate question.
Thymulin was named for a specific zinc-bound state, not for a sequence. Neither registered chemical identity for it actually confirms that state.
The sequence behind Matrixyl was identified in 1993 by researchers studying how collagen is built, years before anyone turned it into a skincare product.
IGF-1 LR3 outperforms native IGF-1 where binding proteins are present and underperforms it where they are absent. The same experiment shows both.
Mitochondria read the genetic code slightly differently from the rest of the cell. For humanin that means two peptides of different lengths, from one gene.
Orphan designation gets read as a milestone reached. It is an incentive granted before the work is done, and thymosin alpha-1 shows the difference.
PT-141 and melanotan II get treated as near-enough the same thing. FDA's compounding safety-risk page names only melanotan II, as a withdrawn nomination.
Selank is tuftsin, a fragment of an antibody, with three amino acids added at one end for a single stated purpose: to stop it degrading before it can act.
Almost everything in pharmacology starts by binding a receptor. The claim made for these peptides is that they skip that step and reach the gene itself.
A cell trims its proteins and discards the offcuts. DNSP-11 is eleven amino acids from one of those offcuts, and whether a living body makes it is an open question.
The names record the organ each compound's original extract came from, and that origin is also the series' central scientific claim.
The origin story everyone repeats about BPC-157 is close to right. The precise version is more interesting, and it changes how you read the whole literature.
The trials that won tesamorelin its approval were sponsor-funded, as approval trials are. What happened next is the part worth paying attention to.
Thymosin beta-4 is 43 amino acids long. The part that binds actin is six of them, and working out which six is a small masterpiece of patient science.
The 1973 paper that introduced GHK had nothing to do with skin, or with copper. How a tripeptide from blood took fifteen years to become a matrix molecule.
MOTS-c sits inside a mitochondrial gene whose job was never to make proteins. The discovery story, and what a sequence in a database does and doesn't prove.
A convincing blue color is easy to fake. Here's the plain-English version of the two checks that actually prove GHK-Cu's copper is real.
