Most peptide writing online either says nothing or promises everything. This page does neither. It explains what these molecules are, which receptor or pathway each class acts on, and how strong the published evidence behind each one actually is — including where it is thin.
A peptide is a short chain of amino acids — the same building blocks as a protein, just fewer of them. The convention is loose, but chains under roughly 50 amino acids are called peptides and anything longer is a protein. Insulin, at 51, sits right on the boundary and gets called both.
That size is the whole point. Proteins are large enough to do structural and enzymatic work. Peptides are small enough to act as signalling molecules: they fit a receptor, the receptor changes shape, and a cascade inside the cell begins. The peptide itself usually does nothing directly. It is a key, not a machine.
This is why peptides are studied so heavily. A molecule that binds one receptor with high specificity is a precise instrument for asking what that receptor does. It is also why the interesting question about any peptide is never "what does it do" in the abstract — it is which receptor does it bind, and what happens downstream.
Almost every research peptide in circulation falls into one of a handful of mechanistic groups. Grouping them this way is far more useful than grouping by the outcome someone hopes for, because compounds in the same family share pharmacology — and share failure modes.
These imitate incretin hormones the gut releases after eating. The archetype binds the GLP-1 receptor, a G-protein-coupled receptor found in the pancreas, gut and brain. Newer compounds are multi-agonists: tirzepatide hits GLP-1 and GIP receptors, retatrutide adds glucagon receptor activity as a third target. More receptors is not automatically better — it means a broader and less predictable effect profile, which is exactly what trials are built to characterise.
This is the most clinically mature family on the list, because several members are approved medicines with large published trial programmes behind them. Read more: GLP-1 peptides compared and retatrutide vs tirzepatide vs semaglutide.
These do not supply growth hormone. They prompt the pituitary to release its own, which is a meaningfully different mechanism. The family splits in two: GHRH analogues such as CJC-1295 and tesamorelin mimic growth-hormone-releasing hormone, while ghrelin mimetics such as ipamorelin act on the GHSR receptor. Because release stays under the body's own feedback control, the resulting pattern is pulsatile rather than a flat elevation.
The DAC modification is a good illustration of how a small structural change alters pharmacokinetics rather than mechanism — covered in CJC-1295 with DAC vs without. For what separates a family member with an approved indication from one without, see tesamorelin vs CJC-1295.
BPC-157 and TB-500 are the best known. Proposed mechanisms centre on angiogenesis, cell migration and growth-factor signalling — TB-500 is a fragment of thymosin beta-4, which binds actin and is involved in cytoskeletal reorganisation.
This is also where the evidence gap is widest. The literature is dominated by rodent and in-vitro work with very little controlled human data. That does not make the mechanisms wrong; it means they are largely uncorroborated in humans, and anyone claiming otherwise is going beyond what has been published. See what the BPC-157 research actually shows and BPC-157 vs TB-500.
A genuinely distinct family: short peptides encoded in mitochondrial DNA rather than nuclear DNA. MOTS-c and humanin are the archetypes, and SS-31 (elamipretide) is a synthetic relative that binds cardiolipin in the inner mitochondrial membrane. The research interest here is metabolic signalling and mitochondrial membrane integrity rather than any single receptor.
This family is the newest and the least written about, which is precisely why it is worth understanding rather than skipping — and why the two compounds most often sold under this heading are not the same kind of molecule at all: SS-31 and MOTS-c compared.
Semax and Selank derive from endogenous regulatory peptides — ACTH(4-10) and tuftsin respectively. Proposed mechanisms involve BDNF expression and modulation of monoamine and GABAergic signalling. Most of the primary literature is Russian-language and predates modern trial standards, a provenance issue worth knowing before weighing any claim about them. Compared in Semax vs Selank.
GHK-Cu is a tripeptide with a high affinity for copper(II). The copper is not incidental — the complex is what participates in the signalling, influencing extracellular-matrix remodelling and collagen expression. This family has more in-vitro dermatological data behind it than most. See copper peptides compared.
The single most useful skill is telling apart claims that sound equally confident but rest on completely different foundations. In rough order of strength:
Two habits catch most bad claims. First, ask what was actually measured — a study reporting a change in a signalling marker has not demonstrated a change in an outcome anyone cares about. Second, check whether a result in one species has been quietly restated as a result in humans. That single substitution is behind most of the overreach in this field.
For most compounds discussed here, controlled human evidence is limited or absent. Mechanism is not outcome: knowing which receptor a molecule binds does not tell you what happens to a person who takes it, and the history of pharmacology is largely a history of that gap.
TXLABS supplies these materials for laboratory research use only. They are not medicines, and they are not for human or veterinary use. We do not publish dosing, we do not suggest protocols, and we will not tell you whether a compound is appropriate for anyone — not out of caution, but because doing so would be outside what we are and unlawful for us. In Australia many of these compounds are Schedule 4, and advertising prescription-only substances to the public is prohibited regardless of how a product is labelled. Those questions belong with a qualified medical practitioner.
What we can tell you is what is in the vial, what documentation exists for that batch, and how to handle it. The regulatory picture is set out in peptide regulations in Australia.
Mechanism only matters if the material in front of you is what the label says and is still intact. Three things decide that:
Every compound in the catalogue is supplied for research use only. Certificates we hold are published in full in the CoA library.