Compare research peptides, side by side.

The core difference is receptor coverage. Semaglutide acts on the GLP-1 receptor only; tirzepatide acts on both the GIP and GLP-1 receptors. Both are fatty-acid-modified for a long half-life and both are approved medicines, so both sit at the top of our evidence scale.

Retatrutide adds glucagon-receptor activity to the GIP and GLP-1 activity that tirzepatide already has. That third receptor is the whole story of the comparison.

This pairing spans the whole incretin story: one receptor versus three. Semaglutide is the established single-receptor medicine; retatrutide is the investigational triple agonist.

These are often mentioned together but are unrelated molecules. BPC-157 is a 15-residue peptide derived from a gastric-juice protein. TB-500 is a fragment of thymosin beta-4, an actin-regulating protein.

They act on two different pituitary receptors. CJC-1295 is a GHRH analogue acting at the GHRH receptor; ipamorelin is a ghrelin-receptor agonist. That is why they are so often studied together rather than instead of each other.

PT-141 was derived from melanotan II. The key difference is selectivity: melanotan II activates several melanocortin receptors broadly, while PT-141 acts more selectively on central receptors, mainly MC4R.

Both are Russian-developed heptapeptides that share a stabilising Pro-Gly-Pro tail, but their parent sequences differ. Semax comes from ACTH(4-10) and is studied for neurotrophic signalling; Selank comes from tuftsin and is studied for stress-response and GABAergic pathways.

Both are acylated GLP-1 analogues that act on the GLP-1 receptor only, and both are approved medicines. The difference is in the engineering: semaglutide has a different N-terminal substitution and a longer fatty-diacid linker, which gives it a half-life of about a week against roughly 13 hours for liraglutide.

These two act on different hormone systems. Semaglutide mimics GLP-1 and activates the GLP-1 receptor. Cagrilintide mimics amylin and activates amylin and calcitonin receptors. Both are acylated for a half-life of about a week.

Both are GHRH analogues acting on the same pituitary receptor. Tesamorelin keeps the full 44-residue GHRH sequence and adds an N-terminal hexenoyl group. CJC-1295 is built on the first 29 residues and comes in versions with and without a drug affinity complex (DAC) that differ greatly in half-life.

Both activate the ghrelin (GHS) receptor. GHRP-6 is a six-residue, first-generation compound. Ipamorelin is a five-residue compound developed later with a more selective profile.

Both came out of the same University of Arizona research programme, but they are different molecules. Afamelanotide, or melanotan I, is a linear 13-residue α-MSH analogue acting mainly at MC1R. Melanotan II is a shorter cyclic peptide that activates several melanocortin receptors.

Both peptides activate the melanocortin-4 receptor, but they come from different design lineages. PT-141 (bremelanotide) derives from melanotan II and also touches other melanocortin receptors. Setmelanotide is a separate cyclic octapeptide designed around MC4R.

Both appear in mitochondrial research, but they work in opposite ways. MOTS-c is a natural 16-residue peptide encoded by mitochondrial DNA that acts as a signal from the mitochondrion to the rest of the cell. SS-31 is a synthetic four-residue peptide designed to enter mitochondria and bind cardiolipin.

These are often confused because of the family name, but they are unrelated. Thymosin alpha-1 is a 28-residue, N-acetylated peptide from the precursor prothymosin alpha, studied for immune signalling. TB-500 is a fragment of thymosin beta-4, an actin-binding protein, studied in cell-migration and wound models.

Both activate the GLP-1 receptor, but they get there differently. Exenatide is a 39-residue copy of exendin-4 from Gila monster saliva with no lipid chain. Liraglutide is a modified human GLP-1 analogue carrying a fatty acid that binds albumin and extends its half-life.

Both act on the GHRH receptor. Sermorelin is the native 1-29 fragment of GHRH and has a half-life of minutes. CJC-1295 is a modified analogue engineered for greater stability and a longer duration.

Both are first-generation synthetic ghrelin-receptor agonists, and both are six residues long. Hexarelin is generally reported as the more potent of the two, while the published work also highlights how rapidly the receptor response to it fades.

Both are amylin analogues, but they come from different design strategies. Pramlintide is a 37-residue human amylin with three proline substitutions, a short-acting soluble version. Cagrilintide is an acylated analogue built for a much longer duration.

The core difference is receptor coverage. Survodutide activates the GLP-1 and glucagon receptors; retatrutide activates those two plus the GIP receptor. Both are fatty-acid-modified for a long half-life and both are investigational, so neither is an approved medicine outside the regional exceptions noted on their pages.

Both compounds activate the GLP-1 and glucagon receptors, but they are different molecules. Mazdutide is an oxyntomodulin analogue developed in China and approved there for obesity; survodutide is built on a glucagon-like backbone and remains investigational.

Both are six-residue peptides that activate the ghrelin (GHS-R1a) receptor, and both sit in the original growth hormone releasing peptide family. They differ in sequence and in how they affect other pituitary hormones and appetite signalling in published studies.

Both peptides activate the PTH1 receptor, so the practical difference is origin and sequence. Teriparatide is a fragment of human PTH. Abaloparatide is a modified analogue of PTHrP that has been reported to engage a different receptor conformation in cell studies.

Both peptides act on the GnRH receptor. Gonadorelin is the synthetic copy of the native decapeptide and is cleared within minutes. Leuprolide is a modified nonapeptide built to resist breakdown, so it persists far longer.