How the compounds work, grouped
Each class page explains the shared mechanism in plain words and how its members differ.
- Mechanism
GLP-1 receptor agonists
GLP-1 receptor agonists are engineered versions of the gut hormone GLP-1 that activate the GLP-1 receptor, a cell-surface receptor that raises cyclic AMP in pancreatic beta cells. According to their FDA labels, this increases insulin release and lowers glucagon only when glucose is elevated, and it delays gastric emptying. GLP-1 receptors are also present in several brain areas involved in appetite regulation. Native GLP-1 lasts only 1.5 to 2 minutes in the blood, so these drugs are modified to resist the enzymes that break it down.
5 compounds - Mechanism
GIP and glucagon co-agonists
These single peptides activate the GLP-1 receptor together with one or two related receptors: the GIP receptor, the glucagon receptor, or both. Tirzepatide's label describes combined GIP and GLP-1 receptor activation as enhancing insulin secretion and lowering glucagon in a glucose-dependent manner. Developers describe glucagon receptor activity as adding energy expenditure in mice and acting directly on the liver to increase fatty acid oxidation and inhibit fat production. Most of these molecules carry a fatty-acid or glycolipid side chain to extend their half-life.
6 compounds - Mechanism
Amylin analogues
Amylin is a pancreatic hormone released together with insulin that induces satiety. It acts through amylin receptors, which form when the calcitonin receptor pairs with a receptor activity-modifying protein (RAMP). Amylin analogues are lipidated, stabilised versions designed to last longer and to avoid native amylin's tendency to form amyloid. In rodents they reduced food intake and body weight, and several are in human trials alone or combined with incretin drugs.
4 compounds - Mechanism
GHRH analogues
Growth hormone-releasing hormone (GHRH) is a hypothalamic peptide that acts on pituitary somatotroph cells to stimulate synthesis and pulsatile release of the body's own growth hormone. GHRH analogues are based on its first 29 amino acids and act at the pituitary GHRH receptor rather than supplying growth hormone itself. Growth hormone released this way then raises IGF-1. The analogues differ mainly in how they are modified to resist breakdown and therefore how long they last.
4 compounds - Mechanism
Ghrelin-receptor agonists (GH secretagogues)
These synthetic peptides activate the growth hormone secretagogue receptor, a G protein-coupled receptor in the pituitary and hypothalamus whose natural ligand was later identified as ghrelin, a peptide from the stomach. Activating it releases growth hormone by a route separate from GHRH. A review described these secretagogues as functional somatostatin antagonists that potentiate GHRH and enhance pulsatile growth hormone secretion. Several have been used in humans as diagnostic growth hormone stimulation tests.
4 compounds - Mechanism
Melanocortin-receptor peptides
Melanocortin-receptor peptides are derived from alpha-melanocyte-stimulating hormone (alpha-MSH) and act at a family of receptors named MC1R to MC5R. MC1R on melanocytes drives eumelanin production and skin pigmentation, while MC3R and MC4R in the brain have been linked to appetite and sexual behaviour in animal work. How selective a compound is across these receptors largely shapes the effects reported for it.
5 compounds - Class
Thymic peptides
Thymic peptides are peptides isolated from, or extracted from, thymus tissue. Several have been studied for effects on immune function, such as T-cell differentiation markers and cytokine release in cell cultures, and immune markers in clinical trials. The group is chemically mixed: it includes a defined peptide, a tissue extract, a dipeptide and a fragment of a protein later recognised mainly for non-immune roles.
5 compounds - Class
Short bioregulator peptides
Short bioregulator peptides, often called Khavinson peptides, are synthetic di-, tri- and tetrapeptides from a St Petersburg research programme, many designed from the amino-acid composition of organ extracts. Their developers propose an epigenetic mechanism: that the peptides enter cells, reach the nucleus and bind DNA or histones to change which genes are expressed. Most of the supporting work is in cultured cells, tissue explants and computational docking, largely from the originating group. No receptor or defined molecular target has been identified for most of them.
14 compounds - Class
Mitochondria-targeted & mitochondrial-derived peptides
This group covers two kinds of peptide linked to mitochondria. Mitochondrial-derived peptides such as humanin and MOTS-c are encoded by short open reading frames in the mitochondrial genome and are described as signalling molecules. Mitochondria-targeted peptides such as elamipretide (SS-31) are synthetic molecules that bind the inner mitochondrial membrane. Apart from elamipretide, the reported effects on metabolism, cell survival and energy production come from cells and animals.
3 compounds - Class
Copper peptides
Copper peptides are short peptides that bind copper ions. GHK is a tripeptide that binds copper(II), and the GHK-Cu complex has been proposed to act in tissue repair and skin remodelling, for example by stimulating collagen, decorin and glycosaminoglycan synthesis in cell and tissue models. Copper is a cofactor for the lysyl oxidase enzymes that cross-link collagen, which a 2026 review discusses as a mechanistic hypothesis. Plasma GHK levels have been reported to decline with age.
1 compounds - Mechanism
Kisspeptin & GnRH axis
Kisspeptins, products of the KISS1 gene, act on the KISS1R receptor on hypothalamic neurons to release gonadotropin-releasing hormone (GnRH). GnRH then acts on pituitary gonadotrophs to release LH and FSH, which drive the ovaries and testes. The axis responds to pulses: pulsatile signals stimulate it, while continuous exposure can desensitise or suppress it. Kisspeptin peptides act one step upstream of GnRH.
5 compounds - Class
Host-defence (antimicrobial) peptides
Host-defence peptides are part of innate immunity. Cathelicidins, one family, are cationic and amphipathic, properties the literature links to their membrane-directed antimicrobial activity, and in cell-based work they also show immunomodulatory actions such as directing chemotaxis and affecting cell differentiation. LL-37 is the only cathelicidin-derived antimicrobial peptide identified in humans, released from its precursor hCAP-18 by proteinase 3 during neutrophil degranulation.
1 compounds - Class
Neuropeptide analogues studied for cognition
This group brings together peptides derived from, or modelled on, natural neuropeptides and brain proteins that have been studied in memory, mood, sleep or brain-injury research. Their starting points differ widely: fragments or analogues of ACTH, tuftsin, angiotensin IV, ciliary neurotrophic factor and the sortilin propeptide, plus a porcine brain extract and a sleep-linked nonapeptide. Proposed mechanisms include changes in BDNF, GABA binding and potassium-channel activity, and none is settled. Cerebrolysin has the most human trial data; for the others, human data are small, non-blinded or absent.
7 compounds - Class
Peptides studied in tissue-repair models
This is a loose grouping of chemically unrelated peptides that share one feature: they have been studied in models of injury, wound healing or fibrosis. Proposed mechanisms range from angiogenic signalling and actin binding to collagen remodelling, a tissue-protective receptor and anti-fibrotic relaxin-receptor signalling. Almost all of the evidence comes from rodents and cells, and the human studies that exist are small or did not meet their primary endpoints.
7 compounds