Peptide encyclopedia
3 of 20 peptides match the filters. Each entry carries mechanism, route of administration, half-life, legal status in your jurisdiction, and the primary sources backing every claim.
- Compounds
- 20
- Source links
- 39
- Therapeutic classes
- 9
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Reset all01·Metabolic / GLP-1
Retatrutide
Also: LY3437943
Retatrutide is a synthetic peptide engineered as a balanced agonist of three receptors: the glucose-dependent insulinotropic polypeptide (GIP) receptor, the glucagon-like peptide 1 (GLP-1) receptor, and the glucagon receptor ([Jastreboff et al., *N Engl J Med* 2023, 389:514–526](https://doi.org/10.1056/NEJMoa2301972)). The first two receptors share their incretin mechanism with tirzepatide and semaglutide, respectively; the addition of glucagon-receptor agonism is what distinguishes retatrutide and is hypothesized to add a pro-energy-expenditure component to the appetite-suppressive and insulin-sensitizing effects of the two incretins. Mechanistically, glucagon-receptor agonism increases hepatic glucose output, mobilizes lipids, and raises basal energy expenditure — a combination that, balanced correctly against the incretin signals, is intended to drive weight loss through both reduced energy intake and increased energy turnover. The fatty-acid modification for albumin binding produces a roughly week-long pharmacokinetic profile suited to weekly dosing.
Prescription only
02·Metabolic / GLP-1
Semaglutide
Also: Ozempic, Wegovy, et al.
Semaglutide is a 31-amino-acid analog of glucagon-like peptide-1 (GLP-1) with two structural modifications: an α-aminoisobutyric acid substitution at position 8 that resists degradation by DPP-4, and a C18 fatty acid chain attached at position 26 through a γ-glutamic acid spacer that binds plasma albumin and extends the half-life to about a week ([Lau et al., *J Med Chem* 2015, 58:7370–80](https://doi.org/10.1021/acs.jmedchem.5b00726)). It acts as a full agonist at the GLP-1 receptor, which is expressed on pancreatic β-cells, on enteric neurons, and on hypothalamic and brainstem appetite-regulating circuits. Three downstream effects matter clinically: glucose-dependent insulin secretion, slowed gastric emptying, and centrally mediated appetite suppression. The central effect is the dominant driver of weight loss, not the peripheral metabolic ones.
Prescription only
03·Metabolic / GLP-1
Tirzepatide
Also: Mounjaro, Zepbound, et al.
Tirzepatide is a 39-amino-acid synthetic peptide engineered from the native glucose-dependent insulinotropic polypeptide (GIP) backbone, with a C20 fatty diacid chain attached via a γ-glutamic-acid / OEG linker to a Lys residue for albumin binding ([Jastreboff et al., *N Engl J Med* 2022, 387:205–216](https://doi.org/10.1056/NEJMoa2206038)). It activates both the GIP and GLP-1 receptors as a full or near-full agonist; the dual incretin engagement is the molecular signature that distinguishes it from semaglutide and the rest of the GLP-1 monoagonist class. Downstream effects span the same three mechanisms as GLP-1: glucose-dependent insulin secretion, slowed gastric emptying, and central appetite suppression. The GIP component contributes additional metabolic effects — including modulation of adipose insulin sensitivity and potential alteration of nausea-pathway signaling — that may explain part of the larger weight-loss magnitude relative to GLP-1 monoagonism, though the contribution of each receptor to clinical effect is still being parsed in the literature.
Prescription only