Comparison
Afamelanotide vs. Kisspeptin-10
Two peptides side-by-side — identity, evidence base, legal status and known adverse events.
Identity
Category
Research other
Research other
CAS no.
75921-69-6
374675-21-5
Molecular weight
1646.87 g/mol
1302.44 g/mol
Half-life
12 h
0.07 h
Sequence
Ac-Ser-Tyr-Ser-Nle-Glu-His-D-Phe-Arg-Trp-Gly-Lys-Pro-Val-NH2H-Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2Mechanism of action
Afamelanotide
Afamelanotide is a synthetic analogue of α-melanocyte-stimulating hormone. It differs from native α-MSH by two substitutions — norleucine at position 4 and D-phenylalanine at position 7 — which make it metabolically more stable and more potent. As an agonist at the melanocortin-1 receptor (MC1R) on melanocytes, it activates adenylate cyclase, raises cAMP and increases tyrosinase activity via the transcription factor MITF. This shifts pigment synthesis toward eumelanin, which absorbs UV and visible light and has antioxidant properties — the presumed mechanism of photoprotection in EPP.
Kisspeptin-10
Kisspeptin-10 comprises the ten C-terminal amino acids sufficient for binding to the KISS1R receptor (also GPR54). KISS1R is a G-protein-coupled receptor expressed predominantly on GnRH neurons in the hypothalamus. Activation signals through the Gq/11-phospholipase C pathway to release gonadotropin-releasing hormone (GnRH), which in turn drives the pituitary to secrete luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Kisspeptin signaling is regarded as an indispensable trigger of puberty; inactivating mutations in KISS1R are associated with absent puberty (idiopathic hypogonadotropic hypogonadism). Beyond the reproductive axis, KISS1R expression is described in limbic brain regions, discussed as a possible mechanism for the effects on sexual and emotional processing observed in imaging studies.
Evidence base
Highest evidence
Human RCT
Human RCT
Studies
4
4
of which in humans
4
4
Effects recorded
4
4
Open conflicts
1
1
Documented adverse events
4
1
Legal status
Full entries
Frequently asked questions
- What is the difference between Afamelanotide and Kisspeptin-10?
- Afamelanotide is classified as "Research other", while Kisspeptin-10 is classified as "Research other". Afamelanotide: Afamelanotide (brand name Scenesse) is a synthetic 13-amino-acid analogue of α-melanocyte-stimulating hormone (α-MSH) and a melanocortin-1 receptor agonist. Unlike most peptides covered here, it is a regularly approved medicine: EMA approval in 2014/2015, FDA approval in 2019, in each case as a subcutaneous implant for the prevention of phototoxicity in adults with erythropoietic protoporphyria (EPP). It promotes eumelanin formation in the skin. Kisspeptin-10: Kisspeptin-10 is the shortest bioactive fragment (10 amino acids) of the endogenous neuropeptide kisspeptin, encoded by the KISS1 gene. It acts as an agonist at the KISS1R (GPR54) receptor and stimulates hypothalamic GnRH neurons, driving release of LH and FSH. Kisspeptin is a master switch of puberty and reproduction and is studied in humans, notably by the group of Waljit Dhillo (Imperial College London), in reproductive disorders and in sexual and emotional brain processing. It is not an approved drug. This page contrasts both neutrally and source-based — with no usage or dosing recommendation.
- Which peptide is better supported by science, Afamelanotide or Kisspeptin-10?
- The highest available evidence level is "Human RCT" for Afamelanotide and "Human RCT" for Kisspeptin-10. A higher evidence level means more robust data, but says nothing about suitability for an individual. The full body of evidence is on each peptide's own page.
- What is the legal status of Afamelanotide and Kisspeptin-10 in Germany and the United States?
- Germany: Afamelanotide — Prescription, Kisspeptin-10 — Unapproved. United States: Afamelanotide — Prescription, Kisspeptin-10 — Research only. These are factual summaries with source and review date on the individual pages.