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Decapeptide · KISS1R (GPR54) ligand
The C-terminal decapeptide of KISS1 and a full agonist at KISS1R (GPR54). Supplied as a lyophilized powder for research purposes only.
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Tested lot by lot at ≥99% purity. The Janoshik certificate for your lot is emailed with the order.
Everything Valtrax Research ships is bench material for in-vitro work. None of it is a drug, a supplement, a cosmetic, or a medical device, and none of it is intended for human or animal use, ingestion, or administration. Placing an order is your confirmation that you are a qualified researcher buying for lawful research, under every Canadian law and regulation that applies to you.
Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe. Ten residues off the C-terminal end of KISS1 — the part the longer kisspeptins get trimmed to in tissue, and the part that holds full activity at GPR54 (KISS1R). Everything past those ten amino acids is scaffold the receptor never needs.
GPR54 lives on GnRH neurons. Engage it and the consequence is one rung up: GnRH release, then the pituitary. That single upstream position is what makes the 10-mer a standing reagent for the switch that gates the reproductive axis.
Three bodies of work, unequal in size. The largest reads the HPG cascade — central and peripheral dosing, GnRH drive, the LH/FSH response, and its split by sex. A receptor-mechanics strand sits beneath it, mapping GPR54 occupancy and the signal it raises. A residual oncology strand carries forward from the gene’s origins as a metastasis suppressor.
Two levels of work run in parallel. At the receptor, binding and second-messenger studies read GPR54 occupancy directly — what the 10-mer touches and what it switches on. At the organism, central and peripheral dosing read the cascade it sets off: pulsatile GnRH, then LH and FSH downstream.
One finding shapes much of the human literature. Jayasena’s 2011 cohort showed the LH response splits by sex, and that dimorphism is part of why the fragment keeps reappearing wherever the reproductive gate — not the receptor alone — is the question.
The gene reached the literature through oncology, not endocrinology. KISS1 was first catalogued as a metastasis suppressor; the reproductive role only landed when GPR54 was paired with its kisspeptin ligands and loss-of-function mutations were found to stall puberty.
That second discovery moved the C-terminal decapeptide to the foreground. Short enough to synthesize cleanly, fully potent at the receptor — once the axis became the subject, it was the obvious thing to put in a vial.
Jayasena, C.N. et al. (2011). The effects of kisspeptin-10 on reproductive hormone release show sexual dimorphism in humans. J Clin Endocrinol Metab 96(12):E1963–E1972.
PubMedThompson, E.L. et al. (2004). Central and peripheral administration of kisspeptin-10 stimulates the hypothalamic-pituitary-gonadal axis. J Neuroendocrinol 16(10):850–858.
PubMedOlbrich, T. et al. (2010). Kisspeptin-10 inhibits bone-directed migration of GPR54-positive breast cancer cells.
PubMedJanoshik Analytical measures identity, purity, and net content, lot by lot.
Janoshik Analytical, a laboratory Valtrax does not own, runs the testing — identity by mass spectrometry, purity by RP-HPLC at ≥99%. The certificate covering the lot you receive is also emailed with your order.
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