Main functions
- "1.Regulates Reproductive Endocrinology: Activates GPR54 receptors on GnRH neurons to stimulate pulsatile LH and FSH release. Clinical studies show that intravenous Kp-10 rapidly elevates LH levels in healthy men within 45 minutes and increases LH pulse frequency. This mechanism demonstrates potential therapeutic applications in reproductive disorders such as hypogonadotropic hypogonadism, delayed puberty, and hypothalamic amenorrhea.
- 2.Antitumor and Metastasis Suppression: The KISS1 gene was initially discovered as a metastasis suppressor. Exogenous Kp-10 treatment in triple-negative breast cancer cells upregulates KISS1 expression, inhibits cell migration, induces apoptosis, and reverses epithelial-mesenchymal transition (EMT). In esophageal cancer studies, Kp-10 overexpression suppresses cell proliferation, migration, and stemness. Its anti-angiogenic mechanism involves inhibiting Sp1-mediated VEGF expression and blocking FAK/Rho GTPase pathways.
- 3.Metabolic Regulation: In a high-fat diet-induced obesity-diabetes mouse model, 21-day Kp-10 treatment reduced body weight, blood glucose, and energy intake to normal levels. In a gestational diabetes mellitus rat model, Kp-10 improved insulin resistance in placental trophoblast cells by activating the cAMP/PKA pathway and restored glucose uptake. Studies indicate Kp-10 directly modulates the gut-pancreatic axis.
- 4.Bone Protection: Kp-10 binding to GPR54 recruits the Dusp18 phosphatase, which dephosphorylates Src kinase at Tyr416, thereby inhibiting osteoclast activity and bone resorption. Animal studies show that Kiss1 or Gpr54 knockout mice exhibit osteoclast hyperactivation and bone loss, which is effectively inhibited by Kp-10.
- 5.Neurovascular Protection: In a mouse cerebral ischemia-reperfusion model, Kp-10 alleviates neurological deficits, reduces infarct volume, and preserves blood-brain barrier integrity via mechanisms involving upregulation of Claudin-10 and activation of the Nrf2 antioxidant pathway."