Evidence Grade B — Strong clinical evidence. 306 published studies, 104 human. 5 registered clinical trials.
Medically reviewed by a licensed medical professional
Kisspeptin-10 is the shortest active fragment of kisspeptin, a brain hormone that controls the reproductive hormone cascade. It has been used extensively in academic research to study reproductive physiology and as a tool in fertility clinic studies. Its very short half-life (about 4 minutes) makes it less practical for therapeutic development than the longer kisspeptin-54 form. It has no pharmaceutical approval.
Kisspeptin-10 is also known by these brand and alternate names:
306 published studies: 104 human, 170 animal, 64 in-vitro, 13 reviews
Kisspeptin-10 has no marketing authorisation as a pharmaceutical product. It has been studied in multiple academic clinical studies, particularly as an alternative trigger for oocyte maturation in IVF — where it may reduce the risk of ovarian hyperstimulation syndrome (OHSS) compared to conventional triggers.
The kisspeptin signalling system is well established in reproductive endocrinology, and kisspeptin-10 has a more advanced clinical evidence base than many research compounds in this database. Its very short half-life (approximately 4 minutes) presents challenges for pharmaceutical development. Clinical investigation is ongoing, primarily in academic reproductive medicine centres.
Research has established that kisspeptin-10 activates the KISS1R receptor on GnRH neurons in the hypothalamus, triggering GnRH release, which in turn stimulates LH and FSH release from the pituitary. This kisspeptin-GnRH-gonadotropin cascade is now recognised as a fundamental regulator of puberty and reproductive function. The mechanism is well characterised through extensive academic research.
Research suggests kisspeptin-10 has been studied in multiple academic clinical settings, particularly as an alternative trigger for egg maturation in IVF — where it may reduce the risk of ovarian hyperstimulation syndrome. Most human studies involve small numbers (2-58 subjects), and no Phase III trials have been completed. The kisspeptin signalling pathway is well established in reproductive biology, and kisspeptin-10 has a more advanced clinical evidence base than many research compounds. However, the approximately 4-minute half-life poses major challenges — the longer kisspeptin-54 is preferred in most clinical research. An active trial for hypothalamic amenorrhoea (loss of periods due to stress or low weight) is ongoing.
PeptideTrace tracks 5 registered clinical trials for Kisspeptin-10 sourced from ClinicalTrials.gov.
Evaluation of Kisspeptin Stimulated Insulin Secretion With Hyperglycemic Clamp
Evaluation of Kisspeptin Glucose-Stimulated Insulin Secretion With Physiologic Mixed Meal Tolerance
Age-dependent Changes in the Responsiveness of Hypothalamic Pituitary Gonadal Axis in Men
Link Between the Sensitivity of Kisspeptin Signalling and Pubertal Onset in Boys.
KP-10 and Insulin Secretion in Men
Kisspeptin-10 is the C-terminal decapeptide of kisspeptin-54 (metastin), retaining full receptor-binding capacity and biological activity. Sequence: Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2. Molecular weight: 1,302.4 Da. CAS: 374675-21-5. Molecular formula: C63H83N17O14. Half-life approximately 4 minutes (3.8+/-0.3 min in men). Receptor: KISS1R (GPR54). Binding affinity: Ki = 2.33 nM (human KISS1R). The KISS1 gene was discovered in 1996 as a metastasis suppressor in melanoma; its reproductive role was recognized in 2003 when loss-of-function GPR54 mutations were found to cause hypogonadotropic hypogonadism. All kisspeptin fragments (KP-54, KP-14, KP-13, KP-10) share the same C-terminal decapeptide and activate KISS1R with equal affinity. Not approved by any regulatory agency.
Research suggests kisspeptin-10 binds KISS1R (GPR54), a Gq/11-coupled GPCR, activating phospholipase C, IP3 accumulation, intracellular calcium mobilization, along with ERK1/2 and p38 MAPK phosphorylation. KISS1R is expressed on GnRH neurons in the hypothalamus, primarily in the arcuate nucleus (ARC) and anteroventral periventricular nucleus (AVPV). These are KNDy neurons co-expressing kisspeptin, neurokinin B, and dynorphin, which together regulate GnRH pulsatility. Kisspeptin-10 activation of KISS1R drives pulsatile GnRH release, anterior pituitary LH and FSH secretion, and downstream gonadal steroid production. This effect is completely GnRH-dependent (abolished by GnRH antagonist pretreatment). Kisspeptin sits upstream of the entire HPG axis, making it a more physiological and self-limiting stimulator than direct GnRH agonists or gonadotropins.
Healthy men (George et al., JCEM 2011; N=6/group): IV KP-10 at 1 ug/kg raised LH from 4.1+/-0.4 to 12.4+/-1.7 IU/L at 30 min (P<0.001). A 22.5-hour infusion at 4 ug/kg/h raised LH from 5.4+/-0.7 to 20.8+/-4.9 IU/L (P<0.05) and testosterone from 16.6+/-2.4 to 24.0+/-2.5 nmol/L (P<0.001). A bell-shaped dose response was observed. IVF (Dhillo/Abbara group; N=53): Subcutaneous kisspeptin-54 triggered oocyte maturation in 96% (51/53) of women at risk of OHSS, yielding 7.9+/-3.9 MII oocytes/cycle with zero cases of OHSS. A Phase 2 RCT (N=58) showed double-dosing improved optimal oocyte yield to 72% vs 45%. Hypothalamic amenorrhea: Twice-daily administration for 2 weeks (N=5/group) produced significant tachyphylaxis by day 14. An active Phase 2 pulsatile trial (NCT05633966) is currently recruiting.
The information on this page is provided for educational and research reference purposes only. This is not medical advice. Always consult a qualified healthcare professional before making any health-related decisions.
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Nafarelin is marketed as Synarel (approved 1990) for endometriosis and central precocious puberty. It requires administration as one spray in each nostril twice daily — a higher frequency than injectable alternatives but avoids needles entirely, which can be a significant advantage for some patients, particularly children. Clinical trials showed symptom improvement in 75–92% of endometriosis patients. However, absorption can be affected by nasal congestion or concurrent use of nasal decongestants, which can be a practical limitation. As with all GnRH agonists, prolonged use leads to bone density loss, and treatment for endometriosis is typically limited to six months. Nafarelin occupies a niche for patients who prefer non-injectable hormone suppression, though it has become less commonly prescribed as longer-acting depot injections and oral alternatives have become available.
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This content is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making decisions about your health.
