Evidence Grade C — Moderate human evidence. 91 published studies, 57 human. 0 registered clinical trials.
Medically reviewed by a licensed medical professional
Kisspeptin-54 is the full-length form of the kisspeptin hormone, a key regulator of reproductive function. With a half-life of about 28 minutes (versus 4 minutes for the shorter kisspeptin-10), it is more practical for clinical use. Academic Phase II trials have shown promising results as an IVF trigger that may eliminate the risk of ovarian hyperstimulation syndrome. It has no pharmaceutical approval.
Kisspeptin-54 is also known by these brand and alternate names:
91 published studies: 57 human, 28 animal, 15 in-vitro, 11 reviews
Kisspeptin-54 has no marketing authorisation. Phase II trials conducted primarily at Imperial College London have investigated its use as an IVF oocyte maturation trigger. One trial (60 patients) reported 95% oocyte maturation with zero cases of ovarian hyperstimulation syndrome.
Kisspeptin-54 has a more advanced clinical evidence base than kisspeptin-10, with multiple Phase II studies in reproductive medicine. Its potential advantage over conventional IVF triggers relates to a lower risk of the serious complication of ovarian hyperstimulation. Clinical development is ongoing in academic settings. No Phase III trials have been completed.
Kisspeptin-54 activates the same KISS1R receptor as kisspeptin-10 (#130), triggering the GnRH-gonadotropin cascade that controls reproductive hormone release. Its longer half-life allows sustained receptor activation. Research has focused particularly on its potential to trigger egg maturation in IVF cycles with a lower risk of ovarian hyperstimulation syndrome compared to conventional triggers.
Research suggests Phase II trials at Imperial College London showed 95% egg maturation with zero cases of ovarian hyperstimulation syndrome in 60 high-risk patients — a notable safety result. Live birth rates of 45% per transfer were achieved at the optimal dose. All clinical data originate from a single centre (Imperial College London), with no independent replication. No Phase III trials have been completed. The tachyphylaxis limitation (loss of response with continuous use) restricts chronic applications. Larger multi-centre trials are needed before clinical adoption, but for high-risk IVF patients the OHSS elimination potential addresses a genuine safety gap.
PeptideTrace tracks 0 registered clinical trials for Kisspeptin-54 sourced from ClinicalTrials.gov.
No trials registered on ClinicalTrials.gov for this compound.
Kisspeptin-54 (Metastin) is a 54-amino acid neuropeptide with a molecular weight of approximately 5,857 Da (CAS 374683-24-6). It is the full-length product of the KISS1 gene and signals through the KISS1R/GPR54 receptor. Research suggests a circulating half-life of approximately 28 minutes, substantially longer than the 10-amino acid fragment Kisspeptin-10 (half-life ~4 minutes). Kisspeptin-54 was originally identified as metastasis suppressor gene product in melanoma research before its central role in reproductive neuroendocrinology was established. It is the primary endogenous regulator of gonadotropin-releasing hormone (GnRH) neurons in the hypothalamus.
Research suggests Kisspeptin-54 binds to the KISS1R (GPR54) receptor, a Gq/11-coupled GPCR expressed on GnRH neurons in the hypothalamus. Activation triggers phospholipase C signaling, IP3/DAG generation, intracellular calcium mobilization, and PKC activation, stimulating pulsatile GnRH release into the hypophyseal portal system. This drives downstream LH and FSH secretion from anterior pituitary gonadotrophs. The kisspeptin-neurokinin B-dynorphin (KNDy) neuronal network in the arcuate nucleus generates the episodic GnRH pulse pattern essential for normal reproductive function. Continuous exposure leads to tachyphylaxis via receptor desensitization by day 14.
Clinical trials conducted primarily by the Dhillo/Abbara group at Imperial College London provide the most robust data. A Phase 2 IVF oocyte maturation study (N=53) reported 75-85% maturation rates with a 49.4% blastocyst rate. An OHSS prevention trial (N=60) demonstrated 95% oocyte maturation with zero OHSS cases (0/60), compared to standard hCG triggers which carry significant OHSS risk. A Phase 2 RCT (N=62) showed 71% versus 45% achieved >=60% oocyte yield (p=0.042) with kisspeptin-54 versus standard trigger. In hypothalamic amenorrhea, acute administration produced LH increases of +24.0 +/- 3.5 IU/L, but tachyphylaxis developed by day 14 of continuous dosing.
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.
Compare prices from 8 vendor listings
View pricing data across vendors and countries for Kisspeptin-54
Carbetocin has not been approved by the FDA. It is registered in over 80 countries for prevention of uterine atony and excessive bleeding after caesarean delivery. A heat-stable formulation was added to the WHO Essential Medicines List in 2019. The CHAMPION trial (WHO, 2018; over 29,000 women) compared a heat-stable carbetocin formulation to oxytocin for preventing postpartum haemorrhage after vaginal delivery, and found it to be non-inferior. The heat-stable formulation addresses a significant limitation of oxytocin, which degrades in warm climates without refrigeration — a major concern in low-resource settings where postpartum haemorrhage causes the most deaths. Its regulatory status varies by jurisdiction.
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.
Triptorelin is marketed as Trelstar (approved 2000) for advanced prostate cancer, available as intramuscular depot injections in monthly (3.75 mg), three-monthly (11.25 mg), and six-monthly (22.5 mg) formulations. It is also widely used internationally for gender-affirming care and central precocious puberty. Triptorelin is one of the most commonly used GnRH agonists globally, though it faces the same competitive pressure as other agents in this class from newer oral GnRH antagonists like relugolix, which avoid the initial hormone flare and offer potential cardiovascular advantages. Clinical data demonstrate reliable testosterone suppression comparable to other GnRH agonists in this class.
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.
