Kisspeptin
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Research Use Only
These products are for laboratory research only and not intended for medical use. They are not FDA-approved to diagnose, treat, cure, or prevent any disease. By purchasing, you certify they will be used solely for research and not for human or animal consumption.
Research Summary
30 PubMed CitationsOverview Kisspeptin refers to a family of neuropeptides derived from the KISS1 gene, originally discovered in 1996 by Danny R. Welch and J.H. Lee in Hershey, Pennsylvania, as a melanoma metastasis suppressor. The gene was named "KiSS-1" to honor the discovery location near the Hershey's Kisses chocolate factory, with "SS" denoting "suppressor sequence."[1] The KISS1 gene encodes a 145-amino acid prepro-kisspeptin precursor that undergoes proteolytic cleavage to produce four biologically active isoforms: Kisspeptin-54 (Kp-54), Kp-14, Kp-13, and Kp-10. All isoforms share a conserved C-terminal decapeptide containing an RF-amide motif (Arg-Phe-NH₂) essential for binding and activating the KISS1R (GPR54) receptor.[2][3] Kp-54 is the major circulating form with a half-life of ~27.6 minutes; the shorter Kp-10 (~4 min half-life) exhibits full intrinsic bioactivity and is highly conserved across species.[5] In 2003, Stephanie Seminara and colleagues made the landmark discovery that loss-of-function mutations in KISS1R (GPR54) cause idiopathic hypogonadotropic hypogonadism and pubertal failure...
Kisspeptin — Research Data at a Glance
| Property | Value |
|---|---|
| PubMed Citations Referenced | 30 |
| Contributing Researchers | 3 |
| Storage Conditions | Store lyophilized kisspeptin at −20°C. |
| Purity Standard | ≥99% (HPLC verified, 3rd-party COA) |
| Research Use Only | Not for human consumption. RUO only. |
Compare Kisspeptin with Other Peptides
Overview
Overview
Kisspeptin refers to a family of neuropeptides derived from the KISS1 gene, originally discovered in 1996 by Danny R. Welch and J.H. Lee in Hershey, Pennsylvania, as a melanoma metastasis suppressor. The gene was named "KiSS-1" to honor the discovery location near the Hershey's Kisses chocolate factory, with "SS" denoting "suppressor sequence."[1]
The KISS1 gene encodes a 145-amino acid prepro-kisspeptin precursor that undergoes proteolytic cleavage to produce four biologically active isoforms: Kisspeptin-54 (Kp-54), Kp-14, Kp-13, and Kp-10. All isoforms share a conserved C-terminal decapeptide containing an RF-amide motif (Arg-Phe-NH₂) essential for binding and activating the KISS1R (GPR54) receptor.[2][3]
Kp-54 is the major circulating form with a half-life of ~27.6 minutes; the shorter Kp-10 (~4 min half-life) exhibits full intrinsic bioactivity and is highly conserved across species.[5]
In 2003, Stephanie Seminara and colleagues made the landmark discovery that loss-of-function mutations in KISS1R (GPR54) cause idiopathic hypogonadotropic hypogonadism and pubertal failure — establishing kisspeptin as the gatekeeper of sexual maturation.[4]
Kisspeptin is currently investigational — not approved by the FDA or EMA for general clinical use. It is prohibited by WADA under S2 (Peptide Hormones, Growth Factors) as it stimulates LH/FSH/testosterone production.[7]
Mechanism of Action
Mechanism of Action
KISS1R (GPR54) Receptor Binding
Kisspeptin acts by binding KISS1R (GPR54/AXOR12), a rhodopsin-like Class A GPCR sharing ~45% identity with galanin receptors (but does not bind galanin). The essential pharmacophore is the C-terminal RF-amide motif; key residues Phe-6 and Arg-9 (Kp-10 numbering) are critical for binding. Cryo-EM studies reveal an orthosteric pocket spanning TM2–7 plus ECL1–3.[2][3]
Primary Gαq/11–PLC–Ca²⁺ Pathway
KISS1R couples primarily to Gαq/11, activating phospholipase C beta (PLCβ), which hydrolyzes PIP₂ into IP₃ and DAG. IP₃ triggers biphasic intracellular Ca²⁺ release from the endoplasmic reticulum; DAG + Ca²⁺ activates PKC.[8]
MAPK and Additional Cascades
Downstream signaling involves robust, sustained ERK1/2 phosphorylation (via PKC-dependent and β-arrestin pathways), p38 MAPK activation, arachidonic acid release, and PI3K/Akt signaling.[8]
GnRH Neuronal Excitation
In GnRH neurons, kisspeptin activates TRPC channels (cation influx) and simultaneously closes Kir channels (preventing K⁺ efflux), causing sustained depolarization and increased action potential firing → pulsatile GnRH secretion → LH/FSH release.[8]
Desensitization (β-Arrestin–Mediated)
Continuous kisspeptin exposure recruits β-arrestin 1/2, causing receptor internalization via clathrin-coated pits → paradoxical HPG axis suppression. This is exploited therapeutically: TAK-448 continuous exposure suppresses testosterone to castrate levels for prostate cancer research.[9][14]
Isoform Pharmacokinetic Comparison
| Isoform | Half-Life | Route | Notes |
|---|---|---|---|
| Kp-54 | ~27.6 min | IV | Major circulating form; SC extends to ~1.7h |
| Kp-10 | ~4 min | IV | Full intrinsic bioactivity; highly conserved |
| MVT-602 (TAK-448) | Peak at ~21h | SC | MMP-resistant; >4x AUC vs Kp-54 |
Research Applications
Research Applications
Kisspeptin is one of the most extensively studied reproductive neuropeptides, with >1,000 human subjects across Phase 1/2 clinical trials:
- IVF Oocyte Maturation Trigger — SC Kp-54 (3.2–12.8 nmol/kg) triggers oocyte maturation with 95% mature oocytes, 45.1% live birth rate, and no clinically significant OHSS (vs high OHSS risk with hCG).[10][11]
- Hypothalamic Amenorrhea — Restores LH pulsatility; twice-weekly dosing sustains LH ~9 IU/L over 8 weeks without complete desensitization. Intranasal delivery validated in HA women.[12][13][19]
- PCOS — IV KP-10 infusion (4 µg/kg/h × 7h) increases LH from 5.2 to 7.8 IU/L and estradiol levels in women with polycystic ovary syndrome.[15]
- Psychosexual Disorders (HSDD) — Enhances limbic brain processing (amygdala, hippocampus) for sexual/bonding stimuli; increases penile tumescence up to 55% in men; modulates sexual desire regions in women.[16][17]
- Metabolic / Fatty Liver Disease — TAK-448 reduces hepatic triglycerides, serum FFA, and ALT in MASLD models via AMPK→SREBP-1c→CIDEA downregulation.[18]
- Cancer Metastasis Suppression — Originally identified as melanoma/breast cancer metastasis suppressor ("metastin"); inhibits MMP-9 via NF-κB pathway suppression.[1]
- Prostate Cancer (Androgen Deprivation) — Continuous TAK-448/MVT-602 exposure → receptor desensitization → testosterone suppression to castrate levels (Phase 1 data).[14]
- Pregnancy Biomarker — Kisspeptin rises 7,000-fold during healthy pregnancy; low levels predict miscarriage/preeclampsia by assessing trophoblast invasion.[20]
- Bone Health — Promotes osteoblast differentiation, inhibits osteoclast activity; acute Kp-54 increases osteocalcin ~24% in men.[21]
- Puberty Disorders — Activating/inactivating KISS1/KISS1R mutations linked to precocious/delayed puberty; kisspeptin challenge tests used diagnostically.[4]
- Intranasal Delivery — First human trial: 12.8 nmol/kg intranasal Kp-54 → rapid LH increase (4.4 IU/L in men); no AEs — validating non-invasive delivery.[19]
- Metabolic Insulin Signaling — IV Kp-54 increases glucose-stimulated insulin secretion ~35% in healthy men.[22]
Biochemical Characteristics
| Property | Value |
|---|---|
| Gene | KISS1 (chromosome 1q32, human) |
| Precursor Size | 145 amino acids (prepro-kisspeptin) |
| Molecular Weight (Kp-54) | ~5.9 kDa |
| Molecular Weight (Kp-10) | ~1.3 kDa |
| Sequence (Kp-10, Human) | YNWNSFGLRF-NH₂ (Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH₂) |
| Sequence (Kp-10, Rodent) | YNWNSFGLRY-NH₂ |
| C-Terminal Motif | RF-amide (Arg-Phe-NH₂) — critical for KISS1R binding |
| Receptor | KISS1R (GPR54/AXOR12) — Class A rhodopsin-like GPCR |
| Isoforms | Kp-54, Kp-14, Kp-13, Kp-10 (all share C-terminal decapeptide) |
| Synonyms | Metastin, KiSS-1-derived peptide, Kp-54, Kp-14, Kp-13, Kp-10 |
| Analogs | MVT-602 (TAK-448), TAK-683 |
| Plasma Half-Life | Kp-10 ~4 min; Kp-54 ~27.6 min (IV); MVT-602 peaks at 21h |
Identifiers
| Purity Standard | |
|---|---|
| Identity Confirmation | |
| Endotoxin | |
| Sterility |
Preclinical Research Summary
Preclinical Research Summary
Key Preclinical Studies
| Study | Model | Key Findings | Ref |
|---|---|---|---|
| Mills et al. (2025) | C57BL/6J mice — intranasal Kp-54 | 12.8–50 nM intranasal: dose-dependent LH to 3.6 ng/mL at 25 min (p < 0.001); GnRH neurons activated in olfactory bulb → novel extra-hypothalamic pathway | [19] |
| Izarraras et al. (2025) | DIAMOND mice — TAK-448 MASLD | 0.3 nmol/h × 6 weeks: reduced liver triglycerides, serum FFA, ALT (p < 0.05); downregulated CIDEA via AMPK-SREBP-1c | [18] |
| Seminara/Ramaswamy (2006/07) | Juvenile rhesus monkeys — IV KP-10 | 200–400 µg/h × 98h: maximal LH at 3h, desensitization by 12h; GnRH bolus still effective but KP-10 bolus was not | [23] |
| Terse et al. (2021) | Dogs — KP-10 1000 µg/kg IV × 14d | NOAEL at 1000 µg/kg; peak LH at 5 min post-dose; no toxicity signs | [24] |
| Thompson et al. (2006) | Adult male rats — chronic SC KP-54 | Chronic SC → testicular degeneration; HPG axis suppression via receptor desensitization | [25] |
| Dinh et al. (2023) | Wistar rats — KP-13 CKD model | 13–26 µg/day IP × 10d: increased BP, exacerbated CKD markers and uremic cardiomyopathy | [26] |
Human Clinical Data (>1,000 Participants)
| Trial | Population | Dose/Route | Key Results | Ref |
|---|---|---|---|---|
| Dhillo et al. (2005) | n=6 healthy men | IV Kp-54 4 pmol/kg/min × 90 min | 2.6-fold LH increase; first-in-human; no AEs | [5] |
| Dhillo et al. (2007) | n=8 healthy women | SC 0.4 nmol/kg | Preovulatory LH rise 20.64 IU/L vs follicular 0.12 IU/L | [6] |
| Abbara et al. (2015) | n=60 IVF, high OHSS risk | SC Kp-54 3.2–12.8 nmol/kg | 95% mature oocytes, 52.9% pregnancy rate, 45.1% live birth rate, no clinically significant OHSS | [10] |
| Abbara et al. (2017) | n=62 IVF RCT | SC 9.6 nmol/kg × 2 doses | 30% live birth rate; 1 case mild OHSS only | [11] |
| Jayasena et al. (2009) | n=10 women with HA | SC 6.4 nmol/kg 2x daily × 2 wk | Acute LH ~24 IU/L; tachyphylaxis to 1.5 IU/L | [12] |
| Jayasena et al. (2010) | n=20 women with HA | SC 6.4 nmol/kg 2x/week × 8 wk | Sustained LH ~9 IU/L without complete desensitization | [13] |
| Mills et al. (2023) | n=32 men with HSDD | IV Kp-54 | Penile tumescence ↑55%; enhanced sexual brain processing | [17] |
| Abbara et al. (2020) | n=21 (HV, HA, PCOS) | SC MVT-602 0.01–0.03 nmol/kg | Peak LH at 21h (vs 4.7h Kp-54); >4x AUC; prolonged action | [9] |
| Mills et al. (2025) | n=34 (men, women, HA) | Intranasal Kp-54 12.8 nmol/kg | Rapid LH ↑4.4 IU/L men; no AEs; non-invasive delivery validated | [19] |
| Izzi-Engbeaya et al. (2018) | n=15 healthy men | IV Kp-54 | Glucose-stimulated insulin secretion ↑35% | [22] |
| Comninos et al. (2022) | n=26 healthy men | Acute Kp-54 | Osteocalcin ↑24% (bone formation marker) | [21] |
Safety Summary: >1,000 Human Exposures
| Parameter | Finding |
|---|---|
| Common AEs | Mild/transient: injection site reactions, headache, nausea, bloating |
| Cardiotoxicity | None — no changes in HR, BP, or ECG |
| Tachyphylaxis | Continuous high-dose → β-arrestin recruitment → receptor internalization → HPG suppression (physiological, not toxic) |
| Dog NOAEL | 1000 µg/kg IV × 14 days — no toxicity |
| Metabolism | Cleaved by MMP-2, MMP-9, furin; C-terminal cleavage inactivates |
The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: in glass) are performed outside of the body. These products are not medicines or drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law.
For Laboratory Research Only. Not for human use, medical use, diagnostic use, or veterinary use.
ALL ARTICLES AND PRODUCT INFORMATION PROVIDED ON THIS WEBSITE ARE FOR INFORMATIONAL AND EDUCATIONAL PURPOSES ONLY.
Authors & Attribution
✍️ Article Author
Prof. Waljit S. Dhillo
Waljit S. Dhillo, BSc MBBS PhD, is Professor of Endocrinology and Metabolism at Imperial College London, Department of Investigative Medicine. Prof. Dhillo conducted the first-in-human kisspeptin administration studies in men (2005) and women (2007), establishing kisspeptin as a potent stimulator of the HPG axis. His research program has characterized the therapeutic potential of kisspeptin across IVF treatment (Phase 2 trials demonstrating safe oocyte maturation without OHSS), hypothalamic amenorrhea, psychosexual disorders, and neuroimaging studies of sexual and emotional brain processing. He led the first human intranasal kisspeptin trial (2025), validating non-invasive delivery. Waljit S. Dhillo is being referenced as one of the leading scientists involved in the research and development of Kisspeptin. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →🎓 Scientific Journal Author
Dr. Stephanie B. Seminara
Stephanie B. Seminara, MD, is affiliated with the Reproductive Endocrine Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School. Dr. Seminara led one of the independent groups that discovered loss-of-function mutations in KISS1R (GPR54) cause idiopathic hypogonadotropic hypogonadism and pubertal failure (NEJM, 2003), establishing kisspeptin as the gatekeeper of sexual maturation. Her subsequent work characterized kisspeptin-induced desensitization of GPR54 in primate models, demonstrating the mechanism underlying tachyphylaxis with continuous exposure. Stephanie B. Seminara is being referenced as one of the leading scientists involved in the research and development of Kisspeptin. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →Dr. Stephanie B. Seminara is being referenced as one of the leading scientists involved in the research and development of Kisspeptin. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide.
🔬 Contributing Researcher
Dr. Danny R. Welch
Danny R. Welch, PhD, is affiliated with the University of Kansas Comprehensive Cancer Center (previously University of Alabama at Birmingham). Dr. Welch led the research team that originally discovered the KiSS-1 gene in 1996, identifying it as a metastasis suppressor in human malignant melanoma cells. He named the gene 'KiSS-1' in homage to the discovery location near the Hershey's Kisses chocolate factory, with 'SS' denoting 'suppressor sequence.' His foundational work established the entire kisspeptin field, which has since expanded from cancer biology into reproductive endocrinology, metabolic science, and neuroscience. Danny R. Welch is being referenced as one of the leading scientists involved in the research and development of Kisspeptin. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →Dr. Danny R. Welch is being referenced as one of the leading scientists involved in the research and development of Kisspeptin. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide.
Referenced Citations
Lee JH, Miele ME, Hicks DJ, Phillips KK, Trent JM, Weissman BE, Welch DR. KiSS-1, a novel human malignant melanoma metastasis-suppressor gene. Journal of the National Cancer Institute. 1996;88(23):1731-1737.
DOIOhtaki T, Shintani Y, Honda S, et al. Metastasis suppressor gene KiSS-1 encodes peptide ligand of a G-protein-coupled receptor. Nature. 2001;411(6837):613-617.
DOIKotani M, Detheux M, Vandenbogaerde A, et al. The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54. Journal of Biological Chemistry. 2001;276(37):34631-34636.
DOISeminara SB, Messager S, Chatzidaki EE, et al. The GPR54 gene as a regulator of puberty. New England Journal of Medicine. 2003;349(17):1614-1627.
DOIDhillo WS, Chaudhri OB, Patterson M, et al. Kisspeptin-54 stimulates the hypothalamic-pituitary gonadal axis in human males. Journal of Clinical Endocrinology & Metabolism. 2005;90(12):6609-6615.
DOIDhillo WS, Chaudhri OB, Thompson EL, et al. Kisspeptin-54 stimulates gonadotropin release most potently during the preovulatory phase of the menstrual cycle in women. Journal of Clinical Endocrinology & Metabolism. 2007;92(10):3958-3966.
DOIWorld Anti-Doping Agency. The Prohibited List. S2 Peptide Hormones, Growth Factors, Related Substances, and Mimetics. WADA. Updated 2025.
WADAde Roux N, Genin E, Carel JC, Matsuda F, Chaussain JL, Milgrom E. Hypogonadotropic hypogonadism due to loss of function of the KiSS1-derived peptide receptor GPR54. Proceedings of the National Academy of Sciences. 2003;100(19):10972-10976.
DOIAbbara A, Eng PC, Phylactou M, et al. Kisspeptin receptor agonist has therapeutic potential for female reproductive disorders. Journal of Clinical Investigation. 2020;130(12):6739-6753.
DOIAbbara A, Jayasena CN, Christopoulos G, et al. Efficacy of kisspeptin-54 to trigger oocyte maturation in women at high risk of OHSS during IVF therapy. Journal of Clinical Endocrinology & Metabolism. 2015;100(9):3322-3331.
DOIAbbara A, Clarke S, Islam R, et al. A second dose of kisspeptin-54 improves oocyte maturation in women at high risk of OHSS: a phase 2 randomized controlled trial. Human Reproduction. 2017;32(9):1915-1924.
DOIJayasena CN, Nijher GM, Chaudhri OB, et al. Subcutaneous injection of kisspeptin-54 acutely stimulates gonadotropin secretion in women with hypothalamic amenorrhea, but chronic administration causes tachyphylaxis. Journal of Clinical Endocrinology & Metabolism. 2009;94(11):4315-4323.
DOIJayasena CN, Nijher GM, Abbara A, et al. Twice-weekly administration of kisspeptin-54 for 8 weeks stimulates release of reproductive hormones in women with hypothalamic amenorrhea. Clinical Pharmacology & Therapeutics. 2010;88(6):840-847.
DOIMacLean DB, Matsui H, Suri A, Neuwirth R, Colombel M. Sustained exposure to the investigational kisspeptin analog, TAK-448, down-regulates testosterone into the castration range in healthy males and in patients with prostate cancer. Journal of Clinical Endocrinology & Metabolism. 2014;99(8):E1445-E1453.
DOISkorupskaite K, et al. KP-10 infusion in PCOS women. Human Reproduction. 2020.
DOIComninos AN, Wall MB, Demetriou L, et al. Kisspeptin modulates sexual and emotional brain processing in humans. Journal of Clinical Investigation. 2017;127(2):709-719.
DOIMills EG, et al. HSDD in men — kisspeptin increases penile tumescence and sexual brain processing. JAMA Network Open. 2023.
PubMedIzarraras L, et al. Kisspeptin agonist reduces hepatic de novo lipogenesis in MASLD via AMPK-SREBP-1c-CIDEA. 2025.
PubMedMills EG, et al. Intranasal kisspeptin-54 rapidly stimulates gonadotropin release in humans: a non-invasive delivery route. eBioMedicine. 2025.
PubMedJayasena CN, Abbara A, et al. Kisspeptin-54 triggers egg maturation in women undergoing in vitro fertilization. Journal of Clinical Investigation. 2014;124(8):3667-3677.
DOIComninos AN, et al. Acute kisspeptin administration increases osteocalcin in healthy men. Journal of Clinical Endocrinology & Metabolism. 2022.
PubMedIzzi-Engbeaya C, et al. Kisspeptin increases glucose-stimulated insulin secretion in healthy men. Diabetes, Obesity and Metabolism. 2018.
PubMedSeminara SB, et al. Continuous human metastin 45-54 infusion desensitizes GPR54-induced GnRH release in juvenile male rhesus monkeys. 2006.
PubMedTerse PS, et al. Kisspeptin-10 toxicology studies in dogs — NOAEL at 1000 µg/kg IV × 14 days. 2021.
PubMedThompson EL, et al. Chronic subcutaneous administration of kisspeptin-54 causes testicular degeneration in adult male rats. 2006.
PubMedDinh TO, et al. Kisspeptin-13 exacerbates chronic kidney disease and uremic cardiomyopathy in rats. 2023.
PubMedGeorge JT, Veldhuis JD, Roseweir AK, et al. Kisspeptin-10 is a potent stimulator of LH and increases pulse frequency in men. Journal of Clinical Endocrinology & Metabolism. 2011;96(8):E1228-E1236.
DOIThurston L, et al. Kisspeptin modulates brain activity in sexual desire regions in women with HSDD. JAMA Network Open. 2022.
PubMedNishizawa N, Takatsu Y, et al. Design and synthesis of TAK-448, an investigational nonapeptide KISS1R agonist. Journal of Medicinal Chemistry. 2016;59(19):8804-8811.
DOIChan YM, Butler JP, Pinnell NE, et al. Kisspeptin resets the hypothalamic GnRH clock in men. Journal of Clinical Endocrinology & Metabolism. 2011;96(6):E908-E915.
DOIRUO Disclaimer
For Research Use Only (RUO). This product is intended solely for in-vitro research and laboratory experimentation. It is not a drug, food, cosmetic, or medical device and has not been approved by the FDA for any human or veterinary use. It must not be used for therapeutic, diagnostic, or any other non-research purpose. Pure US Peptide does not condone or encourage the use of this product for anything other than strictly defined research applications. Users assume full responsibility for compliance with all applicable regulations and guidelines.
Certificate of Analysis (COA)
Every batch is strictly tested by accredited third-party laboratories (ISO 17025) to ensure 99%+ purity.
Latest Lab Report
Storage & Handling
Summary
Store lyophilized kisspeptin at −20°C. Reconstituted Kp-54 in 0.9% saline stable for 60 days at 4°C (>90% retention). Intranasal solution: 3.5 mg/mL in 0.9% saline. Avoid repeated freeze-thaw.
Recommended Laboratory Storage Conditions
Lyophilized Powder: Store at −20°C for long-term stability. Protect from light and moisture.
Reconstituted Solution: Kp-54 in 0.9% saline remains stable (>90% concentration) for up to 60 days at 4°C. For daily use, aliquot to minimize freeze-thaw cycles.
Intranasal Formulation: 3.5 mg/mL in 0.9% saline; store refrigerated (2–8°C) and use within recommended stability window.
Handling: Standard aseptic technique. Dosing regimen matters: pulsatile = stimulation; continuous = desensitization (HPG suppression).
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