Kisspeptin-10 Peptide
Kisspeptin (also known as metastin) is a naturally occurring human protein essential for regulating hormonal signaling during puberty and reproduction. It is also investigated for its effects on mood, behavior, angiogenesis (formation of new blood vessels), and kidney regulation. In the central nervous system, kisspeptin has demonstrated an ability to inhibit tumor growth and metastasis (the spread of cancer). Its primary scientific significance is its capacity to stimulate the release of gonadotropin-releasing hormone (GnRH).
Kisspeptin-10 Peptide - 5mg Overview
Kisspeptins are a group of neuropeptides derived from a larger precursor. Kisspeptin-10 is the smallest known form that retains full biological activity. The mechanism of action involves Kisspeptin-10 binding to the KISS1R receptor, which triggers the pulsatile release of GnRH from the hypothalamus. This is a critical regulatory step for the subsequent secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH).
Kisspeptin-10 is widely used as a research tool in studies encompassing reproductive endocrinology, fertility control, neuroendocrine function, and cancer biology. Its role as a connector between energy balance and reproductive capacity also makes it a subject of metabolic and behavioral research.
Kisspeptin-10 Research
Key Research Areas and Findings
Research Area
Key Role/Effect
Relevant Finding
Reproductive Endocrinology
Master regulator of the HPG axis via GnRH.
Essential for initiating puberty and regulating reproductive hormones.
Testosterone Modulation
Increases LH and FSH secretion.
Caused near-tripling of plasma testosterone in male subjects.
Cancer Biology
Functions as a metastasis suppressor.
Inhibited melanoma spread by up to 95% via migration suppression.
Metabolic Control
Links nutritional status to reproductive function.
Receptor-deficient mice showed increased fat accumulation.
Neurobiology
Involved in brain regions for memory and emotion.
Analogs reversed learning deficits; increases reward-seeking behavior.
Boosting Gonadotropin-Releasing Hormone
GnRH is secreted by specialized hypothalamic neurons and acts as the initial signal in the hypothalamic-pituitary-gonadal (HPG) axis. It dictates the pulsatile release of FSH and LH from the anterior pituitary, which is vital for puberty and reproductive maturation. GnRH is utilized clinically in therapies for menstrual cycle regulation, precocious puberty, and certain cancer treatments.
Increasing Testosterone
Kisspeptin modulates testosterone levels primarily by elevating LH and FSH concentrations. This effect is sexually dimorphic, showing a strong elevation of testosterone in men, with minimal impact in women. Experimental findings in healthy male subjects confirmed that Kisspeptin-10 induces a rapid, dose-dependent rise in serum LH, followed by a corresponding increase in testosterone levels. These observations suggest that kisspeptin derivatives could be explored for therapeutic applications in male hypogonadism (low testosterone) and fertility management.
Cancer Research
Kisspeptin was discovered to be a potent metastasis suppressor, capable of dramatically reducing the spread of melanoma. Its anti-metastatic mechanism involves the suppression of cancer cell migration and interference with cell adhesion. The consistent observation of decreased kisspeptin levels across numerous metastatic cancers (including breast, prostate, and bladder) reinforces its importance in regulating tumor progression. Research continues to investigate how the complexity of the peptide's biological actions can be leveraged for targeted cancer therapy.
Kisspeptin-10 Summary
Kisspeptin is a complex neuropeptide fundamentally involved in reproductive hormone regulation. Scientific research actively explores its diverse roles in testosterone production, cancer metastasis, and energy balance. Preclinical studies indicate moderate bioavailability and a minimal to moderate side-effect profile. Researchers must note that dosage and safety findings from animal models are not directly transferable to humans.
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Storage
Storage Instructions
Kisspeptin-10 is produced via lyophilization (freeze-drying), ensuring stability for 3–4 months during shipping. Upon reconstitution with bacteriostatic water, it must be refrigerated and is stable for up to 30 days.
- Long-Term Storage (Months to Years): Freezer at $-80^{\circ}C$ ($-112^{\circ}F$).
- Short-Term Storage (Days to Months): Refrigeration below $4^{\circ}C$ ($39^{\circ}F$).
Best Practices For Storing Peptides
Proper storage prevents degradation and contamination, ensuring reliable laboratory results.
- Minimize freeze-thaw cycles and avoid frost-free freezers.
- Keep peptides cool and shielded from light.
Preventing Oxidation and Moisture Contamination
Allow vials removed from the freezer to reach room temperature before opening to prevent condensation. Minimize air exposure. Aliquotting the peptide into smaller portions for experiments prevents repeated exposure to air and temperature changes.
Storing Peptides In Solution
Peptide solutions have a shorter shelf life. If solution storage is required, use sterile buffers with a pH between 5 and 6 and aliquot. Solutions remain stable for up to 30 days under refrigeration.
Article Author
Review authored by Dr. Stephen B. Seminara, M.D., a leading endocrinologist. Her discovery of the GPR54 (KISS1R) receptor’s role in GnRH activation provided the fundamental scientific basis for understanding Kisspeptin’s function in reproductive biology.
Scientific Journal Author
Dr. Stephen B. Seminara and her collaborators (including Drs. W.H. Colledge, V.M. Navarro, and W.S. Dhillo) have made extensive contributions through the study of the Kisspeptin-GPR54 pathway, establishing Kisspeptin's central role in hormonal communication, energy balance, and neuroendocrine function.
Note: This credit is solely for scientific acknowledgement and does not imply product endorsement.
Reference Citations
- Lee DK, et al. Endocrinology. 1999;140(2):583-590.
- Kotani M, et al. J Biol Chem. 2001;276(37):34631-34636.
- Seminara SB, et al. N Engl J Med. 2003;349(17):1614-1627.
- Navarro VM, et al. Endocr Rev. 2012;33(6):686-727.
- Messager S, et al. Proc Natl Acad Sci U S A. 2005;102(5):1761-1766.
- Clarkson J, Herbison AE. J Neurosci. 2006;26(19):4986-4995.
- Dhillo WS, et al. J Clin Endocrinol Metab. 2009;94(2):545-550.
- Hori A, et al. Int J Cancer. 2001;92(4):529–534.
- Dhillo WS, et al. J Clin Endocrinol Metab. 2007;92(8):3125-3131.
- d'Anglemont de Tassigny X, et al. Nat Rev Endocrinol. 2010;6(10):564-574.