Kisspeptin-10

Kisspeptin-10 Peptide

Kisspeptin (also known as metastin) is a naturally occurring human protein fundamental to hormonal signaling during puberty and reproduction. Beyond this, it is implicated in mood/behavior, angiogenesis, and kidney function. In the brain, kisspeptin is noted for its ability to inhibit tumor growth and metastasis. Its key scientific value stems from its role in stimulating the release of gonadotropin-releasing hormone (GnRH).

Kisspeptin-10 Peptide - 5mg Overview

Kisspeptins are neuropeptides derived from a larger precursor. Kisspeptin-10 is the smallest fully biologically active form. It initiates the release of GnRH from the hypothalamus by binding to the KISS1R receptor, which in turn regulates the secretion of LH and FSH.

This peptide is a widely used research tool in studies concerning reproductive endocrinology, fertility, neuroendocrine signaling, and cancer biology. It is also examined in metabolic and behavioral research due to its significant function in linking energy balance with reproductive processes.

Kisspeptin-10 Research

Key Areas of Study

Research Focus

Mechanism/Result

Potential Implication

Boosting GnRH

Stimulates initial hormone in the HPG axis; regulates FSH and LH.

Puberty regulation, menstrual cycle management, fertility research.

Increasing Testosterone

Modulates LH/FSH levels; shown to significantly elevate testosterone in men.

Infertility, low testosterone research.

Energy Balance

Kisspeptin neurons respond to nutritional status; regulates energy homeostasis via KISS1R.

Infertility linked to nutrition, metabolic regulation research.

Cancer Research

Potent anti-metastasis agent; levels often decreased in malignancies.

Exploration as a novel cancer therapy, metastasis inhibition.

Memory Enhancement

Analogs reverse learning/navigational impairments in animal models.

Development of nootropic compounds for cognitive deficits.

Impact on Mood

Increases activity in brain regions associated with emotion and motivation.

Role in emotional regulation and positive affect.

Kidney and Heart

Involved in glomerular development and vascular activity (vasoconstriction/angiogenesis).

Cardiovascular health, kidney function, and disease management research.

Boosting Gonadotropin-Releasing Hormone

GnRH, produced by hypothalamic neurons, is the starting point of the HPG axis, controlling the pituitary's release of FSH and LH, which are critical for puberty and reproductive cell maturation. GnRH is a clinical agent for managing menstrual cycles, precocious puberty, and specific cancers.

Increasing Testosterone

Kisspeptin's influence on testosterone via LH and FSH is observed primarily in men, where studies show a rapid, dose-dependent rise in serum LH and a corresponding increase in testosterone (e.g., nearly tripling in one male study within 90 minutes). This regulatory role suggests applications in managing low testosterone and related fertility issues.

Cancer Research

Kisspeptin is recognized for its ability to inhibit cancer cell metastasis (up to 95% reduction in melanoma spread) by suppressing cell migration and adhesion. The consistent finding of decreased kisspeptin levels in various metastatic cancers highlights its tumor-regulating role. Research continues to explore its potential as a complex, multi-functional agent in cancer therapy, particularly leveraging its influence on vascular growth and function.

Kisspeptin-10 Summary

Kisspeptin is a versatile peptide critical for reproductive hormone regulation and under investigation for its roles in testosterone production, cancer metastasis, and energy balance. Preclinical data suggests moderate bioavailability and a mild side-effect profile, though human translation requires further study.

FOR RESEARCH USE ONLY: ALL information is for educational purposes. Products are for in-vitro studies only and are not approved by the FDA as medicines. Bodily introduction into humans or animals is strictly forbidden.

Storage

Storage Instructions

The product is lyophilized (freeze-dried) for shipping stability (3–4 months). Once reconstituted with bacteriostatic water, it must be refrigerated and is stable for up to 30 days.

• Short-Term Use (Days/Months): Refrigerate below 4°C (39°F). Lyophilized peptides are stable at room temperature for several weeks.
• Extended Storage (Months/Years): Freeze at -80°C (-112°F) for optimal long-term integrity.

Best Practices For Storing Peptides

To ensure reliable research results:

• Minimize freeze-thaw cycles.
• Avoid frost-free freezers.
• Upon receipt, keep peptides cool and protected from light.

Preventing Oxidation and Moisture Contamination

Always allow the vial to reach room temperature before opening (when removed from the freezer) to prevent condensation. Minimize air exposure. Aliquot the peptide into smaller portions for individual experiments to limit repeated handling and temperature changes. Peptides with Cysteine (C), Methionine (M), or Tryptophan (W) are particularly sensitive to oxidation.

Storing Peptides In Solution

Peptide solutions degrade faster. Use sterile buffers with a pH of 5-6 and aliquot the solution. Most solutions are stable for up to 30 days at 4°C (39°F).

Article Author

Review authored by Dr. Stephen B. Seminara, M.D., a distinguished endocrinologist. Dr. Seminara’s groundbreaking research on the GPR54 (KISS1R) receptor and GnRH activation established the fundamental role of Kisspeptin in reproductive biology.

Scientific Journal Author

Dr. Stephen B. Seminara and collaborators (including Drs. W.H. Colledge, V.M. Navarro, W.S. Dhillo, and others) have collectively advanced the understanding of the Kisspeptin-GPR54 pathway. Their work confirms Kisspeptin's central role in neuroendocrine communication, reproductive hormone regulation, and energy balance.

Note: This credit is solely for scientific acknowledgement and is not an endorsement or promotion of the product.

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.