Kisspeptin-10 / KP-10
KISS1R-Active Reproductive Signaling Decapeptide
Kisspeptin-10 is a reproductive neuroendocrine research peptide within Alford Molecular Research's Research Compound Library. This molecular fragment is provided solely for nonclinical research objectives within established laboratory settings.
Chemical Class
C-terminally amidated decapeptide derived from kisspeptin
Primary Research Domain
Endocrine & Reproductive Signaling
Evidence Classification
Supported for acute human endocrine pharmacodynamics; Preliminary for longer-term or generalized outcomes
Primary Molecular Target
KISS1 receptor / KISS1R / GPR54
Compound
Kisspeptin-10
Aliases / Synonyms
KP-10; Metastin(45-54)
Chemical Class
C-terminally amidated decapeptide derived from kisspeptin
CAS Number
374675-21-5
Molecular Formula
C63H83N17O14
Average Molecular Weight
1302.47 g/mol
Sequence
Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2
N-Terminal State
Free amino terminus
C-Terminal State
Amidated
Primary Molecular Target
KISS1 receptor / KISS1R / GPR54
Molecular Identity
Kisspeptin-10 is the C-terminal 10-amino-acid bioactive fragment of kisspeptin and retains activity at the KISS1 receptor.
Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2
C-terminal amidation is part of the defined molecular identity for receptor activation and metabolic stability.
Structural Identity Requirement
Kisspeptin-10 should be defined by its exact decapeptide sequence together with C-terminal amidation. A non-amidated form should not be assumed chemically or pharmacologically equivalent.
Molecular Target / Mechanism
The profile of Kisspeptin-10 is centered globally on the KISS1 receptor (KISS1R / GPR54), a G-protein-coupled receptor that serves as a fundamental check-point in reproductive neuroendocrine signaling. Research characterizes Kisspeptin-10 as a potent upstream regulator of hypothalamic GnRH-associated signaling, which in turn modulates the downstream release of pituitary gonadotropins.
Kisspeptin-10
Pituitary LH/FSH Response
→
KISS1R
→
Hypothalamic GnRH Signaling
→
Gonadal Endocrine Signaling
→
Intracellular Signaling Pathways
KISS1R activation is primarily associated with Gq/11-coupled signaling cascades. Investigated pathway framing includes phospholipase C ligation, IP3 / DAG-associated signaling, and robust intracellular calcium mobilization. Research also explores PKC-associated signaling alongside neuronal depolarization and GnRH-neuron activation. Scientific interpretation should remain cautious, as downstream endocrine variations may involve complex regulatory feedback loops rather than direct linear outputs.
Cellular & Tissue-Level Research
Discussing research involving hypothalamic reproductive signaling, GnRH-neuron activity, pituitary gonadotropin responses, LH and FSH signaling, and gonadal endocrine physiology. Alford Molecular Research maintains a clear distinction between acute endocrine pharmacodynamics and long-term reproductive or clinical outcomes.
KISS1R Biology
Research examining ligand-receptor interactions and signaling through the kisspeptin receptor.
GnRH Signaling
Investigation of kisspeptin-associated regulation of hypothalamic gonadotropin-releasing-hormone pathways.
LH & FSH Dynamics
Human and translational research examining downstream pituitary gonadotropin responses.
Reproductive Endocrinology
Investigation of hypothalamic-pituitary-gonadal-axis physiology and endocrine feedback.
Fertility Biology
Research involving reproductive-axis signaling and fertility-related physiology without assuming established clinical fertility benefit.
Pubertal & Developmental Signaling
Study of kisspeptin signaling in reproductive maturation and neuroendocrine development.
Translational Chain
Kisspeptin-10 → KISS1R → GnRH-Associated Signaling → Pituitary LH/FSH Response → Gonadal Endocrine Signaling → Hormonal Biomarkers → Reproductive / Functional Outcomes
The early portions of this translational chain are better established than long-term functional outcomes. Acute changes in LH, FSH, testosterone, estradiol, or other endocrine biomarkers do not automatically establish durable fertility, sexual-function, or wellness benefits.
Evidence Classification: Supported
Evidence Classification: Preliminary
Kisspeptin has credible human pharmacodynamic evidence demonstrating acute activation of the hypothalamic-pituitary-gonadal axis and measurable endocrine responses in appropriate research settings.
Longer-term repeated exposure, durable reproductive outcomes, sustained testosterone changes, fertility outcomes, sexual-function outcomes, generalized endocrine optimization, and wellness applications require substantially more evidence. Alford Molecular Research distinguishes acute endocrine pharmacodynamics from longer-term reproductive or functional outcomes.
Receptor Regulation & Repeated Exposure
Kisspeptin signaling participates in a tightly regulated neuroendocrine system; continuous or repeated stimulation can produce biological responses that differ from a single acute exposure. Research interpretation should consider receptor regulation, GnRH-axis feedback, pulsatile neuroendocrine physiology, endocrine feedback loops, exposure frequency, and possible attenuation of response with repeated stimulation.
Analytical & Quality-Control Considerations
- Identity by Mass Spectrometry (MS)
- RP-HPLC or UPLC Purity Confirmation
- Exact 10-amino-acid sequence confirmation
- C-terminal amidation confirmation
- N-terminal state (Free amino terminus)
- Quantitative net peptide content
- Counterion / salt state
- Residual solvents and water content
- Degradation products (oxidation/hydrolysis)
- Endotoxin and Sterility (where relevant)
C-Terminal Amidation Control
Kisspeptin-10 is C-terminally amidated. Analytical identity should verify amidation because an incorrect terminal state changes the defined molecular species.
Tryptophan-Containing Sequence Note: Kisspeptin-10 contains tryptophan; oxidative or other sequence-related degradation should be considered during analytical characterization where relevant.
Example Analytical Documentation
Alford Molecular Research has reviewed third-party analytical documentation for Kisspeptin-10 research material including molecular identity, quantitative content, purity, sterility, elemental-impurity, and endotoxin testing. Analytical results are lot-specific and should not be generalized to other batches.
Structural / Formulation Considerations
Stability & Handling — Scientific Context
Exact molecular interpretation depends on: C-terminal amidation; N-terminal state; counterion; hydration state; gross versus net peptide reporting. Sequence identity, terminal amidation, chromatographic purity, quantitative content, and salt state are analytically distinct quality attributes.
Stability factors for Kisspeptin-10 research material include exposure to moisture, light, and temperature. Tryptophan residues increase susceptibility to oxidation. Peptide degradation, repeated freeze-thaw cycles, and container integrity should be monitored to ensure research validity.
Research Context Notice
Kisspeptin biology has been investigated extensively in reproductive endocrinology, including human pharmacodynamic research. Human experimental evidence supports acute activity on the reproductive endocrine axis, but the existence of acute pharmacodynamic effects does not establish every proposed fertility, sexual-function, testosterone, reproductive, or wellness application. Regulatory and clinical-development status varies by compound, indication, and jurisdiction. Alford Molecular Research evaluates kisspeptin research according to molecular mechanism, study design, population, endpoint, and translational relevance.
Scientific and Research Context Only: This information is provided for scientific documentation and research context only and is not for treatment, diagnosis, or human use. Alford Molecular Research distinguishes acute endocrine pharmacodynamics from established clinical outcomes.