GH-axis research
Kisspeptin-10
Lyophilisiertes Peptid zur Forschung zu endokrinen Signalen zur Systemüberprüfung
Kisspeptin-10 is a KISS1R / GPR54 research peptide studied around upstream reproductive-axis signaling.
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Get catalog updatesNur für Laborforschungszwecke. Nicht für den menschlichen oder veterinärmedizinischen Gebrauch bestimmt. Nicht zur Diagnose, Behandlung, Heilung, Linderung oder Vorbeugung von Krankheiten bestimmt.
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Forschungskontext
Kisspeptin-10 Forschungsprofil
Kisspeptin-10 is the active carboxyl-terminal decapeptide of kisspeptin and is studied as an agonist at KISS1R, also known as GPR54. Research focuses on upstream reproductive-axis signaling, GnRH-neuron activation, luteinizing-hormone response, receptor pharmacology, pulse behavior, and puberty or fertility model systems. Its position in the pathway distinguishes it from gonadorelin, which directly activates the pituitary GnRH receptor. Kisspeptin-10 is most useful when the study question concerns KISS1R signaling or the regulation of GnRH output. Human physiology studies provide context, but experimental timing, sequence, formulation, and model conditions remain important when comparing results.
Molecular class
10-residue KISS1R ligand fragment
Sequence / composition
Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2, the receptor-active carboxyl-terminal kisspeptin fragment.
Research design note
It is a focused KISS1R / GPR54 probe; short half-life and pulsatile signaling shape experimental interpretation.
Vorgeschlagener Mechanismus
Binds KISS1R/GPR54 on GnRH neurons and activates Gq-related signaling, increasing GnRH output and downstream pituitary LH and FSH release. It acts upstream of gonadorelin in the reproductive endocrine axis.
In Studien berichtete Effekte
- Human studies report acute increases in LH, and sometimes FSH, after kisspeptin exposure in responsive reproductive states.
- Animal and human studies report stimulation of GnRH-dependent reproductive signaling and ovulation-related endpoints in selected models.
- Continuous or repeated exposure can produce tachyphylaxis or desensitization, and responses vary by sex-hormone state.
Häufige Forschungsendpunkte
KISS1R signaling, GnRH release, LH, FSH, pulse dynamics, gonadal steroids, ovulation-related markers, reproductive state, and desensitization.
Evidenz und Grenzen
Mechanistic, animal, and controlled human physiology evidence exists. Response is strongly dependent on endocrine state and exposure pattern.
External reading
Literature for context—not product proof.
Third-party sources describe their own research materials and methods. They do not validate a specific Azure catalog batch.
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