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Kisspeptin-10

Endocrine signaling research

Kisspeptin-10

Lyophilized endocrine-signaling research peptide for systems review

Kisspeptin-10 is a KISS1R / GPR54 research peptide studied around upstream reproductive-axis signaling.

价格范围:53.99 $ 至 229.99 $
98.7%-99.3% Lyophilized powder 5 mg
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仅供实验室研究使用。不适用于人类或兽医用途。并非旨在诊断、治疗、治愈、减轻或预防疾病。

存储

Keep sealed, cold, dry, and protected from heat swings. Confirm product-specific storage on arrival.

Shipping notes

Packed for transit stability with order support available for warm-weather routes.

Batch reference

Batch-linked certificate support is available through the documentation desk.

研究背景

Kisspeptin-10 研究资料

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.

拟议机制

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.

研究中报告的作用

  • 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.

常见研究终点

KISS1R signaling, GnRH release, LH, FSH, pulse dynamics, gonadal steroids, ovulation-related markers, reproductive state, and desensitization.

证据与局限

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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