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Kisspeptin for Isolated Hypogonadotropic Hypogonadism (IHH) — VialBase Research

Trial Summary

Phase 1 trial evaluating kisspeptin as a diagnostic and therapeutic tool in isolated hypogonadotropic hypogonadism. IHH is caused by deficient GnRH secretion or action, leading to absent puberty and infertility. Kisspeptin, as the upstream activator of GnRH neurons, could potentially bypass defective kisspeptin signaling to restore the reproductive axis.

Design

  • Type: Interventional, proof-of-concept
  • Population: Adults with confirmed IHH (congenital or acquired)
  • Arms: Kisspeptin administration (various doses, routes, and infusion patterns)
  • Duration: Acute and repeated-dose protocols
  • Key measures: LH pulse frequency and amplitude, FSH response, testosterone/estradiol levels, inhibin B, follicular development (in women), spermatogenesis markers (in men)

Key Outcomes

Trial is recruiting; no results available yet. Prior academic studies (Dhillo, Seminara groups) have shown that kisspeptin can reliably stimulate LH secretion in both healthy volunteers and some IHH patients, depending on the genetic etiology.

Significance for Peptide Research

IHH is the prototypical disease for kisspeptin therapy because the pathophysiology directly maps to the kisspeptin-GnRH-gonadotropin axis. Different IHH genotypes respond differently: patients with kisspeptin receptor (KISS1R) mutations may not respond, while those with defects upstream of kisspeptin signaling should respond. This creates a precision-medicine framework for kisspeptin-based therapeutics. Long-term pulsatile kisspeptin could potentially replace GnRH pump therapy for fertility induction.

See Also