Where it comes from

Made in
The dorsomedial hypothalamus, projecting widely
Sent out by
Stress raises it; melatonin and day length set it in seasonal animals
Acts on
  • GnRH neurons
  • Pituitary
  • Pain circuits

What it does

  • Its effect on gonadotropins is inconsistent: in hamsters it lowered LH in long days and raised it in short days 3
  • Stimulates prolactin in rats, as its sibling RFRP-3 does 2
  • Takes part in pain signalling, though the opioid-opposing work rests mostly on RFRP-3 1

In medicine

  • No medicine copies it or blocks it, and it is not measured in people
  • Its receptor is the one neuropeptide FF uses, which is the practical obstacle: a blocker of NPFFR1 would act on pain and on reproduction at the same time 1

Beyond the body’s own use

  • Nothing containing it is in trials, approved or obtainable outside the laboratory
  • It is studied with RFRP-3 as the mammalian gonadotropin-inhibitory hormone, and nearly all of that work uses RFRP-3: the two come from one precursor and RFRP-1 is the one left out 3
  • What is unknown is whether it has a role of its own. Its effect on gonadotropins has not settled in either direction, and no antiserum or animal separates it from RFRP-3, so the gene’s two peptides are reported as one system 2

Sources

  1. Hinuma et al., New neuropeptides containing carboxy-terminal RFamide and their receptor in mammals, Nature Cell Biology 2000
  2. Anderson et al., Central and peripheral effects of RFamide-related peptide-3 on LH and prolactin secretion in rats, Endocrinology 2009
  3. Tsutsui et al., Gonadotropin-inhibitory hormone, a key neurohormone of reproduction, Frontiers in Neuroendocrinology 2021

This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.