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
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
- Hinuma et al., New neuropeptides containing carboxy-terminal RFamide and their receptor in mammals, Nature Cell Biology 2000
- Anderson et al., Central and peripheral effects of RFamide-related peptide-3 on LH and prolactin secretion in rats, Endocrinology 2009
- 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.