📚 Wiki Hormonal & Reproductive RFRP-3

RFRP-3

● Preclinical
RFamide-Related Peptide 3
Also known as: RFRP-3, NPVF Peptide, GnIH Mammalian Homolog, Gonadotropin-Inhibitory Hormone
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Quick Summary

RFamide-related peptide 3 (RFRP-3) is a mammalian neuropeptide that is the functional homolog of avian gonadotropin-inhibitory hormone (GnIH). It is derived from the NPVF precursor and inhibits GnRH neuron firing in the hypothalamus, suppressing LH and FSH secretion.

Neuropeptide / Reproductive Regulator Preclinical
RFamide-related peptide 3 (RFRP-3) is a mammalian neuropeptide that is the functional homolog of avian gonadotropin-inhibitory hormone (GnIH). It is derived from the NPVF precursor and inhibits GnRH neuron firing in the hypothalamus, suppressing LH and FSH secretion. RFRP-3 integrates environmental and physiological signals (photoperiod, stress, energy status) to inhibit the HPG axis and serves as a key negative regulator of reproductive function.
Storage Stability
Lyophilized
1–2 years (-20°C)
Reconstituted
~30 days (2–8°C)
Room temp
Avoid

Mechanism of Action

GnRH Neuron Inhibition

RFRP-3 acts directly on GnRH neurons via NPFFR1 receptors, hyperpolarizing these neurons and reducing their firing rate. It also acts on gonadotroph cells in the pituitary, directly reducing LH pulse amplitude. The Gi/Go coupling of NPFFR1 decreases cAMP and activates GIRK channels, providing inhibitory tone to GnRH pulse generation.

Environmental Signal Integration

RFRP-3 neurons in the dorsomedial hypothalamic nucleus receive inputs from the suprachiasmatic nucleus (photoperiod), arcuate nucleus (metabolic signals), and stress circuits (CRH neurons). This positioning allows RFRP-3 to integrate seasonal, nutritional, and stress signals to modulate reproductive timing, explaining why stress and malnutrition suppress fertility.


Research Summary

Seasonal Reproduction

Preclinical

In photoperiod-sensitive species (sheep, hamsters), RFRP-3 neurons are strongly activated during non-breeding seasons (short days), suppressing the HPG axis. Immunoneutralization of RFRP-3 in seasonally anestrous ewes partially restores LH pulsatility. RFRP-3 appears to be the primary seasonal brake on reproductive function.

Stress-Induced Infertility

Preclinical

Stress activates RFRP-3 neurons through CRH-dependent mechanisms, contributing to stress-induced suppression of LH secretion. NPFFR1 antagonists partially block stress-induced LH suppression, confirming the role of RFRP-3 in the stress-reproduction interaction. This makes RFRP-3 a potential therapeutic target for stress-related infertility.


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Research Protocols

GoalDoseFrequencyRoute
LH suppression1-100 nmol ICVSingleIntracerebroventricular
Stress model10-50 nmol SCSingleSubcutaneous

Preclinical research only. NPFFR1 antagonists are the therapeutic development direction.


Interactions

Opposing
Kisspeptin activates; RFRP-3 inhibits GnRH neurons
Upstream
CRH
Stress-released CRH activates RFRP-3 neurons to suppress reproduction
Block
NPFFR1 antagonists
Experimental NPFFR1 antagonists restore LH pulsatility in RFRP-3-suppressed models

Safety Profile

RFRP-3 is an endogenous hypothalamic peptide. Central administration is used in research; no systemic therapeutic use in humans. NPFFR1 antagonists for clinical reproductive applications are in early development. No human clinical data for RFRP-3 itself.


References

  • [1]Tsutsui K et al. (2000). A novel avian hypothalamic peptide inhibiting gonadotropin release. Biochemical and Biophysical Research Communications, 275(2), 661-667.
  • [2]Kriegsfeld LJ et al. (2006). Identification and characterization of a gonadotropin-inhibitory system in the brains of mammals. PNAS, 103(7), 2410-2415.
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Verified Scientific Data Last audited:
Data Sources & External References
Source: peer-reviewed literature  ·  Domain: ascendpeptide.org

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