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Neuropeptide AF

● Preclinical
Neuropeptide AF (NPAF)
Also known as: NPAF, Anti-Opioid Peptide, FMRF-Amide Related Peptide
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Quick Summary

Neuropeptide AF (NPAF) is an 18-amino acid RF-amide neuropeptide originally identified in bovine brain. Together with neuropeptide FF (NPFF), it is processed from the NPFF precursor and shares the C-terminal Phe-Leu-Phe-Gln-Pro-Gln-Arg-Phe-amide motif.

Neuropeptide / Anti-Opioid Preclinical
Neuropeptide AF (NPAF) is an 18-amino acid RF-amide neuropeptide originally identified in bovine brain. Together with neuropeptide FF (NPFF), it is processed from the NPFF precursor and shares the C-terminal Phe-Leu-Phe-Gln-Pro-Gln-Arg-Phe-amide motif. NPAF activates NPFF receptors (NPFFR1 and NPFFR2) and is a potent anti-opioid peptide that modulates opioid analgesia, promotes opioid tolerance, and regulates pain sensitization.
Storage Stability
Lyophilized
1–2 years (-20°C)
Reconstituted
~30 days (2–8°C)
Room temp
Avoid

Mechanism of Action

NPFF Receptor Activation

NPAF activates both NPFFR1 and NPFFR2, which are Gi/Go-coupled GPCRs. These receptors are expressed throughout pain-modulating circuits including the spinal cord dorsal horn, periaqueductal gray, and rostral ventromedial medulla. NPAF activation opposes opioid receptor signaling at multiple levels, reducing cAMP responses, counteracting opioid-induced receptor desensitization, and increasing excitatory neurotransmitter release.

Anti-Opioid and Pro-Nociceptive Effects

NPAF and related NPFF peptides are among the best-characterized anti-opioid peptides. They reduce morphine analgesia, accelerate tolerance development, and may produce hyperalgesia (pain sensitization) at higher doses. These effects are mediated through NPFFR1/2 and are blocked by RF-amide antagonists. NPAF may contribute to the rebound hyperalgesia observed after opioid withdrawal.


Research Summary

Opioid Tolerance

Preclinical

Co-administration of NPAF with morphine accelerates analgesic tolerance development in rodents. Conversely, NPFFR antagonists slow tolerance development and extend morphine efficacy. These findings have driven interest in developing NPFF receptor antagonists as opioid adjuvants that could extend analgesic benefit and reduce tolerance in chronic pain management.

Spinal Pain Processing

Preclinical

Intrathecal NPAF produces hyperalgesia and facilitates nociceptive transmission in the spinal dorsal horn. NPAF neurons in the superficial dorsal horn receive input from primary afferents and modulate pain signal processing. Their activation under inflammatory conditions contributes to central sensitization.


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Research Protocols

GoalDoseFrequencyRoute
Opioid tolerance acceleration10-100 nmol ICVBefore opioid dosingIntracerebroventricular
Pain modulation1-10 nmol ITSingleIntrathecal

Research tool only. NPFF receptor antagonists are the therapeutic development direction.


Interactions

Anti-Opioid
Morphine
NPAF reduces morphine analgesia and accelerates tolerance
Synergy
NPFF
Both processed from same precursor; similar anti-opioid properties
Opposing
Sialorphin amplifies opioid effects while NPAF opposes them

Safety Profile

NPAF is an endogenous CNS peptide. Central administration produces hyperalgesia and pain sensitization. No therapeutic use. NPFF receptor antagonists that block NPAF/NPFF effects are in preclinical development as opioid adjuvants with potential clinical applications for chronic pain.


References

  • [1]Yang HY et al. (1985). Neuropeptide FF, a F-8-F-amide peptide, antagonizes morphine analgesia without changing morphine induction. Science, 228(4701), 891-893.
  • [2]Mollereau C et al. (2002). Distribution of NPFF1 and NPFF2 receptors in the rat brain and spinal cord. Synapse, 45(3), 191-203.
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Verified Scientific Data Last audited:
Data Sources & External References
Source: peer-reviewed literature  ·  Domain: ascendpeptide.org

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