Storage Stability
Neuropeptide K (NPK) is a 36-amino-acid N-terminally extended form of neurokinin A (NKA), derived from the PPT-A (preprotachykinin-A) gene via alternative processing. It incorporates the full NKA sequence at its C-terminus and acts as a potent agonist at the NK2 receptor, with a pharmacological profile distinct from NKA due to its longer half-life and additional N-terminal domain interactions.
Mechanism of Action
- N-terminal extension (aa1-26) beyond the NKA core (aa27-36) slows aminopeptidase degradation, extending biological half-life vs NKA
- NK2 agonism produces bronchoconstriction, gut smooth muscle contraction, and vasodilation in peripheral tissues
- In airway: NPK is among the most potent endogenous bronchoconstrictors acting via airway smooth muscle NK2 receptors
- Enteric: stimulates peristalsis and colonic motility via myenteric plexus NK2 signaling
- More potent than NKA at NK2 in several bioassays due to combined N-terminal stabilization and C-terminal receptor activation
Research Findings
- NPK and neuropeptide gamma are the two extended tachykinins from PPT-A with tissue-specific expression patterns vs substance P
- NPK bronchoconstriction in guinea pig airways used as standard assay to characterize NK2 antagonist potency
- Elevated NPK-like immunoreactivity in bronchoalveolar lavage of asthma patients during challenge
- NK2 antagonists (saredutant, MEN10207) developed partly using NPK as reference agonist in preclinical assays
- Gastrointestinal: NPK potently contracts human colon circular muscle via NK2; relevant for IBS research
Research Protocols
- Bronchoconstriction assay (guinea pig): 1-100 nM NPK aerosol or IV to characterize NK2 bronchospasm
- GI motility: 10-100 nM NPK bath application to isolated gut smooth muscle preparations
- NK2 receptor binding: NPK as displacement competitor vs [3H]-NKA in receptor binding assays
- Not used clinically; research tool for NK2 receptor pharmacology
Interactions
- Saredutant (SR 48968): NK2 antagonist; competitively blocks NPK bronchoconstriction reference agonist
- Neutral endopeptidase (NEP 24.11): primary degradation enzyme; NEP inhibitors prolong NPK activity
- Substance P and NKA: co-released from same neurons; cooperative tachykinin signaling
Safety Profile
Endogenous peptide; bronchoconstrictor and smooth muscle contractor. Not used clinically. NK2 agonism contributes to asthma and IBS pathophysiology; NK2 antagonists derived from NPK pharmacology tested in Phase II trials.
Legal & Regulatory
Research peptide; not approved as therapeutic
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Categories:
NeuropeptideTachykininNK2 AgonistPPT-A Gene ProductBronchoconstrictionExtended Tachykinin
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