Storage Stability
Hemokinin-1 (HK-1) is an 11-amino-acid tachykinin peptide encoded by the TAC4 gene, distinct from substance P (TAC1 gene). It is the only tachykinin preferentially expressed in the immune system rather than neurons, produced by B-lymphocytes, mast cells, and dendritic cells, and acts as a full agonist at the NK1 receptor with potency comparable to substance P.
Mechanism of Action
- NK1 receptor agonism with potency matching substance P; identical C-terminal sequence -Phe-X-Gly-Leu-Met-NH2 mediates binding
- Released from immune cells (mast cells, B cells) during allergic and inflammatory responses, amplifying neurogenic inflammation
- Promotes B lymphocyte proliferation and differentiation via autocrine NK1 signaling in bone marrow
- Stimulates IL-6, IL-8, and TNF-alpha release from macrophages, linking innate immunity to tachykinin signaling
- Central administration produces analgesia; in spinal cord contributes to pain sensitization and wind-up similar to substance P
Research Findings
- HK-1 discovered in 2000 as a novel NK1 agonist expressed in mouse and human bone marrow hematopoietic cells
- TAC4-knockout mice show reduced B cell proliferation and impaired humoral immune responses
- HK-1 elevated in bronchoalveolar lavage fluid of asthma patients during exacerbations
- HK-1 promotes angiogenesis via NK1 activation on endothelial cells; potential role in tumor vascularization
- NK1 antagonists (aprepitant, netupitant) block HK-1-mediated immune cell activation in vitro
Research Protocols
- In vitro immune cell assay: 1-100 nM HK-1 on B cells or mast cells; measure cytokine release
- Pain behavior: 10-100 nmol intrathecal in rodents for NK1-mediated nociception (reference tool)
- NK1 binding competition assay: HK-1 as competitor vs substance P at 1-1000 nM
- Not used clinically; NK1 antagonists (aprepitant) clinically relevant for CINV and derived from this pathway
Interactions
- Substance P: same NK1 receptor; HK-1 is a full agonist with similar potency at NK1
- Aprepitant/fosaprepitant: NK1 antagonists clinically used for CINV; block HK-1 effects
- Neprilysin (NEP): primary degrading enzyme; NEP inhibitors prolong HK-1 half-life
Safety Profile
Endogenous peptide not used clinically. NK1 agonism contributes to neurogenic inflammation and pain sensitization; NK1 antagonists derived from studying this system have excellent safety profiles in clinical use (CINV treatment).
Legal & Regulatory
Research peptide; not approved as therapeutic
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