Where it comes from
- Made in
- B cell precursors, macrophages, T cells, and the lining of airway, gut and skin
- Sent out by
- Immune activation and inflammation
- Acts on
- B cells (survival)
- Mast cells and macrophages
- Pain neurons
- Vessels
What it does
In medicine
- No medicine targets hemokinin-1 itself. The approved NK1 blockers, aprepitant and its relatives, act at the receptor it shares with substance P, so blocking that receptor blocks both peptides at once 2
- It is not measured in practice. The antisera used for substance P cross-react with it strongly, which is why some older reports of substance P in blood, gut and immune tissue may have been reading hemokinin-1 instead 2
Beyond the body’s own use
- Nothing containing hemokinin-1 is in trials, approved or obtainable outside the laboratory: it is a target and a measurement, not a treatment 3
- The claim that it is simply a peripheral substance P does not hold. It binds the same receptor with similar strength, yet several of its effects differ from substance P’s or run opposite to them, and some persist where NK1 is blocked, which points to a target of its own that has not been found 3
- Its firmest evidence is in pain rather than immunity: mice lacking the TAC4 gene feel less inflammatory and neuropathic pain 4, while the B cell survival effect that gave the peptide its name was shown in mouse bone marrow and has not been established in people 12
Sources
- Zhang et al., Hemokinin is a haematopoietic-specific tachykinin that regulates B lymphopoiesis, Nature Immunology 2000
- Page, Hemokinins and endokinins, Cellular and Molecular Life Sciences 2004
- Borbély & Helyes, Role of hemokinin-1 in health and disease, Neuropeptides 2017
- Hunyady et al., Hemokinin-1 is an important mediator of pain in mouse models of neuropathic and inflammatory mechanisms, Brain Research Bulletin 2019
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.