Where it comes from
- Made in
- Sensory neurons, enteric neurons, and the brain, with substance P
- Sent out by
- Nerve activation by irritants, stretch and inflammation
- Acts on
- Airway smooth muscle
- Gut smooth muscle
- Bladder
- Spinal cord pain neurons
What it does
- Contracts airways, which made it a candidate asthma mediator 1
- Drives gut contraction and the gut-brain signalling of cramp
- Carries pain with substance P
In medicine
- No medicine. NK2R blockers were trialled for asthma and for irritable bowel syndrome: ibodutant improved symptoms in women with the diarrhoea-predominant form in a phase 2 study, and the programme went no further 2
- Neurokinin A is not measured in practice. In research it has to be separated by chromatography before assay, because an antiserum to the shared end of the molecule also reads the longer peptides that contain it 3
Beyond the body’s own use
- Nothing containing neurokinin A is approved or obtainable outside the laboratory, and infusing it constricts airways, which is why it was studied in asthma at all 1
- The honest summary of the NK2 story is that the target is real and the drugs have not delivered: airway and gut tissue respond to NK2 blockade, and no trial has turned that into an approved medicine 1
- What is still asked of it is whether the gut rather than the lung is the right organ, since the one positive signal came in women with diarrhoea-predominant irritable bowel syndrome 2
Sources
- Steinhoff et al., Tachykinins and their receptors, Physiological Reviews 2014
- Tack et al., The neurokinin-2 receptor antagonist ibodutant in diarrhoea-predominant irritable bowel syndrome, Gut 2017
- Takeda et al., Regional distribution of neuropeptide gamma and other tachykinins of the substance P gene, Regulatory Peptides 1990
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.