Neurokinin A
The tachykinin of the airways and gut, used to challenge asthmatic lungs and measured to follow neuroendocrine tumours
Neurokinin A comes from the same gene as substance P and is released by sensory nerves. Breathed in, it tightens the airways of people with asthma while leaving healthy airways unaffected, which made it a research tool for probing airway sensitivity. In the gut it speeds motility. It also spills into the blood from small-bowel neuroendocrine tumours, where its level tracks how the disease is doing. Neurokinin A itself is not a medicine; the drugs built around it block its receptor.
Used in human trials: 1 to 125 µg/mL (nebulised, 0.5 mL per dose), Rising inhaled doses, Inhaled (nebulised) (Study: asthma bronchial challenge, inhaled dose-response) Details ↓
Recommended Dosing
Used in human trials
No manufacturer dose exists for this use: these are amounts given in published trials, not recommendations.
What is it?
Neurokinin A is one of the tachykinins, a peptide family named for the quick muscle contractions they cause. It shares its gene, TAC1, and much of its biology with substance P: both are cut from the same precursor and released together by sensory nerves. Where substance P prefers the neurokinin 1 receptor, neurokinin A prefers the neurokinin 2 receptor, and that difference shows most clearly in the lung.
Its best-studied human role is in the airways. When six healthy and six asthmatic volunteers inhaled rising doses of substance P and neurokinin A, neither peptide changed the healthy airways and substance P did nothing in asthma, but neurokinin A narrowed the asthmatic airways by almost half. Later work showed this response closely tracks the response to methacholine, the standard test agent, which suggests both act through a final common path on airway muscle. Inhaled neurokinin A is also the main tachykinin recovered from the airway fluid of both normal and asthmatic people, rising further after an allergen challenge.
A series of challenge studies used neurokinin A to probe how the airways are controlled. Blocking neutral endopeptidase, the enzyme that breaks tachykinins down, made the airways more sensitive to inhaled neurokinin A, showing the enzyme normally limits the response. Two weeks of an inhaled steroid, either fluticasone or beclomethasone, reduced sensitivity to neurokinin A, more so than to methacholine or histamine. These were research measurements, not treatments: the peptide was the probe.
In the gut, neurokinin A drives movement. Infused into healthy men it stimulated contractions of the small intestine, an effect that a neurokinin 2 receptor blocker could switch off, confirming the receptor at work. This motility role is why drugs targeting its receptor were studied for conditions such as irritable bowel.
Neurokinin A also matters in cancer medicine as a marker. Tumours of the gut's hormone-producing cells, small-bowel neuroendocrine tumours, can secrete it into the blood. In large patient series, a persistently high plasma level, above about 50 pg/mL, marked a poor outlook, and a level that stayed high after surgery to remove tumour bulk identified the patients who did worst. An assay comparison across the United States and United Kingdom found the measurements agree well between laboratories.
Mechanism of Action
Neurokinin A is released from sensory nerves in the airways and gut and acts mainly on the neurokinin 2 receptor, narrowing airways and driving gut contractions; the enzyme neutral endopeptidase normally breaks it down.
Airway narrowing
Inhaled, it constricts asthmatic but not healthy airways through the NK2 receptor on airway muscle; inhaled steroids reduce the response.
Enzyme control
Neutral endopeptidase degrades it; blocking that enzyme makes the airways more sensitive to it.
Tumour marker
Small-bowel neuroendocrine tumours secrete it, and a high plasma level marks a poor prognosis.
Published Research
These are studies of neurokinin A itself, read from their PubMed abstracts: inhaled and intravenous challenge studies in healthy and asthmatic people, measurements in airway fluid and blood, the prognostic studies in neuroendocrine tumours, an assay validation, and the gene's cloning. Studies whose point is a receptor-blocking drug are listed under References.
Infused, it narrows airways; substance P widens them
In six normal volunteers, intravenous neurokinin A and substance P both raised skin temperature and heart rate, but substance P was far more potent at each. Substance P caused bronchodilation while neurokinin A caused bronchoconstriction, pointing to different receptor actions.
Inhaled, it narrows only asthmatic airways
Six healthy and six asthmatic subjects inhaled rising concentrations of substance P and neurokinin A. Neither peptide changed airway conductance in the healthy subjects, and substance P did nothing in the asthmatics, but neurokinin A cut asthmatic airway conductance by a mean of 48%, recovering within an hour.
The breakdown enzyme limits the response
Eight atopic asthmatic men inhaled the neutral endopeptidase blocker thiorphan or placebo before a neurokinin A challenge in a crossover study. Thiorphan significantly lowered the dose of neurokinin A needed to drop lung function, showing the enzyme normally restrains the airway response.
A second enzyme blocker, the same effect
In six atopic asthmatic patients, inhaled phosphoramidon, another neutral endopeptidase inhibitor, significantly potentiated the airway narrowing caused by inhaled neurokinin A, with no effect on baseline lung function.
The response tracks methacholine
In 27 people with mild asthma, the provocative concentration of neurokinin A that dropped lung function correlated strongly with that of methacholine, suggesting both agents narrow the airways through a shared final pathway, likely the neurokinin 2 receptor on airway muscle.
An inhaled steroid blunts the response
In a double-blind crossover study, six weeks of inhaled beclomethasone raised the provocative concentration of both histamine and neurokinin A about fivefold, reducing airway sensitivity to each to a similar degree.
Fluticasone reduces sensitivity more than for methacholine
Eleven people with mild asthma took inhaled fluticasone or placebo for 14 days. Fluticasone significantly reduced bronchial responsiveness to neurokinin A, and the reduction was larger than the change in responsiveness to methacholine.
The main tachykinin in airway fluid
Using radioimmunoassay and HPLC on bronchoalveolar lavage fluid, neurokinin A was detected in significant amounts in both asthmatic and normal subjects while substance P and CGRP were not, and its level rose after allergen challenge. It was the predominant tachykinin in the airways.
Persistently high level, worst survival
In 267 patients with small-bowel neuroendocrine tumours followed after surgical cytoreduction, those whose plasma neurokinin A stayed elevated despite treatment had a 10-year survival of 0%, against 62% to 78% in those whose levels were normal or normalised.
A simple cutoff predicts survival
Among 180 patients with metastatic midgut neuroendocrine tumours, those with plasma neurokinin A consistently above 50 pg/mL had a median survival of 20 months and a 24-month survival of 48%, while those below 50 pg/mL had not reached median survival and a 24-month survival of 93%.
The assay agrees across continents
Frozen clinical samples were exchanged between laboratories in the United States and United Kingdom and assayed by different methods. Neurokinin A values agreed closely (r = 0.88 and 0.96), supporting its use as a biomarker in international studies.
Raised in carcinoid, but not the whole flush story
In 10 patients with metastatic carcinoid tumours, circulating neurokinin A and substance P were measured during meal-induced flushing. Several patients had raised baseline tachykinins, but the rises after food were erratic and did not track the flush, so the tachykinins could not solely explain it.
Where neurokinin A fits among NET markers
A review of 500 raised results each for chromogranin A, urinary 5-HIAA and neurokinin A in a regional service found neurokinin A the most specific of the three for small-bowel neuroendocrine tumours, though values near the reference limit sat within assay precision.
Cut from the substance P precursor
The human beta-preprotachykinin complementary DNA, cloned from a laryngeal carcinoid tumour, encodes a 129-amino-acid precursor carrying both substance P and neurokinin A, each flanked by basic residues, with neuropeptide K being an N-terminally extended form of neurokinin A.
Dosing Data
Neurokinin A is not approved anywhere as a medicine. These are research challenge amounts from published human studies, as stated in their abstracts; none was a treatment course.
Educational information, not medical advice. Each dose above is tagged with its source: an approved label, a published human study, animal data, or amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
What a Buyer Needs to Know
What is sold, how it is mixed, stored and taken, and what is known about its safety, quality and legal status. Each part names its source. Where we have none, it says unknown.
What is sold
Unknown: we hold no label and no published test that says what forms or vial sizes Neurokinin A is sold in. A vial's own label is a seller's claim, not a source.
Mixing a vial: a worked example
No worked example: none of the doses on this page is a fixed amount in mg or mcg injected under the skin or into a muscle (the routes given are: inhaled (nebulised), intravenous). There is no home-mixing step to show. The reconstitution calculator does the arithmetic for any vial.
Source: the route and amount of each dose row in Dosing Data below.
Storage before and after mixing
Unknown: no label or published stability study on file says how to store Neurokinin A, before or after mixing. The mixing guide sets out the general rules, with their sources: keep a mixed vial in the fridge, and use it promptly, as the bacteriostatic water label says of any drug dissolved in it. The 28 days often quoted is the limit for an opened multiple-dose vial from a manufacturer, an outer limit set for sterility, not a time a mixed solution has been shown to keep. Nobody has published how long Neurokinin A stays intact once mixed.
How it is taken
As it was given in human studies: Inhaled (nebulised) (Rising inhaled doses; Study: asthma bronchial challenge, inhaled dose-response); Intravenous (Continuous infusion; Study: healthy men, small-intestine motility).
For injection technique, sites and needle disposal, see the mixing guide.
Source: Used in human trials: the route and frequency of each row in Dosing Data below.
What to expect, and when
How long it stays in the body: not established by a measurement cited on this entry.
How long the doses were given: Study: asthma bronchial challenge, inhaled dose-response: Single challenge session; Study: healthy men, small-intestine motility: During motility recording.
When effects appear: unknown; no source on this page gives a time to effect for Neurokinin A. Results reported in the studies are under Published Research.
Source: Used in human trials, the duration of each row in Dosing Data below.
Side effects, and when to stop or get help
From the Side Effects section: Bronchoconstriction when inhaled by people with asthma, the intended effect of the challenge (PMID 2447663); A faster heart rate and warmer skin during an intravenous infusion (PMID 2451930); No safety data beyond single research challenges. Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Neurokinin A. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“From the challenge studies above, whose point was to provoke a measured response”).
Interactions
- neutral endopeptidase inhibitors (inhaled phosphoramidon): blocking the enzyme that degrades neurokinin A potentiated its bronchoconstriction in asthmatic patients
Every peptide's record, with its source: the interaction matrix.
Source: human study, PMID 8187026.
Checking what you bought
Unknown: no published independent test of Neurokinin A products is in our lab-results database yet, so how products sold under this name measure up is not known.
To read a certificate of analysis, paste it into the COA decoder; it checks the measured mass against Neurokinin A's expected mass, 1,133.3 Da, from this entry's molecular data. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Research Chemical (Not a medicine anywhere in the sources read). Sport: Prohibited (S0 catch-all).
Country by country ↓ · Regulatory tracker
Source: this entry's approval status and the WADA Prohibited List, as in Legal Status below.
Side Effects & Contraindications
Reported Side Effects
From the challenge studies above, whose point was to provoke a measured response.
Contraindications & Cautions
No product label exists. These cautions follow from the evidence.
Legal Status
Neurokinin A is a research peptide; it is not approved as a medicine anywhere in the sources read.
Frequently Asked Questions
?What is neurokinin A?
A 10-amino-acid tachykinin peptide made from the same gene as substance P and released by sensory nerves. It acts mainly on the neurokinin 2 receptor.
?What does inhaled neurokinin A do?
It narrows the airways of people with asthma while leaving healthy airways unchanged, which is why it was used as a research challenge agent.
?Why is neurokinin A measured in cancer?
Small-bowel neuroendocrine tumours can release it into the blood. A persistently high level, above about 50 pg/mL, marks a poor prognosis.
?How is it different from substance P?
They come from the same precursor, but substance P prefers the neurokinin 1 receptor and neurokinin A prefers the neurokinin 2 receptor; in the lung, only neurokinin A narrowed asthmatic airways.
?Is neurokinin A a medicine?
No. It has no approval anywhere; it has been given to people only in short research challenges, inhaled or infused.
?What is neuropeptide K?
An N-terminally extended form of neurokinin A, cut from the same precursor; it appears in the blood of some carcinoid patients.
References
- [clinical-trial] Evans TW, et al. "Comparison of neurokinin A and substance P on cardiovascular and airway function in man." Br J Clin Pharmacol, 1988;25(2):273-5. PMID: 2451930.
- [clinical-trial] Joos G, et al. "Effect of inhaled substance P and neurokinin A on the airways of normal and asthmatic subjects." Thorax, 1987;42(10):779-83. PMID: 2447663.
- [clinical-trial] Cheung D, et al. "Neutral endopeptidase activity and airway hyperresponsiveness to neurokinin A in asthmatic subjects in vivo." Am Rev Respir Dis, 1993;148(6 Pt 1):1467-73. PMID: 8256886.
- [clinical-trial] Crimi N, et al. "Inhibition of neutral endopeptidase potentiates bronchoconstriction induced by neurokinin A in asthmatic patients." Clin Exp Allergy, 1994;24(2):115-20. PMID: 8187026.
- [clinical-trial] Cohen J, et al. "Relationship between airway responsiveness to neurokinin A and methacholine in asthma." Pulm Pharmacol Ther, 2005;18(3):171-6. PMID: 15707850.
- [clinical-trial] Prosperini G, et al. "Beclomethasone dipropionate attenuates airways hyperresponsiveness to neurokinin A and histamine in asthma." Respir Med, 2006;100(6):1006-12. PMID: 16290928.
- [clinical-trial] Van Schoor J, et al. "Effect of inhaled fluticasone on bronchial responsiveness to neurokinin A in asthma." Eur Respir J, 2002;19(6):997-1002. PMID: 12108885.
- [clinical-trial] Heaney LG, et al. "Neurokinin A is the predominant tachykinin in human bronchoalveolar lavage fluid in normal and asthmatic subjects." Thorax, 1998;53(5):357-62. PMID: 9708226.
- [clinical-trial] Woltering EA, et al. "Plasma Neurokinin A Levels Predict Survival in Well-Differentiated Neuroendocrine Tumors of the Small Bowel." Pancreas, 2018;47(7):843-848. PMID: 29939909.
- [clinical-trial] Diebold AE, et al. "Neurokinin A levels predict survival in patients with stage IV well differentiated small bowel neuroendocrine neoplasms." Surgery, 2012;152(6):1172-6. PMID: 23102678.
- [clinical-trial] Mamikunian P, et al. "Validation of neurokinin a assays in the United States and Europe." Pancreas, 2011;40(7):1000-5. PMID: 21926539.
- [clinical-trial] Conlon JM, et al. "Circulating tachykinins (substance P, neurokinin A, neuropeptide K) and the carcinoid flush." Scand J Gastroenterol, 1987;22(1):97-105. PMID: 2882598.
- [review] Ardill JE, et al. "Neuroendocrine tumours of the small bowel: interpretation of raised circulating chromogranin A, urinary 5 hydroxy indole acetic acid and circulating neurokinin A." QJM, 2016;109(2):111-5. PMID: 25979268.
- [pubmed] Harmar AJ, et al. "cDNA sequence of human beta-preprotachykinin, the common precursor to substance P and neurokinin A." FEBS Lett, 1986;208(1):67-72. PMID: 3770210.
- [pubmed] Lördal M, et al. "A novel tachykinin NK2 receptor antagonist prevents motility-stimulating effects of neurokinin A in small intestine." Br J Pharmacol, 2001;134(1):215-23. PMID: 11522614.
- [other] UniProt P20366 (TAC1_HUMAN), protachykinin-1; peptide 98-107 is neurokinin A (HKTDSFVGLM), C-terminal methionine amide. Read October 30, 2026. https://www.uniprot.org/uniprotkb/P20366/entry
Sources & Citations
Every study on this page was read from its PubMed record on October 30, 2026. Regulatory status comes from Drugs@FDA (openFDA) and the EMA medicines list, read the same day. Grey Peptides sells nothing and links to no vendor.
Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Talk to a licensed clinician about your own situation.