Research compounds
Bradykinin
BK, kinin
Bradykinin is a nine-amino-acid inflammatory peptide of the kallikrein-kinin system, responsible for the swelling in hereditary angioedema and for the cough caused by ACE inhibitors.
Also known as: kinin
- Status
- Bradykinin is a research compound and not approved by the FDA for human use.
- Evidence
- Early human data. Only small or early-phase studies in people so far.
- Half-life
- Approximately 15 to 30 seconds.
- How it's taken
- Not used therapeutically; research administration only
- Mechanism
- Other
How Bradykinin works
Bradykinin is cleaved from high-molecular-weight kininogen by plasma kallikrein and acts at B2 receptors on endothelium, causing vasodilation, increased vascular permeability and pain. It is degraded chiefly by angiotensin-converting enzyme — which is why ACE inhibitors raise bradykinin levels and produce cough and, occasionally, angioedema.
What research has looked at
- It is the mediator that explains an entire therapeutic area: icatibant blocks its B2 receptor, ecallantide blocks the kallikrein that makes it, and C1-inhibitor concentrates restrain the cascade upstream.
- Its degradation by ACE explains two of the best-known ACE inhibitor adverse effects, cough and angioedema.
- Bradykinin-mediated vasodilation contributes to some of the beneficial haemodynamic effects of ACE inhibition.
Evidence level: Early human data. Only small or early-phase studies in people so far. These are areas studied or reported, not promised effects.
Reported side effects and risks
- Bradykinin causes pain, swelling and hypotension — it is a mediator of pathology, and every approved drug in this space blocks it rather than supplies it. No regulator has approved it, the human evidence base is limited, and material sold under this name is research chemical supply with unverified identity, purity, sterility and dose accuracy.
- It is degraded within seconds in circulation.
- Bradykinin-mediated angioedema does not respond to antihistamines or corticosteroids, a distinction that matters clinically and is frequently missed.
Sources
- PubMed research on bradykinin B2 receptor ACE inhibitor angioedema · NIH · National Library of Medicine
- DrugBank record for bradykinin · DrugBank
- Active clinical trials for bradykinin · U.S. National Library of Medicine
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Related compounds
Bradykinin FAQ
What is Bradykinin?
Bradykinin is a nine-amino-acid inflammatory peptide of the kallikrein-kinin system, responsible for the swelling in hereditary angioedema and for the cough caused by ACE inhibitors.
How does Bradykinin work?
Bradykinin is cleaved from high-molecular-weight kininogen by plasma kallikrein and acts at B2 receptors on endothelium, causing vasodilation, increased vascular permeability and pain. It is degraded chiefly by angiotensin-converting enzyme — which is why ACE inhibitors raise bradykinin levels and produce cough and, occasionally, angioedema.
Is Bradykinin FDA approved?
No. Bradykinin is a research compound and not approved by the FDA for human use. Evidence level: early human data. Only small or early-phase studies in people so far.
What is the half-life of Bradykinin?
Reported half-life: Approximately 15 to 30 seconds.
How is Bradykinin taken?
Not used therapeutically; research administration only.
What side effects have been reported with Bradykinin?
Reported in the sources: Bradykinin causes pain, swelling and hypotension — it is a mediator of pathology, and every approved drug in this space blocks it rather than supplies it. No regulator has approved it, the human evidence base is limited, and material sold under this name is research chemical supply with unverified identity, purity, sterility and dose accuracy; It is degraded within seconds in circulation; Bradykinin-mediated angioedema does not respond to antihistamines or corticosteroids, a distinction that matters clinically and is frequently missed.
Educational summary compiled from the sources listed above. Not medical advice. Peptide Vault does not sell, source or recommend any compound. Talk to a qualified clinician before starting or changing anything.