Bradykinin is a 9-amino-acid vasoactive peptide (sequence: Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg, MW ~1060.2 g/mol) generated by the kallikrein-kinin system through proteolytic cleavage of high-molecular-weight kininogen by plasma kallikrein. It is a potent endogenous vasodilator, pain mediator, and inflammatory agent with no approved therapeutic use as an exogenous drug. It is the primary target of ACE inhibitor-mediated cough and angioedema.
Category: Cardiovascular / Vasoactive. Evidence rating: B (meaningful human data).
Clinical status: Reference peptide. Not used therapeutically. Clinically relevant as mediator of ACE inhibitor side effects and hereditary angioedema.
Bradykinin binds primarily to constitutively expressed B2 receptors (BDKRB2), a Gq-coupled GPCR, on endothelial cells and smooth muscle. B2 activation stimulates phospholipase C, increasing IP3/DAG and intracellular calcium, leading to eNOS activation and nitric oxide release, as well as…
Safety considerations: Not used as an exogenous therapeutic agent; Endogenous bradykinin excess causes angioedema, hypotension, and pain; Bradykinin accumulation is the mechanism of ACE inhibitor cough (5-35% of patients) and angioedema (0.1-0.7%).
Reviewed by the PeptideAtlas Editorial Team.
| Amino-acid sequence | Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg (RPPGFSPFR) |
|---|---|
| Molecular weight | ~1060.2 g/mol |
| CAS number | 58-82-2 |
| Half-life | ~15-30 seconds (plasma) |
| Production method | synthetic |
| Anti-doping status | not-listed |
| US regulatory status | Not an approved drug. Available as research reagent. Bradykinin pathway antagonists (icatibant) and kallikrein inhibitors (ecallantide, lanadelumab) are FDA-approved for HAE. |
Related peptides: Angiotensin II, Angiotensin 1-7, Endothelin-1.
Bradykinin is clinically relevant as the mediator of ACE inhibitor-associated cough and angioedema, the central pathogenic molecule in hereditary angioedema (HAE), and an important pain and inflammation mediator. Drugs targeting the bradykinin pathway (icatibant, ecallantide, lanadelumab) are approved for HAE treatment.
ACE (angiotensin-converting enzyme) is also known as kininase II, the primary enzyme that degrades bradykinin. ACE inhibitors block this degradation, leading to elevated bradykinin levels. This causes the characteristic dry cough in 5-35% of patients and rarely angioedema. The bradykinin pathway may also contribute to ACE inhibitors' cardioprotective effects.
No. Bradykinin is too potent, non-selective, and rapidly degraded (half-life ~15-30 seconds) to be useful as a therapeutic agent. Instead, drugs targeting the bradykinin system include B2 receptor antagonists (icatibant) for HAE and kallikrein inhibitors (lanadelumab) to prevent bradykinin generation.