PeptaHub
The comprehensive peptide reference
OTHERPEPTIDE PROFILE

Bradykinin

Also known as Kallidin-9, BK, Bradykinin (1-9)

Bradykinin is an endogenous nonapeptide generated from kininogens by the enzyme kallikrein. It is a potent vasodilator and pain-sensitizing mediator involved in inflammation, blood pressure regulation, and the pain cascade. Its receptor antagonist Icatibant is FDA-approved for treatment of hereditary angioedema (HAE), validating the clinical significance of this kinin pathway.

Last updated April 10, 2026

TL;DR

Quick summary

Bradykinin is a 9-amino acid endogenous vasodilator and pain-sensitizing mediator generated by the kallikrein-kinin system. Its B2 receptor antagonist Icatibant is FDA-approved for hereditary angioedema, and bradykinin potentiation by ACE inhibitors explains the cough side effect of that drug class.

§ 01

Overview

Bradykinin is an endogenous nonapeptide generated from kininogens by the enzyme kallikrein. It is a potent vasodilator and pain-sensitizing mediator involved in inflammation, blood pressure regulation, and the pain cascade. Its receptor antagonist Icatibant is FDA-approved for treatment of hereditary angioedema (HAE), validating the clinical significance of this kinin pathway.

§ 02

Mechanism of action

Bradykinin acts on two G-protein-coupled receptors: B1 (inducible, involved in chronic inflammation) and B2 (constitutively expressed, mediates acute effects). B2 receptor activation stimulates phospholipase C, increases intracellular calcium, triggers nitric oxide synthase, and releases prostaglandins. These combined effects produce vasodilation, increased vascular permeability, smooth muscle contraction, and sensitization of nociceptors underlying pain and inflammation.

§ 03

Dosing protocols

PurposeRouteDosageFrequency
cardiovascular/pain researchintravenous1001000 ng/kg/mincontinuous infusion per protocol

Dosing information is for educational purposes only. Consult a qualified healthcare professional before using any peptide.

§ 04

Research summary

Bradykinin is extensively studied in cardiovascular physiology, pain research, and inflammatory disease. Its role in ACE inhibitor-induced cough (potentiation of bradykinin via reduced degradation) is well established. Icatibant, a B2 receptor antagonist, received FDA approval in 2011 for HAE. Ongoing research examines bradykinin's role in COVID-19 pathophysiology and potential therapeutic targets in the kinin-kallikrein system.[1][2][3][4]

📄This section cites 4 peer-reviewed sources. View all references →
§ 04b

Evidence grading

Each claimed benefit is graded by the strength of available evidence. Grades reflect study quality, not effect size.

strong
Icatibant (B2 antagonist) FDA-approved for HAECicardi 2010 NEJM RCT (FAST-3) supported FDA approval of icatibant for hereditary angioedema
strong
ACE inhibitor cough caused by bradykinin accumulationMechanism established through decades of clinical pharmacology; affects 10-20% of ACE-inhibitor users
strong
Potent vasodilator via B2 receptor and NO releaseFoundational cardiovascular pharmacology establishes PLC/calcium/NOS signaling cascade
strong
Extremely short plasma half-life (~17 seconds)Well-characterized pharmacokinetics across human and animal studies due to rapid kininase degradation
preliminary
Implicated in COVID-19 pathophysiologyHypothesized role in ACE2-mediated kinin dysregulation during COVID-19; clinical evidence emerging

Strong = multiple RCTs · Moderate = limited trials or observational · Preliminary = animal or in vitro only · Insufficient = anecdotal or no published data

§ 05

Side effects

Hypotension
Flushing
Pain at injection site
Bronchoconstriction

Side effects vary by individual. This is not an exhaustive list. Report unusual symptoms to a healthcare professional.

§ 06

Common stacks

Peptides commonly paired with Bradykinin for synergistic effects.

§ 08

Sourcing & access

Research compound

Bradykinin is classified as a research compound. Regulatory status varies by jurisdiction. Always verify current legal status and source from vendors providing third-party certificates of analysis (COA).

§ 09

Frequently asked questions

Bradykinin is an endogenous nonapeptide generated from kininogens by the enzyme kallikrein. It is a potent vasodilator and pain-sensitizing mediator involved in inflammation, blood pressure regulation, and the pain cascade.

Bradykinin acts on two GPCRs: B1 (inducible, involved in chronic inflammation) and B2 (constitutively expressed, mediating acute effects). B2 receptor activation stimulates phospholipase C, increases calcium, triggers nitric oxide synthase, and releases prostaglandins, producing vasodilation, increased vascular permeability, and pain sensitization.

Bradykinin is a research compound with an extremely short half-life of about 17 seconds. Effects include hypotension, flushing, pain at injection site, and bronchoconstriction. Icatibant, a B2 receptor antagonist, is FDA-approved for hereditary angioedema and has an established clinical safety profile.

ACE (angiotensin-converting enzyme) also degrades bradykinin. ACE inhibitors reduce bradykinin breakdown, leading to accumulation that causes the well-known dry cough side effect in approximately 10-20% of patients. This potentiation also contributes to the vasodilatory benefits of ACE inhibitor therapy.

§ 10

Research references

  1. Bradykinin and the kallikrein-kinin system in cardiovascular homeostasisBhoola KD, Figueroa CD, et al.Pharmacol Rev, 1992PubMed
  2. Bradykinin B2 receptor antagonist icatibant in hereditary angioedemaCicardi M, Banerji A, et al.N Engl J Med, 2010PubMed
  3. Role of bradykinin in ACE inhibitor cardiovascular protection beyond blood pressureUnger T, et al.J Cardiovasc Pharmacol, 1999PubMed
  4. Kinin receptors: pharmacology and therapeutic implicationsRegoli D, Barabe J, et al.Pharmacol Rev, 1980PubMed
● READER REVIEWS

What readers say about Bradykinin

No reader reviews yet. If you’ve used Bradykinin, share your experience — your review helps the next person decide.