Peptide Basics
Bradykinin: The Nine-Amino-Acid Peptide Behind Swelling and Pain, Its Two Receptors and the Medicines That Block It
Bradykinin is a peptide of nine amino acids, cut from a blood protein called kininogen, that widens small blood vessels, makes them leaky and signals pain, and is inactivated by enzymes including ACE. This page sets out where the molecule comes from, its close relative kallidin, its two receptors, how it is inactivated, its link to hereditary angioedema, and the medicines in FDA’s records that act on its pathway. Every figure is taken from UniProt, PubChem, MeSH or FDA’s own databases and labels.
What bradykinin is
MeSH, the U.S. National Library of Medicine’s subject index, describes bradykinin as a nonapeptide messenger: a potent but short-lived agent that dilates arterioles and makes capillaries more permeable. It is released from damaged tissue as a pain signal, from mast cells during asthma attacks and from the gut wall, and it may also act as a neurotransmitter, which is why MeSH files it among the neuropeptides. It belongs to the kinins, peptides MeSH calls autacoids: they act locally, near where they are made, to produce pain, vasodilatation, leakier vessels and the synthesis of prostaglandins.
Its sequence reads RPPGFSPFR: arginine, proline, proline, glycine, phenylalanine, serine, proline, phenylalanine, arginine. It is a straight chain with no ring. PubChem gives it a molecular formula of C50H73N15O11 and a molecular weight of 1,060.2 (CID 439201).
Where it comes from: kininogen and the kallikreins
Bradykinin is not made on its own. It sits in the middle of a 644-amino-acid blood protein, kininogen-1, made from the KNG1 gene, and is cut out by enzymes called kallikreins. UniProt maps the protein like this:
| Piece | Positions | Amino acids | Note |
|---|---|---|---|
| Signal peptide | 1-18 | 18 | Steers the precursor out of the cell; removed first. |
| Heavy chain | 19-380 | 362 | The front part of kininogen, on the near side of the kinin stretch. |
| T-kinin | 376-389 | 14 | ISLMKRPPGFSPFR. UniProt records it in some ovarian, colon and breast cancers, not in benign tumours. |
| Lysyl-bradykinin (kallidin) | 380-389 | 10 | KRPPGFSPFR: bradykinin with one extra lysine at the front, released by tissue kallikrein. |
| Bradykinin | 381-389 | 9 | RPPGFSPFR: released by plasma kallikrein from high-molecular-weight kininogen. |
| Light chain | 390-644 | 255 | The back of kininogen, left joined to the heavy chain by a disulfide bond once the kinin is cut out. |
The three kinins overlap: T-kinin contains kallidin, and kallidin contains bradykinin. Which one is released depends on the enzyme. UniProt records that plasma kallikrein releases bradykinin from high-molecular-weight kininogen, and that tissue kallikrein releases lysyl-bradykinin, also called kallidin. MeSH describes kallidin as a decapeptide homologue of bradykinin and records that bradykinin can be produced from kallidin in the blood. PubChem gives kallidin the formula C56H85N17O12 and a weight of 1,188.4 (CID 5311111).
The same system is tied to blood clotting. UniProt records that plasma kallikrein and factor XII activate each other, and that high-molecular-weight kininogen helps hold prekallikrein and factor XI next to factor XII. That loop, factor XII to kallikrein to bradykinin, is where every medicine in the hereditary angioedema table below acts. The first piece of the precursor is a signal sequence, explained on our signal peptides page.
Sources: UniProt P01042 (KNG1), P03952 (KLKB1) and P06870 (KLK1); MeSH D001920, D007609, D007705 and D016234; PubChem CID 439201 and 5311111. Read 5 November 2026.
What bradykinin does
UniProt describes bradykinin as a potent vasodilator and lists its effects: it contracts smooth muscle, lowers blood pressure, increases the kidneys’ loss of salt and water, lowers blood glucose, and acts as a mediator of inflammation. In that last role it makes vessels leakier, stimulates the nerve endings that sense pain, and triggers the release of other mediators such as prostaglandins. UniProt also records a protective effect on the heart, directly and through the relaxing factor released by the vessel lining.
All of this happens close to where the peptide is made: MeSH describes kinins as acting locally and bradykinin’s action as short-lived.
Sources: UniProt P01042; MeSH D001920 and D007705. Read 5 November 2026.
The two bradykinin receptors, B1 and B2
Bradykinin acts through two G protein-coupled receptors. MeSH records that both are coupled to the Gq/11 and Gi/o families of G proteins; UniProt records that B2 activates the phosphatidylinositol-calcium second-messenger system. They differ in when they are present and which kinins they recognise:
| Receptor (gene) | Amino acids | When and where | Recognises |
|---|---|---|---|
| B2 (BDKRB2) | 391 | Present all the time (MeSH: constitutive); UniProt records it as ubiquitous, in normal smooth muscle and neurons | Intact bradykinin and kallidin |
| B1 (BDKRB1) | 353 | Induced in response to inflammation (MeSH); UniProt notes it could be a factor in chronic pain and inflammation | Kinins that have lost their last arginine: des-Arg9-bradykinin and des-Arg10-kallidin |
By MeSH’s descriptions, a kinin that has lost its last arginine is recognised by B1, the receptor that inflammation switches on, rather than by B2.
Sources: UniProt P30411 (BDKRB2) and P46663 (BDKRB1); MeSH D043782 and D043783. Read 5 November 2026.
How bradykinin is switched off: ACE and the kininases
UniProt records that angiotensin-converting enzyme, ACE, inactivates bradykinin by removing its last two amino acids, Arg-Phe. ACE is the same enzyme that turns angiotensin I into angiotensin II, and UniProt lists bradykinin and enkephalins among the other hormones it trims. The U.S. label for lisinopril, an ACE inhibitor, states that ACE is identical to kininase, an enzyme that degrades bradykinin, and its warnings section describes angioedema, swelling of the face, lips, tongue, throat or gut, in patients treated with ACE inhibitors.
This page does not interpret those warnings for any individual. Anyone taking a blood-pressure medicine should take questions about side effects to their own clinician and the product label.
Sources: UniProt P01042 and P12821 (ACE); current U.S. label for lisinopril (mechanism of action; warnings and precautions); MeSH D000799. Read 5 November 2026.
Bradykinin and hereditary angioedema: what FDA’s records show
MeSH describes hereditary angioedema as an inherited condition of swelling under the skin and the lining of the airways and gut. The Firazyr label states that it is caused by an absence or dysfunction of C1-esterase inhibitor, a key regulator of the factor XII and kallikrein cascade that leads to bradykinin production, and that bradykinin is thought to be responsible for the localised swelling, inflammation and pain of an attack. The medicines in Drugs@FDA for the condition each act at one step of that cascade: on factor XII, on kallikrein or its precursor, or on the B2 receptor. The table lists them by the approval year Drugs@FDA records for each original application:
| Medicine | Application | Approved | Where it acts and what the label names it for |
|---|---|---|---|
| Kalbitor (ecallantide) | BLA 125277 | 2009 | Blocks plasma kallikrein, so less bradykinin is cut from kininogen. A 60-amino-acid protein made in yeast; labelled for acute attacks of hereditary angioedema from age 12. |
| Firazyr (icatibant) | NDA 022150 | 2011 | Blocks the B2 receptor itself. A synthetic decapeptide with five non-proteinogenic amino acids; labelled for acute attacks in adults. Generic icatibant injections are recorded from 2019. |
| Takhzyro (lanadelumab) | BLA 761090 | 2018 | A monoclonal antibody against plasma kallikrein; labelled to prevent attacks, from age 2. |
| Orladeyo (berotralstat) | NDA 214094 | 2020 | A small-molecule plasma kallikrein blocker taken by mouth; labelled to prevent attacks, from age 2, and not for treating an attack. A second application is recorded in 2025. |
| Andembry (garadacimab) | BLA 761367 | 2025 | A monoclonal antibody one step further up, against activated factor XII; labelled to prevent attacks, from age 12. |
| Ekterly (sebetralstat) | NDA 219301 | 2025 | A plasma kallikrein blocker in tablet form; labelled for acute attacks, from age 12. |
| Dawnzera (donidalorsen) | NDA 219407 | 2025 | An antisense oligonucleotide that lowers the liver's production of prekallikrein; labelled to prevent attacks, from age 12. |
Only one of them is a peptide. Icatibant, a synthetic decapeptide, was built to block the B2 receptor with an affinity similar to bradykinin’s own; PubChem gives it the formula C59H89N19O13S and a weight of 1,304.5 (CID 6918173). The table covers Drugs@FDA only; it is not a list of every treatment for the condition.
Sources: Drugs@FDA via openFDA (original approval dates); current U.S. labels for Kalbitor, Firazyr, Takhzyro, Orladeyo, Andembry, Ekterly and Dawnzera (indications, description, mechanism of action); MeSH D054179 and D065094; PubChem CID 6918173. Read 5 November 2026. Doses are not reproduced here; the full list of approved peptides is on our FDA-approved peptides page.
Medibact does not manufacture or sell peptides. We supply USP-grade bacteriostatic water, made in the USA, for research use only, and publish reference material like this page.
Where this sits in the rest of the reference
FAQ
What is bradykinin?
Bradykinin is a peptide of nine amino acids, RPPGFSPFR, that widens small blood vessels and makes them leakier. MeSH, the U.S. National Library of Medicine's subject index, describes it as a potent but short-lived agent of arteriolar dilation and increased capillary permeability, released from damaged tissue as a pain signal and from mast cells and the gut wall. It belongs to the kinins, a family of peptides that act locally, close to where they are made.
What does bradykinin do?
UniProt lists its effects as smooth muscle contraction, a fall in blood pressure, increased salt and water loss through the kidneys, a lower blood glucose level and a role in inflammation: it makes vessels leakier, stimulates pain-sensing nerve endings and triggers the release of other inflammatory mediators such as prostaglandins. MeSH adds that it may also act as a neurotransmitter.
How is bradykinin made?
It is cut out of a larger protein, kininogen-1, by enzymes called kallikreins. UniProt records that plasma kallikrein releases bradykinin from high-molecular-weight kininogen, and that tissue kallikrein releases lysyl-bradykinin, also called kallidin, which has one extra lysine at the front. In kininogen, bradykinin sits at positions 381 to 389, between the heavy chain and the light chain.
What is the difference between bradykinin and kallidin?
One amino acid. Kallidin is KRPPGFSPFR, ten amino acids; bradykinin is RPPGFSPFR, nine. MeSH describes kallidin as a decapeptide bradykinin homologue cleaved from kininogen by kallikreins, and records that bradykinin can be produced from kallidin in the blood. Both act on the same B2 receptor.
What are the bradykinin receptors?
Two G protein-coupled receptors, B1 and B2. MeSH describes B2 as present all the time and specific for intact bradykinin and kallidin, and B1 as induced by inflammation and specific for kinins that have lost their final arginine. UniProt records B2 as found throughout the body, in smooth muscle and neurons, and notes that B1 could be a factor in chronic pain and inflammation.
How is bradykinin broken down, and what has ACE got to do with it?
UniProt records that angiotensin-converting enzyme (ACE) inactivates bradykinin by removing its last two amino acids, Arg-Phe, and that the same enzyme converts angiotensin I. The U.S. label for lisinopril, an ACE inhibitor, states that ACE is identical to kininase, an enzyme that degrades bradykinin, and carries a warning about angioedema. Anyone taking these medicines should raise questions about side effects with their own clinician.
What is the link between bradykinin and hereditary angioedema?
The Firazyr label states that hereditary angioedema is caused by an absence or dysfunction of C1-esterase inhibitor, a key regulator of the factor XII and kallikrein cascade that leads to bradykinin production, and that bradykinin is thought to be responsible for the swelling, inflammation and pain of an attack. Every medicine in the table on this page works at one step of that cascade.
Is icatibant a peptide?
Yes. Its label describes icatibant as a synthetic decapeptide with five non-proteinogenic amino acids, built to block the B2 receptor with an affinity similar to bradykinin's. PubChem gives it the formula C59H89N19O13S (CID 6918173). Drugs@FDA records Firazyr from 2011 and generic icatibant injections from 2019. It is the only peptide among the medicines in the table; ecallantide is a 60-amino-acid protein and the others are antibodies, small molecules or an antisense oligonucleotide.
Is this medical advice?
No. This page explains what bradykinin is, from public scientific and regulatory sources. It gives no dose, schedule or recommendation; anyone treated with these medicines should follow their own clinician and product label. Peptides sold for research are labelled research use only, not for human use. Medibact supplies USP-grade bacteriostatic water, made in the USA, and is not affiliated with any manufacturer of the products named here.
References: UniProt P01042, P03952, P06870, P12821, P30411, P46663; MeSH D001920, D007609, D007705, D016234, D043782, D043783, D054179, D065094, D000799; PubChem CID 439201, 5311111, 6918173; Drugs@FDA via openFDA and the current U.S. labels named above. Read 5 November 2026.
Educational use only — not medical advice. This guide summarizes information reported in published research and community practice for educational purposes. It is not medical advice and not a recommendation to use any compound. Any doses, schedules, or combinations shown are examples of what has been reported, not instructions for you. Many peptides described here are research compounds that are not FDA-approved for the uses discussed and may be investigational or restricted. Effects, risks, and legal status vary; individual needs and results vary. Consult a qualified, licensed healthcare professional before making any decision. Do not use this content to diagnose, treat, or dose yourself.