Bradykinin_Dosage, benefits & legal status
Also known as BK, Kallidin I, Bradykinin (1-9)
The reason a common blood pressure drug makes you cough.
Common vial size is what vendors typically sell, not a recommendation. Enter your own vial in the calculator.
What is Bradykinin?
Plain language first. The technical label stays, but it never stands alone.Overview
Nothing you would take. Bradykinin is on this site because it explains things readers actually encounter. If you take an ACE inhibitor such as lisinopril or ramipril for blood pressure, the enzyme that drug blocks is also the enzyme that destroys bradykinin. Block the enzyme and bradykinin builds up, and the result is the persistent dry cough that is among the most common reasons people stop taking these drugs, and in rarer cases sudden facial or throat swelling. The same peptide is the target of icatibant, a drug already on this site: icatibant works by blocking bradykinin's B2 receptor to stop hereditary angioedema attacks. Understanding bradykinin is what makes both of those make sense.
Bradykinin is a nine amino acid peptide, residues 381 to 389 of the 644 amino acid kininogen-1 precursor, reading RPPGFSPFR. The related kallidin, or lysyl-bradykinin, is residues 380 to 389 and adds a single N-terminal lysine. Bradykinin acts at two receptors, B1 and B2, and through B2 it produces vasodilation, increased vascular permeability, pain and the tissue swelling characteristic of angioedema. It is degraded by angiotensin-converting enzyme, whose alternative name is kininase II, in a reaction cleaving the C-terminal dipeptide to give bradykinin(1-7). That single fact explains two of the best known adverse effects in cardiovascular medicine. It is not a therapeutic and has no approval anywhere.
What it's used for
Nothing. It has no approval anywhere and is not used as a treatment. It has been given to humans only in small physiology studies, typically infused into an artery to study local blood vessel responses or injected to study pain.
How does Bradykinin work?
What it does in the body, and where.Bradykinin is best understood through the enzyme that destroys it, because that is where it touches ordinary medicine.
- 01Where it comes fromBradykinin is cut out of kininogen-1, a 644 amino acid precursor, at residues 381 to 389. The resulting peptide is nine residues long and reads RPPGFSPFR. Kallidin, also called lysyl-bradykinin, is the same chain with one extra lysine at the front, residues 380 to 389. The kallikrein enzymes do the cutting, and in hereditary angioedema that cutting runs out of control, and that is why drugs for that condition target either the kallikrein or the receptor.
- 02One enzyme, two famous side effectsAngiotensin-converting enzyme is best known for making angiotensin II and raising blood pressure, and ACE inhibitors are prescribed to block it. The reference database for that enzyme lists kininase II among its names and records that it also inactivates bradykinin, a potent vasodilator, cleaving the terminal two residues to leave bradykinin(1-7). So an ACE inhibitor does two things at once: less angiotensin II, and more bradykinin. The extra bradykinin is the accepted explanation for the dry persistent cough these drugs cause, and for the rarer angioedema. A reader who knows this understands why switching to an angiotensin receptor blocker usually resolves the cough: those drugs block the receptor downstream and leave the enzyme alone, so bradykinin is still cleared normally.
- 03Two receptors, and the one drugs aim atBradykinin signals through B1 and B2 receptors. B2 is the one present under normal conditions and the one responsible for vasodilation, vascular leak and swelling, and it is the target icatibant blocks. B1 is induced during inflammation and tissue injury. A claim about bradykinin without saying which receptor is involved is incomplete.
- 04Why there is no bradykinin productEverything bradykinin does is something medicine wants less of: pain, leaky vessels, swelling. There is no therapeutic reason to administer it, and the entire drug development effort around it has gone into blocking it or blocking its production. That is why this page has no dose, no supplier and no protocol, and that is the answer for anyone who finds the peptide listed by a reagent company and wonders what it is for.
What else is it used for?
Each group carries its own evidence level.Approved means regulators have cleared it for that purpose. Investigational means it is in trials. Early research means it is being studied and is not established.
Why it matters to people taking common medication
Clinical use- lab-analysisThe reference entry for angiotensin-converting enzyme lists kininase II among its names and records that it inactivates bradykinin, cleaving it to bradykinin(1-7).
- ReviewBlocking that enzyme with an ACE inhibitor raises bradykinin levels, and that accumulation is the accepted explanation for the dry cough associated with the drug class and for its rarer angioedema.
- ReviewAngiotensin receptor blockers act downstream of the enzyme and leave bradykinin clearance intact, and that is why switching usually resolves the cough.
The approved drug targets it by blocking it
FDA-approved- RegulatoryIcatibant's label describes it as a selective, competitive inhibitor of the bradykinin B2 receptor, dosed at 30 mg subcutaneously for acute hereditary angioedema attacks.
- No dataNo approved product supplies bradykinin. Every drug on this pathway blocks either the peptide's receptor or its production.
A naming mismatch worth knowing
none- No dataThe reference database annotates T-kinin at fourteen residues, ISLMKRPPGFSPFR. Suppliers commonly sell an eleven-residue peptide under that name. The two are not the same molecule.
The most useful correction here is not about bradykinin itself but about the cough. People told that an ACE inhibitor cough is an allergy or an unexplained side effect are missing a well-characterized mechanism: the enzyme the drug blocks is the same enzyme that clears bradykinin, so bradykinin accumulates. That also explains why switching to an angiotensin receptor blocker generally fixes it, and why the swelling form of the reaction is treated with a bradykinin receptor blocker rather than with antihistamines or epinephrine the way an allergic reaction would be. Beyond that, bradykinin and kallidin differ by a single lysine and are sometimes used interchangeably when they should not be. The reference sequence for T-kinin is fourteen residues and does not match the eleven-residue peptide sold under that name, so a supplier listing and a database entry can disagree about what T-kinin even is.
The published record
Papers and trials about Bradykinin
Searched: bradykinin angioedema, bradykinin cough, bradykinin ACE inhibitor, bradykinin B2 receptor, kininase II.
Left out: bradykinin (the bare name returns on the order of tens of thousands of records across vascular physiology, pain and inflammation, far beyond the clinical questions this card answers); kinin (a broader family term); icatibant (has its own slug; this card is the mechanism page behind it); kallikrein (the upstream enzyme family, with its own large literature and its own drugs); T-kinin (unreliable as a search term: the reference database annotates T-kinin as fourteen residues while suppliers sell an eleven-residue peptide under that name, so the term does not identify one molecule); angiotensin (an enormous cardiovascular literature that overlaps only at the enzyme).
290 papers tagged human · 169 not reviews or lab · 15 clinical trial publications
25 registered trials · 5 with posted results
Furthest stage reached: Published trials only, 15 clinical trial publications, no phased trial registered
Counted from Europe PMC indexing, not read by a person; a human tag can land on reviews, commentary or lab papers; clinical trial publications is the narrower count. 477 papers and 25 trials indexed in detail.
At a glance
Four things to know about Bradykinin
How much, and do you cycle it?
The range, and whether you take breaks.No established dose, not applicable. Not applicable No range
There is no approved product and no established route of use, so no cycling scheme exists.
Under a minuteNo figure
Bradykinin is cleared very rapidly in the circulation, principally by angiotensin-converting enzyme. We did not find a specific measured human half-life figure in the sources read for this page, so no number is plotted. The rapid clearance is itself the mechanistically important point, since blocking the enzyme that performs it is what produces the ACE inhibitor cough.
You can compare this against the whole library to see where it sits.
What does it cost?
Typical dose and cost, in plain numbers.Bradykinin is not injected in the forms covered here
It is not taken as a treatment.
How do you store it?
Before mixing, and after.Nothing to store: it is not taken as a treatment.
Bradykinin is not used as a medicine or a supplement, so no home storage question arises. Laboratory suppliers ship research material frozen and state their own handling conditions on the certificate that comes with it.
What are the side effects and cautions?
Known cautions and warnings for this compound.Solubility, computed: 44% charged residues, 56% hydrophobic. Water usually sufficient.
A first-pass rule from peptide manufacturers' guidance. It does not account for disulfide bridges, salt form or how the powder was dried, and it predicts what should be easy rather than what will happen in your vial.
Who should avoid it
- Any use at all: there is no approved product, and the therapeutic direction on this system is to block bradykinin rather than supply it
- Confusing it with the vendor product sold as T-kinin, since the reference database range for T-kinin does not match the peptide commonly sold under that name
Stop and get help
- Not applicable as a treatment. If you take an ACE inhibitor and develop sudden swelling of the face, lips, tongue or throat, that is an emergency and needs immediate medical attention.
Common effects
- Nothing established as a treatment. In physiology studies, local vasodilation and pain at the site.
Where this page says nothing is established, that means nobody has studied it, not that a compound is safe.
Is Bradykinin approved?
And where the numbers on this page come from.No. Bradykinin is not approved for any use, anywhere. It is sold labeled for laboratory research only, and there is no legal route to buy it for human use.
- Approval statusResearch only
- RouteNot taken as a treatment
- Checked26 October 2026
- DoseNo dose has been established in people.
- Vial sizeFrom what vendors typically list; not a recommendation.
- Sources
What has happened recently
Not approved anywhere, and the drugs built on this system all oppose it. Icatibant, marketed as Firazyr and already covered on this site, is described in its own prescribing information as a selective, competitive inhibitor of the bradykinin B2 receptor, given at 30 mg by subcutaneous injection into the abdomen for acute attacks of hereditary angioedema, with no more than three doses in 24 hours. Berotralstat works further upstream on the same pathway. Bradykinin itself is a research reagent. Note the pattern across several pages on this site: for bradykinin, for substance P and for angiotensin, the licensed medicine is an antagonist or an enzyme inhibitor, never the peptide.
You can compare this against the whole library, or read how to check a seller.
What else is like Bradykinin?
Others in Healing and recovery, side by side.If you're weighing Bradykinin, it's worth reading Calcitonin (salmon), Canvuparatide, and Cerluten in the same class.
The reason a common blood pressure drug makes you cough.
- Dose
- No established dose
- How often
- Not applicable
A bone hormone borrowed from salmon, and the weakest option in its own category.
- Dose
- Set by the label
- How often
- Daily, by spray or injection
Parathyroid hormone fitted with fatty tails and a self-releasing cap so one injection lasts a week. Phase 3 started in August 2026.
- Dose
- 400 to 1,600 mcg once weekly (phase 3 range; 600 mcg for the first 4 weeks)
- How often
- Once weekly
A bioregulator for brain and nerve support, with thin evidence.
- Dose
- Varies (course-based)
- How often
- Courses
Guides for this compound
- How to Reconstitute a Peptide
Mix peptide powder with bacteriostatic water, step by step.
- How to Read an Insulin Syringe
Read the units, convert to millilitres, and draw the exact dose.
- mcg vs mg: The Peptide Dosing Mistake to Avoid
Your vial says mg and your protocol says mcg. Here is the conversion and how to check it.
- How to Read a Peptide COA
What the purity number does and does not tell you, and how to spot an edited report.
- How to Vet a Peptide Vendor
Independent COAs, HPLC purity, and the red flags that mean walk away.
Sources
- UniProt P01042, human kininogen-1(2026)The reference sequence record, read positionally from the full sequence rather than taken from a summary. The precursor is 644 amino acids. Bradykinin, listed as Kallidin I, is annotated at residues 381 to 389, and counting the sequence out gives RPPGFSPFR, nine residues. Lysyl-bradykinin, Kallidin II, is residues 380 to 389, giving KRPPGFSPFR, ten residues. One discrepancy is worth recording: T-kinin is annotated at residues 376 to 389, counting out to ISLMKRPPGFSPFR, fourteen residues, and that does not match the eleven-residue peptide commonly sold by suppliers under the name T-kinin. The mismatch does not affect bradykinin or kallidin, and T-kinin is therefore left off this page.
- UniProt P12821, human angiotensin-converting enzyme(2026)The source of the link between ACE inhibitors and bradykinin, read directly. The entry lists Kininase II among the enzyme's alternative names. Its function comment states that it is also able to inactivate bradykinin, a potent vasodilator, and therefore enhance the blood pressure response. The catalytic activity is recorded as bradykinin plus water giving L-Phe-L-Arg plus bradykinin(1-7), so the enzyme removes the terminal two residues. This is the mechanism behind the cough and the angioedema associated with this drug class.
- Firazyr (icatibant) prescribing information(2026)The label for the approved drug that acts on this peptide. States the mechanism verbatim as a selective, competitive inhibitor of the bradykinin B2 receptor. Indicated for acute attacks of hereditary angioedema in adults aged 18 and older, at 30 mg as a subcutaneous injection into the abdomen, repeatable after six hours if the response is inadequate or symptoms recur, with no more than three doses in 24 hours. Cited to establish both the receptor involved and the therapeutic direction.
Beyond these, 502 records are indexed. Browse the records