Bradykinin dosage and evidence
Written by Aaron CuhaReviewed Sep 2026
The short answer
Bradykinin is a small inflammation signal, not a treatment. It is the reason some blood pressure pills cause a cough and face swelling. Human studies of blood flow and nerve tissue have measured what it does. There is no medical use for giving it.
Evidence grade for Bradykinin: Limited. The rule: people have taken it in a published study, but fewer than 100 of them. The sum on this page: 2 completed trials, 47 people given it. A grade counts how much has been done to people, not whether it works.
- People given it
- 47
- Human studies
- 2
- Found nothing
- 0
Dose
No human dose established
Amounts that were given in studies sit in Human evidence on this page. None of them is a personal dose.
2 completed trials, 47 people given it
2 effects reported, 2 unwanted, by people using it, not a trial
Goal pages: Heart and circulation
In plain English
In plain English, from Aaron
This is how I would explain it to a friend. The evidence, with the numbers, is further down the page.
Bradykinin is a small signal your body makes during swelling and injury. It widens blood vessels, makes them leaky and makes pain nerves touchy. It is why some blood pressure pills cause a cough. Nobody takes it as a treatment.
What people take it for
- Nobody takes it. It shows up in peptide lists because it is famous.
- People look it up to understand the cough and swelling from ACE inhibitor pills.
What studies in people showed
There is no study of giving bradykinin as a treatment. The human studies measure what it does. In 17 people with heart failure on ACE inhibitors, blocking bradykinin tightened blood vessels. So it helps those pills work. In 20 healthy men, blocking it did not change the protection from a tight arm cuff. Human nerve tissue showed it makes pain nerves fire more easily. Swelling from ACE inhibitors hits up to about 0.5 percent of users.
What people report
Reports, not study results
The good
- We have not collected user reports on this one yet.
The bad
- Raised bradykinin is behind the dry cough some people get on ACE inhibitors.
- It is also behind a rare, dangerous swelling of the face and throat on those pills.
Where these come from: No user reports. These come from the blood flow studies, the nerve tissue study and the swelling reviews on this page.
My bottom line
Nobody should be injecting this. If a blood pressure pill gives you a cough or any swelling, tell your doctor. Throat swelling is an emergency.
An opinion, not a finding. I am a coach, not a doctor.
What it has been measured to do
Measured in people
Goals Bradykinin has been tested for in people, biggest studies first. We count only what the studies on this page say, so the real numbers may be higher.
- Heart attacks and strokesno headcount stated · 1 study
35 of the 36 indexed goals have no study of any kind behind Bradykinin
No study in people, animals or cells on this page reports a result for these. That does not prove Bradykinin does nothing for them. It does mean anything you have heard about Bradykinin and one of these did not come from a study cited here.
Show full evidence
What is Bradykinin?
Bradykinin is a small inflammation signal, not a treatment. It is the reason some blood pressure pills cause a cough and face swelling. Human studies of blood flow and nerve tissue have measured what it does. There is no medical use for giving it.
Bradykinin is a small signal, 9 building blocks long. Enzymes release it from a larger protein during inflammation and injury. It widens blood vessels, makes them leaky and makes pain nerves more sensitive. The enzyme ACE destroys it. That is the single most useful fact about it. ACE inhibitors, a common kind of blood pressure pill, lower angiotensin II. As a side effect, they raise bradykinin. That is why they cause a dry cough in a minority of users. It is also why up to about 0.5 percent of users get a dangerous swelling called angioedema.
What we know about bradykinin in people comes from measuring it, not treating with it. Blood flow studies in the forearm used a bradykinin blocker called B9340. In 8 healthy volunteers, bradykinin did not hold resting blood vessel tone. But in 17 people with heart failure on ACE inhibitors, the blocker tightened blood vessels. That stopped when the pills were stopped. So bradykinin helps those pills widen blood vessels. A separate study took 20 healthy men. Each got a bradykinin blocker once and a dummy once. Blocking bradykinin did not remove the protection that comes from squeezing an arm with a cuff first. That goes against a popular idea about how that protection works. Work on nerve tissue from organ donors found bradykinin receptors packed onto pain nerve cells. Bradykinin made those human nerve cells fire more easily. That confirms in human tissue what was first seen in rats and mice.
Bradykinin itself is not a drug and is not approved anywhere for anything. The drug in this family blocks it. That drug is icatibant, and it has its own page.
How does Bradykinin work?
In people, bradykinin works through two receptors. B2 is always there. B1 appears with inflammation. B2 on blood vessel linings releases nitric oxide and prostacyclin. That widens blood vessels and makes them leaky. B2 on pain nerves makes them fire more easily. ACE and other enzymes break bradykinin down within seconds. So blocking ACE both lowers angiotensin II and raises bradykinin. Human nerve tissue confirms that B2 is packed onto pain nerve cells. In that tissue, B1 showed up more in older donors and in donors with a history of long-term pain.
What have studies in people found about Bradykinin?
There is real human data on bradykinin, and none of it is about giving it as a treatment. People have been given bradykinin and bradykinin blockers by drip in careful blood flow tests. Human nerve tissue has been studied directly. And the drug studies that matter are studies of blocking it.
- Forearm blood flow, 8 healthy volunteers and 17 people with heart failure: bradykinin does not hold resting blood vessel tone in healthy people. But it does help blood vessels widen in people on long-term ACE inhibitors. That help disappears when the pills are stopped.
- 20 healthy men, each tested on a blocker and on a dummy: blocking the B2 receptor did not remove the protection from squeezing an arm with a cuff first. That argues against bradykinin as the cause of that effect.
- Nerve tissue from organ donors: B2 receptors are packed onto pain nerve cells, and bradykinin makes human sensory nerve cells fire more easily. This confirms a rat and mouse finding in human tissue.
- Learning by blocking: the face and throat swelling from ACE inhibitors hits up to about 0.5 percent of users. It clears faster when the B2 receptor is blocked with icatibant. That is human evidence that bradykinin causes it.
What this does not tell you: These are small studies that test how the body works, several in healthy volunteers. They measure blood flow and nerve firing, not any health outcome. Nothing here supports giving bradykinin for any reason, and no study has tried. The nerve work used tissue outside the body. It shows what nerve cells do in a dish, not what a person feels.
The state of the research
Bradykinin shows up in peptide catalogues because it is a famous peptide, not because anyone takes it. It belongs here for another reason. It explains two of the most common side effects in all of heart medicine. ACE breaks bradykinin down, so an ACE inhibitor raises it. That is the accepted reason for the ACE inhibitor cough, and for the swelling that sends people to the emergency room.
The field went on to block bradykinin rather than supply it. That is why the drug in this system is a blocker, icatibant. The one place a drug that copies bradykinin was seriously pursued is lobradimil, which was meant to open the barrier around the brain. It is not covered here because we could not confirm a current human record for it. It is worth being exact about where this page stops. There is no published human study of giving bradykinin as a treatment. That is different from saying it was tried and failed.
The evidence, in charts
Fig. 1a · how many people
47people, across 2 studies in people cited here
| Study | People | Share |
|---|---|---|
| New England Journal of Medicine 2015 | 27 | 57% |
| Heart 2011 | 20 | 43% |
One study holds 57% of these people, so the total rests more on one study than its size suggests. Counts are the number of people each study on this page says it signed up. That includes studies that only watched people and gave nobody the compound. 2 more studies in people give no headcount and are not counted here. Studies still signing people up are left out, and only studies cited on this page are counted.
Fig. 1b · evidence mix
4 of 6 sources here are studies in people. The rest are not.
- Study in people · done in people467%
- Review of studies · sums up other studies233%
Counted from the list of sources on this page. It counts only what we cite, so there may be more studies out there. A review counts once, however many studies it sums up.
Fig. 2 · evidence over time
The studies cover 6 different years, 2001 to 2024, counted from the list of sources on this page.
Fig. 3 · legal status at a glance
US
Not approved
UK
Not approved
AU
Not approved
CA
Not approved
Not approved in any of the four countries shown. This is what the law says, not a verdict on the science. See Legal status below for the full text and any notes.
Fig. 4 · how much does what
Nobody has tested different amounts in people
This chart would show how the effect changes as the amount goes up. For this compound, nobody has measured that in people. So we leave it empty. We will not borrow an animal chart and pretend it works the same in people.
Fig. 5 · what the molecule is
- Kind of compound
- Peptide
- Molecule weight
- Not on file
- Half-life
- None on file
- Chain length
- 9 amino acidscounted from the chain below
RPPGFSPFR
- Water-shy 6
- Water-loving 1
- Basic 2
One square per amino acid, left to right from the start of the chain, coloured by type. The type is a fact about the amino acid, not a finding about this compound.
The studies we cite
- Study in people2001Bradykinin contributes to the vasodilator effects of chronic angiotensin-converting enzyme inhibition in patients with heart failure
This showed that bradykinin is part of how blood pressure tablets actually work. Researchers measured blood flow in the forearm while blocking the bradykinin receptor. In 8 healthy volunteers, blocking it stopped the response to injected bradykinin but left resting blood flow alone. In 17 people with heart failure taking ACE inhibitors, blocking it tightened the vessels. That effect vanished when the tablet was stopped and came back when it was restarted. These are small groups, and a forearm is not an outcome.
Forearm plethysmography studies: in 8 healthy volunteers the antagonist B9340 blocked vasodilation to infused bradykinin without changing resting blood flow. In 17 patients with NYHA class II to IV heart failure on chronic ACE inhibitors, B9340 caused dose-dependent vasoconstriction (p = 0.01), which disappeared after the ACE inhibitor was withdrawn and returned when it was restarted.
- Study in people2011Bradykinin does not mediate remote ischaemic preconditioning or ischaemia-reperfusion injury in vivo in man
A popular theory was tested directly in people and it did not hold up. 20 healthy men each took part twice, once on a bradykinin blocker and once on a dummy, and nobody involved knew which was which. Blocking bradykinin did not stop blood vessel damage caused by a short cut in blood supply. It also did not remove the protection that comes from squeezing an arm beforehand. So bradykinin is not the messenger behind that effect. 20 men is small, and they were healthy.
Randomised double-blind crossover study in 20 healthy men. The B2 antagonist HOE-140 did not prevent the impairment of endothelium-dependent vasodilation caused by ischaemia-reperfusion, and did not abolish the protection from remote ischaemic preconditioning. A null result against a widely proposed bradykinin mechanism.
- Study in people2024Bradykinin receptor expression and bradykinin-mediated sensitization of human sensory neurons
Donated human nerve tissue confirmed what rodents had suggested. Researchers examined nerve clusters taken from organ donors and found bradykinin receptors sitting on pain carrying nerve cells and their support cells. Adding bradykinin made those human nerve cells fire more easily. Leaving it on longer calmed a portion of them instead. This is tissue in a dish, not a living person, and nobody was treated. Public money from the National Institutes of Health paid for it.
Human dorsal root ganglion tissue from organ donors. B2 and, less so, B1 receptors were found on sensory neurons and satellite glial cells, with B2 enriched in nociceptors. Patch-clamp recording showed acute bradykinin increases human sensory neuron excitability, while prolonged exposure decreases it in a subpopulation. NIH supported.
- Study in people2015A randomized trial of icatibant in ACE-inhibitor-induced angioedema
Blocking bradykinin cleared the swelling that blood pressure tablets sometimes cause, and it cleared it fast. 27 people whose faces and airways had swollen on an ACE inhibitor got either icatibant or the usual steroid and antihistamine. Swelling settled in about 8 hours on icatibant against about 27 hours on the usual treatment. This is the strongest sign that bradykinin drives that reaction. 27 people is a small trial. Shire, which sells the drug, paid for it. A larger trial later found no benefit.
Phase 2 trial, 27 patients analysed per protocol. Blocking the bradykinin B2 receptor resolved ACE inhibitor angioedema in a median 8.0 hours versus 27.1 hours on prednisolone plus clemastine (p = 0.002). This is the clearest human evidence that bradykinin is the mediator of that reaction. Funded by Shire.
- Review of studies2018Pharmacotherapy for Angiotensin-Converting Enzyme Inhibitor-Induced Angioedema: A Systematic Review
A review of 5 papers covering 218 cases. It says the swelling called angioedema happens in up to 0.5 percent of people on ACE inhibitors, and blames raised bradykinin. In 1 of 2 icatibant studies, swelling improved faster than on steroids plus antihistamines. Two other drugs, ecallantide and C1 inhibitor, showed no clear benefit.
Systematic review of 5 articles covering 218 cases. States that angioedema occurs in up to 0.5 percent of ACE inhibitor users and is attributed to raised bradykinin. Of the treatments tested, 1 of 2 icatibant studies beat corticosteroids plus antihistamines on speed of improvement; ecallantide and C1 inhibitor replacement showed no significant benefit.
- Review of studies2004Bradykinin receptor ligands: therapeutic perspectives
A review of the kinin system and of attempts to make drugs for it. It covers the B1 and B2 receptors, and why the field moved to blockers rather than copies.
Review of the kinin system and of attempts to drug it, covering B1 and B2 receptor pharmacology and why antagonists rather than agonists became the therapeutic direction.
Where to buy Bradykinin
1 seller lists Bradykinin in our latest read. They are ranked by trust score, then by archive rating, then by certificate tier, then by the lowest price per milligram. Archive evidence is counted before source-backed. Each path is out of 4, and the two are not added. A higher price does not raise the score. The letter is the certificate chip. 0 of them have a published certificate that names Bradykinin.
Some seller links may pay this site when you buy through them. A payment never changes a seller's tier or rank, and no seller has a say in any page.
| Seller | Trust score | Vial sizes | From, per mg | Certificate for Bradykinin | Seller link |
|---|---|---|---|---|---|
| Boston Molecules | 28 InsufficientSource-backed 1 of 4. Archive evidence 1 of 4.C | 10 mg | $22.4 | None found for Bradykinin | View |
- LC Lab-confirmed: the issuing laboratory echoed this certificate back
- A Current certificate, independent laboratory named, laboratory not yet checked
- B Certificate published, but no laboratory link, older than a year, or the laboratory did not recognise the published lookup
- C No certificate could be read
Every listing and vial size for Bradykinin · How the trust score is counted
Sellers named on the price pages are ranked by certificate tier, then price, and any affiliate income is disclosed there. Naming a seller is not a recommendation to buy or use anything.
Common questions
Has Bradykinin been tested in people?
Yes. 47 people given it across 2 completed trials cited here, 0 of which found nothing. Bradykinin is a small inflammation signal, not a treatment. It is the reason some blood pressure pills cause a cough and face swelling. Human studies of blood flow and nerve tissue have measured what it does. There is no medical use for giving it.
What is the Bradykinin dosage?
No human dose established. Amounts that were given in studies sit in Human evidence on this page. None of them is a personal dose. 2 completed trials, 47 people given it
Is Bradykinin FDA-approved?
Not an approved drug. Bradykinin is a signal the body makes, and a chemical used in labs. No bradykinin product showed up in our checks of the FDA drug database (Drugs@FDA). The approved medicine that works on this system is icatibant, which blocks bradykinin's B2 receptor.
Can you take bradykinin?
No. There is no bradykinin medicine anywhere. In human studies it is only used as a research tool given by drip, or as the signal that drugs are built to block.
Why do ACE inhibitors cause a cough?
Because ACE, the enzyme these pills block, also destroys bradykinin. Blocking the enzyme raises bradykinin, which makes the nerves in the airway more sensitive. The same thing explains the face and throat swelling from ACE inhibitors. That swelling hits up to about 0.5 percent of users, and it clears faster when the bradykinin B2 receptor is blocked.
Does bradykinin cause pain?
In human nerve tissue, yes. B2 receptors are packed onto pain nerve cells, and bradykinin makes them fire more easily. That finding comes from organ donor tissue. It is not a measure of pain in a living person.
Is bradykinin involved in COVID-19?
It was put forward as a cause and tested by blocking it. A study gave the blocker icatibant to 73 people in hospital with COVID-19 pneumonia, and everyone knew who got it. It missed its main goal. So the bradykinin idea in COVID-19 is still unproven.