Peptide Schedule
Bradykinin9 residuesRPPGFSPFREach bubble = one amino acid. Size = residue mass. Color = chemical class.Bradykinin Dosage Calculator
Bradykinin is a 9-amino-acid vasoactive peptide (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) generated through the enzymatic cleavage of high-molecular-weight kininogen (HMWK) by the serine protease kallikrein.
25mcg · Daily
Summary: Add 2mL BAC water to your 1mg vial. Draw to 5.0 units on a U-100 syringe for a 25mcg dose. This vial will last 40 doses.
Cycle Planner
Bradykinin Pharmacokinetics
Bradykinin Dosing Protocol
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 25mcg | Daily |
| Moderate | 50mcg | Daily |
| Aggressive | 100mcg | Daily |
Note: Bradykinin is an endogenous 9-amino-acid peptide (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) of the kallikrein-kinin system. It is one of the most potent endogenous vasodilators known and plays central roles in inflammation, pain signaling, vascular permeability, and blood pressure regulation. Due to its extraordinarily short half-life of approximately 15-30 seconds — rapidly degraded by kininase II (ACE) and kininase I — exogenous administration for therapeutic purposes is extremely challenging. Most clinical strategies targeting this pathway involve either ACE inhibitors (which raise endogenous bradykinin levels) or B2 receptor antagonists like icatibant (for hereditary angioedema). Direct bradykinin administration remains strictly a research tool for studying vascular physiology, pain mechanisms, and inflammation. Handle with appropriate caution given its potent hypotensive and pro-inflammatory effects.
About Bradykinin
Bradykinin is a 9-amino-acid vasoactive peptide (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) generated through the enzymatic cleavage of high-molecular-weight kininogen (HMWK) by the serine protease kallikrein. First isolated and characterized by Maurício Rocha e Silva and colleagues in 1949, its name derives from the Greek "bradys" (slow) and "kinein" (to move), referring to its slow contraction of smooth muscle. Bradykinin is a central mediator of the kallikrein-kinin system (KKS), one of the most important vasoactive pathways in human physiology. It acts primarily through two G-protein coupled receptors: the constitutively expressed B2 receptor and the inducible B1 receptor, which is upregulated during tissue injury and inflammation. Through the B2 receptor, bradykinin triggers potent vasodilation by stimulating endothelial nitric oxide synthase (eNOS) and prostacyclin (PGI2) release, producing profound effects on vascular tone and blood pressure. Bradykinin is rapidly degraded in vivo by angiotensin-converting enzyme (ACE, also known as kininase II), which cleaves it into inactive fragments. This relationship between ACE and bradykinin is clinically significant — ACE inhibitors, among the most widely prescribed cardiovascular drugs, exert part of their therapeutic benefit by preventing bradykinin degradation, thereby augmenting its vasodilatory effects. The peptide also plays a critical role in hereditary angioedema (HAE), where deficiency of C1-inhibitor leads to excessive bradykinin generation and severe episodic swelling. This has led to the development of the B2 receptor antagonist icatibant (Firazyr) as an FDA-approved treatment for HAE. Bradykinin has been implicated in the dry cough side effect of ACE inhibitors, allergic responses, pain sensitization, and more recently in the proposed "bradykinin storm" hypothesis related to severe inflammatory respiratory conditions.