Icatibant (Firazyr) Dosage Calculator
Icatibant is a synthetic decapeptide containing five non-natural amino acids, designed as a highly selective competitive antagonist of the bradykinin B2 receptor.
30mcg · Single dose
Summary: Add 0mL BAC water to your 30mg vial. Draw to < 0.1 units on a U-100 syringe for a 30mcg dose. This vial will last 0 doses.
Cycle Planner
Icatibant (Firazyr) Pharmacokinetics
Pharmacokinetics — Active Dose Over Time
t½ = ~1-2 hoursDisclaimer: This curve is a simplified first-order exponential decay model. Actual pharmacokinetics vary based on injection site, individual metabolism, body composition, and other factors. Half-life values are approximate and based on available preclinical and clinical literature. Many research peptides lack formal human pharmacokinetic studies. This is for educational purposes only — not medical advice.
Icatibant (Firazyr) Dosing Protocol
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 30mg | Single dose |
| Moderate | 30mg | Single dose |
| Aggressive | 30mg | Single dose |
Note: Icatibant (Firazyr) is an FDA-approved synthetic decapeptide (H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Tic-Oic-Arg-OH) that acts as a selective and competitive antagonist of the bradykinin B2 receptor. It is supplied as a 30 mg/3 mL pre-filled syringe for subcutaneous self-injection during acute hereditary angioedema (HAE) attacks in adults 18 years and older. Icatibant was the first bradykinin B2 receptor antagonist approved for HAE, receiving EMA approval in 2008 and FDA approval in 2011. The recommended dose is 30 mg SC injected in the abdominal area. If symptoms persist or recur, additional 30 mg doses may be administered at intervals of at least 6 hours, with a maximum of 3 injections (90 mg) per 24-hour period. No reconstitution or dilution is required.
About Icatibant (Firazyr)
Icatibant is a synthetic decapeptide containing five non-natural amino acids, designed as a highly selective competitive antagonist of the bradykinin B2 receptor. Developed by Jerini AG (later acquired by Shire, now part of Takeda), it was specifically engineered to block the pathological effects of excessive bradykinin signaling that drives the edema characteristic of hereditary angioedema (HAE). HAE is a rare autosomal dominant disorder caused by deficiency or dysfunction of C1-esterase inhibitor (C1-INH), which leads to uncontrolled activation of the contact system and overproduction of bradykinin. Bradykinin binds the constitutive B2 receptor on vascular endothelial cells, triggering vasodilation and increased vascular permeability that manifests as unpredictable, potentially life-threatening episodes of subcutaneous and submucosal swelling affecting the extremities, face, gastrointestinal tract, and most dangerously, the larynx. Icatibant competes directly with bradykinin for B2 receptor binding with high affinity (Ki ~0.7 nM), effectively blocking the downstream signaling cascade responsible for endothelial gap formation and plasma extravasation. Its incorporation of non-natural amino acids — including D-Arg, hydroxyproline (Hyp), thienylalanine (Thi), D-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid (D-Tic), and octahydroindole-2-carboxylic acid (Oic) — confers resistance to enzymatic degradation by ACE and other peptidases, giving it a dramatically longer half-life (~1-2 hours) compared to the natural bradykinin substrate (~15-30 seconds). In the pivotal FAST-3 trial (NCT00912093), icatibant demonstrated statistically significant superiority over placebo in time to onset of symptom relief for cutaneous and abdominal HAE attacks, with a median time to clinically significant relief of approximately 2 hours. The drug has since become a standard of care for acute HAE management alongside C1-INH replacement therapies and kallikrein inhibitors.