Icatibant

Symptomatic patients were predominantly female (86.3% vs 30.8% male, p<0.0001), with a mean age at first attack of 24±12 years.; 49% of HAE-FXII patients were estrogen-dependent versus 0% of HAE-PLG patients (p<0.01).; 91% of HAE-PLG patients received at least one icatibant treatment with 100% efficacy; 67% of HAE-FXII patients were treated at least once (56% icatibant, 54% C1Inh concentrate during pregnancy).; Long-term prophylaxis was used in 12.6% of HAE-FXII and 47.4% of HAE-PLG patients; tranexamic acid rendered 66.7% of HAE-PLG attack-free, and lanadelumab rendered 100% of HAE-FXII asymptomatic.

Icatibant effectiveness in real-world settings is comparable to clinical trials.; One dose is effective for the majority of attacks.; Early treatment, facilitated by self-administration, leads to faster resolution and shorter attack duration.; Effectiveness and safety are demonstrated across diverse patient subgroups, including children/adolescents and elderly patients.

Bradykinin-mediated angioedema is caused by vasodilation and increased vascular permeability from bradykinin, affecting abdominal and upper airways without urticaria.; Main causes include C1 inhibitor deficiency (hereditary or acquired) and drug-induced factors; diagnosis relies on clinical presentation and biological tests (C1-INH level, activity, and C4).; Acute attacks are managed with C1-inhibitor concentrates and icatibant, while long-term prophylaxis is needed before surgical or dental procedures.; New treatments, including gene therapy, are currently being tested.

ACEi-AE prevalence is 0.1-0.7% and shows ethnic predisposition, with higher rates in African-Americans and Hispanics.; Clinical manifestations include edema of face, lips, tongue, uvula, and upper airways, often requiring hospital admission.; Pathogenesis involves bradykinin accumulation from reduced ACE-mediated catabolism, with genetic polymorphisms contributing.; Corticosteroids and antihistamines are ineffective; icatibant shows conflicting efficacy, with benefit in Caucasian but not black patients.

New techniques isolate and purify human-derived C1 inhibitor.; Recombinant C1 inhibitor has been produced.; Drugs targeting the kallikrein-kinin pathway have been developed.; The paper reviews mechanisms, efficacy, and adverse reactions of these treatments.

Four treatments (plasma-derived C1 inhibitor, recombinant C1 inhibitor, ecallantide, icatibant) are effective for all HAE attacks.; All four treatments have been shown to be superior to placebo.; On-demand use is preferred to keep control with the patient and avoid treatment delays.; Treatment options are available in North America, Europe, UK, and Australia, but few exist in developing countries.

What is Icatibant?

**Mechanism of Action** Icatibant is a synthetic decapeptide that acts as a selective, competitive antagonist of the bradykinin B2 receptor. By blocking bradykinin binding, it inhibits downstream signaling pathways (e.g., nitric oxide and prostaglandin release) that mediate vasodilation, increased vascular permeability

How does Icatibant work?

Selective bradykinin B2 receptor antagonist decapeptide approved for acute attacks of hereditary angioedema.

What is the research status of Icatibant?

Icatibant is currently classified as approved, with 777 research references on record. This is for research purposes only and is not medical advice.

What is the molecular weight of Icatibant?

Icatibant has a molecular weight of approximately 1304.5 g/mol (formula C59H89N19O13S).