Clinical efficacy of icatibant in the treatment of acute hereditary angioedema during the FAST-3 trial

Abstract

Bradykinin is the key mediator of symptoms of hereditary angioedema (HAE), a rare genetic disorder characterized by recurrent episodes of edema of the skin, mucosa and muscle. Icatibant, a bradykinin B₂ receptor antagonist, is an effective and generally well-tolerated treatment option for acute attacks of type I and II HAE. A Phase III randomized, double-blind, placebo-controlled study, FAST-3 (NCT00912093), was designed to further evaluate the efficacy and safety of icatibant in patients presenting with moderate to very severe cutaneous and/or abdominal or mild-to-moderate laryngeal symptoms. Severe laryngeal attacks were treated with open-label icatibant. The controlled phase of FAST-3, completed in October 2010 with results published in December 2011, demonstrated that compared with placebo, icatibant evoked clinically meaningful and statistically significant efficacy across multiple end points in the treatment of type I and II HAE attacks. In addition, icatibant was generally well tolerated and no drug-related serious adverse events were experienced.

Keywords::

• acute treatment
• B₂ receptor antagonist
• bradykinin
• FAST-3
• hereditary angioedema
• icatibant
• self-administration

Financial & competinng interests disclosure

The FAST-3 study, part of the clinical trial program of icatibant, was funded by Jerini AG/Shire Human Genetic Therapies, Inc. Study NCT01154361 is also funded by Jerini AG/Shire Human Genetic Therapies, Inc. M Bas¸ has received consulting fees and honoraria from Shire Human Genetic Therapies Inc. and Jerini AG. He has also received consulting fees and honoraria from Viropharma and research funding from CSL Behring and Pharming. The author has no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Medical writing assistance during the preparation of this manuscript was provided by Lucy Johnson, PhD, at Prime Medica Ltd (supported by Shire Human Genetic Therapies Inc.). Responsibility for opinions, conclusions and interpretation of data lies with the author.