1st and only HAE treatment indicated for use in pediatrics. Learn more ►
Berinert on demand is an essential part of your treatment plan.

Help your patients take control with the only approved C1-INH treatment for acute HAE attacks in adult and pediatric patients.

Mechanism of Action and Therapy Features Berinert replaces the missing C1-INH protein in multiple pathways, regulating and preventing the generation of bradykinin.6, 12

See how Berinert inhibits the reuptake of bradykinin at multiple pathways, differing from other non-C1-INH therapies.

It has been postulated that increased vascular permeability and the clinical manifestation of HAE attacks may be primarily mediated through contact system activation. Regulation of contact system activation by C1-INH through the inactivation of plasma kallikrein and factor XIIa is thought to modulate this vascular permeability by preventing the generation of bradykinin, a potent mediator of vascular permeability.

C1-INH exerts its effect by acting as a brake on target proteases in multiple systems, including the complement system, kallikrein-kinin system (KKS), fibrinolytic system, and coagulation cascade. By preventing the initial fall of various “dominoes” early in these cascades, C1-INH inhibits the production of bradykinin that occurs downstream in the KKS. Without this regulation, individuals with hereditary angioedema develop spontaneous episodes of localized cutaneous or mucous membrane edema.5, 6, 12

Taking a closer look, C1-INH has a reactive loop, which attracts and traps the target protease. Once the protease is trapped, the chain is cleaved and the C1-INH molecule springs closed, forming a covalent bond with the enzyme.5

Berinert Clinical Overview - Mechanism of Action Chart

Understanding the Role of C1-INH in the Treatment of HAE

Kalbitor® (ecallantide) binds to the plasma kallikrein system and blocks its binding site, inhibiting the conversion of high molecular weight (HMW) kininogen to bradykinin. By directly inhibiting plasma kallikrein, Kalbitor reduces the conversion of HMW kininogen to bradykinin and thereby treats symptoms of the disease during acute episodic attacks of HAE.13

Firazyr® (icatibant) is a competitive antagonist selective for the bradykinin B2 receptor, with an affinity similar to bradykinin. Icatibant inhibits bradykinin from binding to the B2 receptor and thereby treats the clinical symptoms of an acute, episodic attack of HAE.14

Save on Co-Pays: The Berinert Co-Pay BENefit™ may cover up to $12,000 of your eligible out-of-pocket expenses per year.

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Efficacy and Safety

Berinert has proven efficacy and safety, alleviating symptoms of acute abdominal, facial, and laryngeal attacks of hereditary angioedema.

Home About Berinert Clinical Overview

Important Safety Information

Berinert®, C1 Esterase Inhibitor (Human), is a plasma-derived concentrate of C1 Esterase Inhibitor (Human), indicated for the treatment of acute abdominal, facial or laryngeal attacks of hereditary angioedema (HAE) in adult and pediatric patients. The safety and efficacy of Berinert for prophylactic therapy have not been established.

Berinert is contraindicated in individuals with a history of life-threatening systemic reactions to C1 esterase inhibitor preparations (including anaphylaxis).

Monitor patients for early signs of allergic or hypersensitivity reactions (including hives, generalized urticaria, chest tightness, wheezing, hypotension, and anaphylaxis). If hypersensitivity is suspected, immediately discontinue administration of Berinert and initiate appropriate treatment. Epinephrine should be immediately available for treatment of acute severe hypersensitivity reactions.

Serious arterial and venous thromboembolic (TE) events have been reported following administration of recommended doses of C1 Esterase Inhibitor (Human) products to patients with HAE. Risk factors may include presence of an indwelling venous catheter/access device; prior history of thrombosis; underlying atherosclerosis; use of oral contraceptives or certain androgens; morbid obesity; and immobility. Weigh benefits/risks before administering to patients with known risk factors for TE events and closely monitor such patients during and after Berinert administration. TE events also have been reported with C1 Esterase Inhibitor (Human) products when used for unapproved indications at higher than recommended doses.

Appropriately trained patients may self-administer Berinert upon recognition of an HAE attack. Advise patients to seek medical attention immediately following selfadministration for laryngeal attacks, and to seek medical attention if progress of any attack makes them unable to properly prepare or administer dose of Berinert.

Berinert is derived from human plasma. The risk of transmission of infectious agents, including viruses and theoretically, the agents of Creutzfeldt-Jakob Disease (CJD) and its variant form (vCJD), cannot be completely eliminated.

The most serious adverse reaction reported in subjects who received Berinert in clinical studies was an increase in severity of pain associated with HAE. Dysgeusia was the most common adverse reaction reported in over 4% of subjects and more frequently than in the placebo group.

Berinert has not been evaluated in pregnant women or nursing mothers, and should be used only if clearly needed. In clinical trials, the half-life of Berinert was shorter and clearance was faster in children than in adults; the clinical implication of this difference is not known.

Please see full prescribing information for Berinert, including the patient product information.

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© 2017 CSL Behring. The product information presented on this site is intended for US residents only. BRN/03-13-0059(1)d