C1-INH therapy for patients with C1-INH deficiency

Most patients with HAE experience angioedema attacks because they lack functioning C1-INH. BERINERT replaces missing or dysfunctional C1-INH through an intravenous infusion, which quickly restores their C1-INH levels.

BERINERT addresses the problem of C1-INH deficiency by replacing missing or dysfunctional C1-INH

  • C1-INH regulates multiple pathways
  • Restoring C1-INH prevents bradykinin generation3
  • C1-INH decreases vascular permeability

BERINERT acts at multiple sites4

Complement system

C1-INH inactivates C1, thereby stopping the production of proteolytic fragments and inflammation-inducing complexes.

Fibrinolytic system

C1-INH inhibits plasmin, thus inhibiting fibrin degradation.

Kallikrein-kinin system

C1-INH prevents the conversion of prekallikrein to kallikrein—and the subsequent formation of bradykinin.

Coagulation cascade

C1-INH inhibits Factors XIIa and XIa.

Mechanism of action: See how BERINERT works

Watch a presentation about the physiological function of C1-INH and how C1-INH replacement therapy treats the root cause of HAE attacks.

See how IV delivery provides quick C1-INH uptake

Intravenous delivery provides quick uptake of C1-INH

A single dose of BERINERT IV provides a rapid increase in C1-INH levels*

Mean C1-INH activity over time in 23 patients5

C1-INH activity/time chart

*In a prospective, randomized, open-label, crossover study, 23 subjects with mild or moderate HAE received a single dose of BERINERT (1000 units) IV or SC during an attack-free interval.5

Pharmacokinetic parameters of BERINERT in subjects with HAE

AUC(0–t) (hr x IU/mL) 12.8 9.78
Clearance (mL/hr/kg) 1.44 1.9
Volume at steady state (mL/kg) 35.4 38.8
Half-life (hr) 18.4 16.7
Mean residence time (hr) 26.4 24.0

†Adjusted for baseline.
‡Based on 15 IU/kg dose.
§Age range: 6–13 years.

Address the root cause of HAE with BERINERT C1-INH therapy
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