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.
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
*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
| Adults (n=35) |
Children§ (n=5) |
|
|---|---|---|
| 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.