General Information

Beovu (brolucizumab-dbll) is a human vascular endothelial growth factor (VEGF) inhibitor.

Beovu is specifically indicated for the treatment of Neovascular (Wet) Age-related Macular Degeneration (AMD).

Beovu is supplied as a solution for intravitreal injection. The recommended dose is 6 mg (0.05 mL of 120 mg/mL solution) administered by intravitreal injection monthly (approximately every 25-31 days) for the first three doses, followed by 6 mg (0.05 mL) by intravitreal injection once every 8-12 weeks.

Clinical Results

FDA Approval

The FDA approval of Beovu was based on the phase 3 HAWK and HARRIER trials. The 96-week prospective, randomized, double-masked multi-center studies were designed to compare the efficacy and safety of intravitreal injections of brolucizumab 6 mg (HAWK and HARRIER) and 3 mg (HAWK only) versus aflibercept 2 mg in patients with wet AMD. The trials enrolled over 1,800 patients across nearly 400 centers worldwide. In both trials patients on Beovu achieved vision gains that were non-inferior to Regeneron’s Eylea (aflibercept) at year one with longer treatment intervals in a majority of patients. In both clinical trials, approximately 30% of patients gained at least 15 letters at year one. Beovu showed greater reduction in central subfield thickness (CST) as early as week 16 and at year one, and fewer patients had intra-retinal (IRF) and/or sub-retinal fluid (SRF). Retinal fluid is a key marker of disease activity. In both trials eligible patients could be maintained on a three-month dosing interval immediately after the loading phase. At year one, over half of patients were maintained on the three-month dosing interval (56% in HAWK and 51% in HARRIER). The remaining patients in the study were treated on a two-month dosing schedule.

Mechanism of Action

Beovu (brolucizumab-dbll) is a human vascular endothelial growth factor (VEGF) inhibitor. Brolucizumab binds to the three major isoforms of VEGF-A (e.g., VEGF110, VEGF121, and VEGF165), thereby preventing interaction with receptors VEGFR-1 and VEGFR-2. By inhibiting VEGF-A, brolucizumab suppresses endothelial cell proliferation, neovascularization, and vascular permeability.