brolucizumab

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brolucizumab

GtoPdb Ligand ID: 8713

Synonyms: Beovu® | brolucizumab-dbll | ESBA-1008 | ESBA1008 | RTH258

brolucizumab is an approved drug (FDA (2019), EMA (2020))

Comment: Brolucizumab is a single-chain variable fragment (scFv) anti-VEGF antibody targeting vascular endothelial growth factor A (VEGFA). This immunobinder was derived from a humanised anti-VEGFA rabbit monoclonal [2].
Peptide sequence and secondary structural information are available from brolucizumab's IMGT/mAb-DB record.
Peptide sequence alignment analysis of patented peptide sequences using the heavy chain variable region of brolucizumab identifies a 100% match with SEQ ID NO: 164 in patent US8349322 B2 [1].

Following regulatory approval brolucizumab took its place as a wet age-related macular degeneration therapy alongside aflibercept (Eylea®) and ranibizumab (Lucentis®), which were previously the main drugs used for this indication. However, with patent protection for both of these older dugs due to expire in the next 2-5 years [4], brolucizumab will likely face competition from aflibercept and ranibizumab biosimilars.

No information available.

No information available.

Summary of Clinical Use
Outcomes from Phase 3 studies that compared brolucizumab therapy to treatment with the VEGF trap agent aflibercept, were published in April 2019 [3]. Brolucizumab was found to be non-inferior to the comparator agent and overall safety was similar to aflibercept, but brolucizumab produced more favourable anatomical outcomes. FDA approval was granted in October 2019 for the treatment of wet age-related macular degeneration (AMD).

Summary of Clinical Use

Outcomes from Phase 3 studies that compared brolucizumab therapy to treatment with the VEGF trap agent aflibercept, were published in April 2019 [3]. Brolucizumab was found to be non-inferior to the comparator agent and overall safety was similar to aflibercept, but brolucizumab produced more favourable anatomical outcomes. FDA approval was granted in October 2019 for the treatment of wet age-related macular degeneration (AMD).

Mechanism Of Action and Pharmacodynamic Effects
Intraocular administration of anti-VEGF agents inhibits the aberrant vascularisation in AMD which results from overexpression of VEGF, thereby controlling or slowing disease progression.

Mechanism Of Action and Pharmacodynamic Effects

Intraocular administration of anti-VEGF agents inhibits the aberrant vascularisation in AMD which results from overexpression of VEGF, thereby controlling or slowing disease progression.