Brolucizumab

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Brolucizumab
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INN
Drug class
Routes of administration Intravitreal
Pregnancy category
Bioavailability
Metabolism
Elimination half-life
Excretion
Legal status
CAS Number 1531589-13-5
PubChem
DrugBank
ChemSpider none
KEGG D11083


Brolucizumab (INN) is a humanized single-chain antibody fragment designed for the treatment of wet age-related macular degeneration.<ref>Statement On A Nonproprietary Name Adopted By The USAN Council - Brolucizumab, American Medical Association.</ref><ref>World Health Organization,

 International Nonproprietary Names for Pharmaceutical Substances (INN). Proposed INN: List 112, 
 WHO Drug Information, 
 2014,
 Vol. 28(Issue: 4),
 
 
 
 
 
 Full text,</ref>

This drug was developed by ESBATech (discovery to phase 2a), Alcon Laboratories (phase 2b) and Novartis (phase 3).

Laboratory development names are RTH258 (Novartis Compound Code) and ESBA1008 (ESBATech AG).

Brolucizumab successfully completed phase 3 development in wet age-related macular degeneration (AMD) meeting the primary efficacy endpoint of non-inferiority to aflibercept in mean change in best corrected visual acuity (BCVA) from baseline to week 48. Furthermore, brolucizumab demonstrated superiority to aflibercept in key secondary endpoint measures of disease activity in wet AMD, a leading cause of blindness in two head-to-head pivotal Phase III studies.

Whilst brolucizumab was initially developed for ophthalmology, non-ophthalmology indications (to which Cell Medica hold development rights) are also under investigation, under the name DLX1008. DLX1008 is under preclinical development for Kaposi sarcoma<ref name="EasonSin2018">,

 Abstract 4: Antitumor activity of DLX1008, a single chain antibody fragment binding to VEGF-A, in in vivo preclinical models of Kaposi sarcoma and glioblastoma, 
 Cancer Research, 
 2018,
 Vol. 78(Issue: 13 Supplement),
 pp. 4–4,
 DOI: 10.1158/1538-7445.AM2018-4,</ref> and glioblastoma.<ref name="SzabóPhillips2018">, 
 Antitumor Activity of DLX1008, an Anti-VEGFA Antibody Fragment with Low Picomolar Affinity, in Human Glioma Models, 
 Journal of Pharmacology and Experimental Therapeutics, 
 2018,
 Vol. 365(Issue: 2),
 pp. 422–429,
 DOI: 10.1124/jpet.117.246249,</ref>

References

<references/>



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