Faricimab

Specification

• Cat#: THA-0131
• Product Name: Faricimab
• Description: Faricimab is an IgG1-derived bispecific antibody against VEGF-A and Ang-2 for the treatment of age-related macular degeneration and diabetic macular edema.
• Sequences: Not Available
• Molecular Weight: 149000.0 Da (approximate)
• Introduction: Retinal vascular diseases (RVDs) such as diabetic macular edema (DME), age-related macular degeneration (AMD), and retinal vein occlusion (RVO) are typically caused by retinal ischemia and subsequent neovascularization (NV). Vascular endothelial growth factor A (VEGF-A) is a well-known mediator of retinal NV, and many currently approved RVD therapies such as aflibercept and ranibizumab solely target VEGF-A. However, another set of factors, the Tie/Ang axis, comprising the transmembrane Tie-2 receptor and its soluble ligands Ang-1 and Ang-2, has been shown to play critical roles in mediating VEGF-A-induced NV. Faricimab is an IgG1-derived bispecific antibody capable of simultaneously binding to and depleting VEGF-A and Ang-2, which has been developed to improve therapeutic efficacy, especially in patients that respond poorly to anti-VEGF-A monotherapy. Faricimab was approved by the FDA on January 28, 2022, and is currently marketed under the trademark VABYSMO by Genentech, Inc. It received subsequent approval for the same indications in Canada in May 2022. In July 2022, the EMA's Committee for Medicinal Products for Human Use (CHMP) recommended faricimab be granted marketing authorization for the treatment of neovascular age-related macular degeneration and diabetic macular edema.
• Purity: >99% by SDS-Page and HPLC analysis
• Formula: C6506H9968N1724O1026S45
• Appearance: Solid

Pharmaceutical Information

• Pharmacodynamics: Faricimab is a bispecific antibody (bsAb) based on human IgG1 comprising two different heavy and two different light chains capable of simultaneously binding to both VEGF-A and Ang-2. Faricimab suppresses endothelial proliferation, neovascularization, and vascular permeability, which are associated with the increased retinal thickness observed in nAMD and DME. In four phase 3 studies in nAMD and DME, faricimab reduced central subfield thickness through the first year in all treatment arms. As with other medications administered intravitreally, faricimab carries a risk of transient increases in intraocular pressure, endophthalmitis, and retinal detachment. Proper injection techniques should always be observed, and patients monitored carefully following injection. Low risk of arterial thromboembolic events, defined as nonfatal stroke or myocardial infarction and vascular death, has been documented with faricimab.
• Targets: Vascular endothelial growth factor A, long form Angiopoietin-2