Vascular endothelial growth factor A


  • Accession: P15692
  • Swissprot: VEGFA_HUMAN
  • Organism: Homo sapiens
  • Gene: VEGFA
  • Target classes: Secreted, Unclassified

Drug Relations:

has antiangiogenic activity; consists of the second and third Ig domains of VEGFR1 and VEGFR2, respectively, fusion to the Fc region of IgG1; putative antineoplastic agent that binds all VEGF-A isoforms; possible medicine for eye disorders Bioactivity details MOA
An anti-VEGF humanized murine monoclonal antibody. It inhibits VEGF RECEPTORS and helps to prevent PATHOLOGIC ANGIOGENESIS. Bioactivity details MOA
Brolucizumab-dbll is a humanized monoclonal single-chain Fv (scFv) antibody fragmentand a human 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. Bioactivity details MOA
a pegylated modified oligonucleotide that binds with high specificity and affinity to extracellular Vascular Endothelial Growth Factor (VEGF165) inhibiting its activity, VEGF is a secreted protein that induces angiogenesis, vascular permeability and inflammation, all of which are thought to contribute to the progression of the neovascular (wet) form of AMD Bioactivity details MOA
A recombinant humanized monoclonal antibody fragment that binds VEGF-A to prevent its binding to VEGFR-1 and VEGFR-2 receptors. This activity reduces vessel permeability and angiogenesis in the treatment of neovascular age-related MACULAR DEGENERATION. Bioactivity details MOA
The N-acetyl derivative of CYSTEINE. It is used as a mucolytic agent to reduce the viscosity of mucous secretions. It has also been shown to have antiviral effects in patients with HIV due to inhibition of viral stimulation by reactive oxygen intermediates. N-Acetylcystene (NAC) as a precursor to the antioxidant glutathione modulates glutamatergic, neurotrophic, and inflammatory pathways. The potential applications of NAC to facilitate recovery after traumatic brain injury, cerebral ischemia, and in treatment of cerebrovascular vasospasm after subarachnoid hemorrhage. Bioactivity details MOA