Novel VEGFR-2 Kinase Inhibitors as Anticancer Agents: A Review Focusing on SAR and Molecular Docking Studies (2016-2021).
Vishakha SKumari KajalSitanshu MondalSimranpreet K WahanBalak Das KurmiGhanshyam Das GuptaPreeti PatelPublished in: Chemistry & biodiversity (2023)
Cancer growth, annexation, and metastatic spread are all aided by the formation of new blood vessels (angiogenesis). The commencement of the VEGF pathway leads to signal transduction that enhances endothelial cell survival, relocation, and divergence from pre-existing vasculature. The ability of solid malignancies to bloom and spread depends critically on their ability to establish their independent blood circulation (tumor angiogenesis). VEGFR is a major receptor tyrosine kinase that regulates angiogenesis, cell growth, and metastasis, diminishing apoptosis, cytoskeletal function, and other biological processes VEGFR has proven to be a remarkable focus for a variety of anticancer medicines in clinical studies. This Review explores the development of anti-VEGF-based antiangiogenic therapies having different scaffolds. This review had focused on SAR and docking studies of previously reported molecules.
Keyphrases
- vascular endothelial growth factor
- tyrosine kinase
- molecular docking
- endothelial cells
- molecular dynamics simulations
- epidermal growth factor receptor
- case control
- oxidative stress
- squamous cell carcinoma
- small cell lung cancer
- papillary thyroid
- endoplasmic reticulum stress
- single cell
- cell therapy
- cell death
- protein protein
- stem cells
- cell cycle arrest
- squamous cell
- mesenchymal stem cells
- tissue engineering