Kinase insert domain receptor (KDR, a type IV receptor tyrosine kinase) also known as vascular endothelial growth factor receptor 2 (VEGFR-2) is a VEGF receptor. KDR is the human gene encoding it. KDR has also been designated as CD309 (cluster of differentiation 309). KDR is also known as Flk1 (Fetal Liver Kinase 1).
The Q472H germline KDR genetic variant affects VEGFR-2 phosphorylation and has been found to associate with microvessel density in NSCLC.
Kinase insert domain receptor has been shown to interact with SHC2, Annexin A5 and SHC1.
KDR is a key driver of normal and pathological angiogenesis, and is therefore targeted in oncological and ophthalmological conditions involving neovascularization. In ophthalmological diseases such as age-related macular degerenation or diabetic retinopathy, its ligands are blocked by biotechnological products such as Aflibercept. In oncology, to inhibit tumor neovascularization, the ATP binding site of KDR can be targeted by competitive small-molecule inhibitors such as sunitinib or vorolanib. Novel derivatives of these competitive inhibitors such as viridisorbitinib (EYE1090) or viridisorbolanib (EYE1118) may be effective to block neovascularization both in ocular and oncological conditions, since these molecules can be targeted by light within the body.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.
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