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VEGFR-3vascular endothelial growth factor C/D receptor
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In addition, to clarify the mechanisms of antitumor and antimetastatic actions through lymph nodes, we examined the effects of wogonin on VEGFR-3 expression and VEGF-C-induced the phosphorylation of VEGFR-3 in lymphatic endothelial cells, on VEGF-C and hypoxia inducible factor (HIF-l[alpha]) expression in LM8 cells, and on cyclooxygenase (COX)-2 and cytokine production in macrophages.
Importantly, the authors showed that combined use of antibodies blocking growth factor binding VEGFR-3 dimerization provided not only an additive, but also a synergistic inhibition.
inhibits FLT-3, KIT, VEGFR-1, VEGFR-2, VEGFR-3, PDGFR-[alpha], PDGFR-[beta], CSF1-R, RET
Sorafenib tosylate (Nexavar; Bayer Pharmaceuticals, West Haven, CT, and Onyx Pharmaceuticals, Richmond, CA) is an oral, bi-aryl urea molecule that was designed as a c-Raf and b-Raf kinase inhibitor but was also found to inhibit several receptor tyrosine kinases, including VEGFR-1, VEGFR-2, VEGFR-3, PDGFR-[beta], Flt3, and c-kit (36-40).
According to the most recent findings, VEGFR-3 halts angiogenesis (blood vessel growth) by acting as a "sink" to bind or neutralize the growth factors sent by the body to stimulate the spread of blood vessels.
VEGF-C and VEGF-D are also the only known proteins to bind and activate VEGFR-3 which drives lymphatic vessel and tumour-associated blood vessel growth.
Specific targets include insulin-like growth factor-1 receptor (IGF-1R), vascular endothelial growth factor receptor-1 (VEGFR-1), VEGFR-2, VEGFR-3, platelet-derived growth factor receptor alpha (PDGFR[eth]), FMS-like tyrosine kinase 3 receptor (FLT3), fibroblast growth factor receptor 3 (FGFR3), among others.
CureFAKtor Pharmaceuticals recently presented pre-clinical research results at the AACR- EORTC-NCI Molecular Targets and Cancer Therapeutics Conference in San Francisco, California and at European Society for Medical Oncology (ESMO) 13th World Congress on Gastrointestinal Cancer in Barcelona, Spain demonstrating that FAK inhibitors targeting the binding site of VEGFR-3 decrease pancreatic tumor blood flow and reduce blood vessel density in vivo.
Circadian's wholly owned subsidiary, Vegenics Pty Ltd, owns worldwide rights to an extensive intellectual property portfolio covering the angiogenesis and lymphangiogenesis targets VEGF-C, VEGF-D and the receptor protein VEGFR-3.
VEGF-C, along with the molecule VEGF-D, are also the only known proteins to bind and activate VEGFR-3 which drives lymphatic vessel and tumour-associated blood vessel growth.
This current study builds on our previous findings demonstrating that VEGF-C, VEGF-D and VEGFR-3 are upregulated in DED corneas, and demonstrates for the first time that an anti-lymphatic effect, caused by the blockade of VEGF-C, has significant beneficial effects in treating the condition.