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VEGFR

VEGF family - VEGF-A, B, C, D, E and PLGF VEGFR - VEGF receptor-1, 2, and 3 Formation and maintenance of vasculature... [Pg.566]

Bevacizumab (Avastin) Monoclonal antibody against ligand VEGFR Cancer Clinic... [Pg.1011]

Bevacizumab (Avastin ) Roche mAb VEGFR Metastatic colorectal cancer... [Pg.1193]

S orafenib (Nexavar ) Bayer TKI VEGFR, PDGFR, KIT, FTL-3, RAF Unresectable or metastatic renal cell carcinoma... [Pg.1193]

S unitinib (Sutent ) Pfizer TKI VEGFR, PDGFR, KIT, FLT-3, RET 1 matinib-resistant KIT overexpressing unresectable or metastatic gastro-intestinal stromal tumor... [Pg.1193]

Sorafenib is a multitargeted cancer therapy that inhibits VEGFR, PDGFR, KIT, fetal liver tyrosine kinase 3 (FLT-3), and the serine/threonine kinase RAF. RAF kinase is a key downstream effector of Ras in the MAPK/Ras signal-transduction pathway that has been linked to various cancers. Sorafenib is both a tyrosine kinase inhibitor and serine/threonine signal-transduction inhibitor. Sorafenib has been approved in renal cancer. [Pg.1194]

Sunitinib is also a multitargeted cancer therapy targeting VEGFR, PDGFR, KIT, FLT-3, and RET. Sunitinib has been approved in GIST refractory to imatinib and renal cancer. [Pg.1194]

Optimization of the large (MW = 512), lipophilic (clogP = 7.6), and very potent (Kj = 0.22 nM) Vascular Endothelial Growth Factor Receptor Tyrosine Kinase (VEGFR TK) inhibitor 8 (LLE = 2.1) to produce the development candidate axitinib (9) was recently reported [17]. [Pg.390]

VEGFR/Flk-1/KDR Activation of tumor vascularization by the anoxic tumor All cancers... [Pg.4]

Figure 18.5 Alcohol containing VEGFR-2 inhibitor used for a prodrug approach. Figure 18.5 Alcohol containing VEGFR-2 inhibitor used for a prodrug approach.
SU11248 Tyrosine kinase inhibitor, VEGFR, PDGFR, Kit... [Pg.453]

Cortes F, Debacker C, Peault B, Labastie MC (1999). Differential expression of KDR/VEGFR 2 and CD34 during mesoderm development of the early human embryo. Mech. Dev. 83 161 164. [Pg.145]

Figure 1. Superimposition of the structures of tyrosine kinases, Tie-2 (yellow), VEGFR-3 (red) and IGFIR (blue). Figure 1. Superimposition of the structures of tyrosine kinases, Tie-2 (yellow), VEGFR-3 (red) and IGFIR (blue).

See other pages where VEGFR is mentioned: [Pg.81]    [Pg.83]    [Pg.87]    [Pg.87]    [Pg.569]    [Pg.569]    [Pg.1192]    [Pg.1256]    [Pg.1256]    [Pg.1270]    [Pg.1270]    [Pg.1271]    [Pg.1271]    [Pg.373]    [Pg.4]    [Pg.527]    [Pg.469]    [Pg.514]    [Pg.131]    [Pg.9]    [Pg.506]    [Pg.544]    [Pg.426]    [Pg.440]    [Pg.444]    [Pg.444]    [Pg.444]    [Pg.455]    [Pg.453]    [Pg.235]    [Pg.243]    [Pg.64]    [Pg.67]    [Pg.69]    [Pg.69]   
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Kinase Growth Factor VEGFR-2 and FGFR-1 Inhibitors

Protein kinases VEGFR

VEGFR (vascular endothelial growth

VEGFR-2, Vascular endothelial growth factor

Vascular endothelial growth factor receptor 2 (VEGFR

Vascular endothelial growth factor receptor VEGFR) inhibitors

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