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Vascular endothelial growth factor receptors (VEGFRs), Raf kinase, Platelet-derived growth factor receptor beta (PDGFRβ), and Fibroblast growth factor receptor 1 (FGFR1) (VEGFR, RAF, PDGFRβ, FGFR1)

Target
VEGFR, RAF, PDGFRβ, FGFR1
Molecular classification
Receptor tyrosine kinase, transmembrane receptor, Serine/threonine kinase, enzyme
01

Overview

These targets are central molecules in key signaling pathways and include VEGFRs (which regulate angiogenesis and lymphangiogenesis, critical in tumor growth and metastasis), Raf kinase (a major component of the RAS/RAF/MEK/ERK pathway central to cell proliferation and survival), PDGFRβ (which drives cell proliferation, migration, and angiogenesis in normal and malignant tissues), and FGFR1 (modulates cell growth, differentiation, and angiogenesis). Aberrant activation or overexpression is implicated in oncogenesis, tumor maintenance, therapeutic resistance, and vascular pathologies. Drugs targeting these molecules are mainly kinase inhibitors, frequently used in cancer therapy, particularly for tumors driven by abnormal angiogenesis or growth factor signaling. Note: Presenting them together as a single target is not standard scientific practice; each name refers to a distinct protein. For proper structured information, individual records should be generated per target, rather than grouping as above.

Other names
Vascular endothelial growth factor receptor familyFLT-1 for VEGFR1KDR for VEGFR2c-RafRaf-1BRAFPDGF receptor betaCD140bFGF receptor 1
02

Mechanism of action

Inhibition of kinase activity via ATP-competitive binding—blocks phosphorylation, halts downstream signaling and cellular responses. Anti-angiogenesis: blocking blood vessel formation via VEGFR, FGFR, PDGFRβ inhibition.

03

Biological functions

Signal transductionCell proliferationCell survivalMigrationAngiogenesisApoptosis
04

Disease associations

Cancer (angiogenesis, tumor growth, metastasis)Cardiovascular diseaseInflammationDrug resistanceFibrosis
05

Safety considerations

CytotoxicityDrug resistance (e.g., compensatory pathways like FGFR in VEGFR-resistant tumors)Vascular toxicity (hypertension, bleeding, thromboembolic events)Off-target effects due to broad kinase inhibition
06

Interacting drugs

Sunitinib

13 more in the full profile.

07

Biomarkers

Overexpression or mutation of VEGFROverexpression or mutation of FGFR1Overexpression or mutation of PDGFRβOverexpression or mutation of BRAF (e.g., BRAF V600E)FGFR alterationsVEGF/VEGFR levels

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