Transforming growth factor-beta receptor (TGFBR), Vascular endothelial growth factor receptor (VEGFR), Fibroblast growth factor receptor (FGFR), and Platelet-derived growth factor receptor (PDGFR) (TGFBR/VEGFR/FGFR/PDGFR)

This target entry represents a collective group of four distinct receptor families: Transforming growth factor-beta (TGF-β) receptor, Vascular endothelial growth factor receptor (VEGFR), Fibroblast growth factor receptor (FGFR), and Platelet-derived growth factor receptor (PDGFR). These receptors are critical transmembrane proteins that initiate intracellular signaling cascades—primarily via tyrosine kinase activity for VEGFR, FGFR, and PDGFR, and serine/threonine kinase activity for TGFBR—to regulate essential cellular processes such as angiogenesis, cell proliferation, and extracellular matrix deposition [1, 2]. In the context of oncology, these pathways are frequently co-opted by tumors to promote vascularization, survival, and resistance to therapy, while in fibrotic diseases like idiopathic pulmonary fibrosis, they drive the activation and proliferation of myofibroblasts [3, 4]. Therapeutic strategies often involve multi-kinase inhibitors, such as nintedanib, which are designed to simultaneously block multiple pathways (VEGFR, FGFR, and PDGFR) to overcome redundant signaling and improve clinical outcomes [3, 5]. While TGF-β receptors are often targeted by more specific inhibitors like galunisertib, the combined inhibition of these four pathways is a major area of research for treating complex, multi-factorial diseases [4].

Other names

Receptor tyrosine kinases (RTKs)Serine/threonine kinase receptorsAngiogenic growth factor receptorsFibrogenic growth factor receptors

ATP-competitive inhibition of the intracellular kinase domains of VEGFR, FGFR, and PDGFR, and inhibition of the serine/threonine kinase activity of TGFBR1.