Multi-kinase Receptor Tyrosine Kinase panel (Multi-kinase RTK panel) (Multi-kinase RTK panel)

A multi-kinase RTK panel refers to a collective group of receptor tyrosine kinases (RTKs) that are targeted by broad-spectrum inhibitors or evaluated in screening assays. RTKs are essential cell surface receptors that regulate key cellular processes including growth, differentiation, and angiogenesis by transducing extracellular signals into the cytoplasm (Lemmon & Schlessinger, 2010, Cell). This panel typically includes receptors such as Vascular Endothelial Growth Factor Receptor (VEGFR), Platelet-Derived Growth Factor Receptor (PDGFR), Fibroblast Growth Factor Receptor (FGFR), and KIT, which are frequently overexpressed or mutated in various cancers (Casaletto & McClatchey, 2012, Nat Rev Cancer). Because tumors often utilize multiple redundant signaling pathways to survive, targeting a panel of these kinases simultaneously can provide more robust therapeutic efficacy than single-target inhibition (Jiao et al., 2018, Mol Cancer). However, the inhibition of multiple kinases also leads to a broader range of systemic side effects, such as hypertension and hand-foot syndrome, due to the disruption of normal physiological signaling in healthy tissues (Chu et al., 2007, Clin Cancer Res). Consequently, the multi-kinase RTK panel is a critical concept in precision oncology for both drug design and the development of companion diagnostics.

Other names

RTK panelMulti-kinase panelReceptor tyrosine kinase familyKinome panel

Multi-kinase inhibitors typically function by binding to the highly conserved adenosine triphosphate (ATP) binding site within the intracellular catalytic domain of various receptor tyrosine kinases (Jiao et al., 2018, Mol Cancer). By competing with ATP, these drugs prevent the autophosphorylation of the receptor and the subsequent activation of downstream signaling pathways, such as the Ras/Raf/MEK/ERK and PI3K/Akt/mTOR cascades, which are vital for tumor cell survival and proliferation (Lemmon & Schlessinger, 2010, Cell).