Quizartinib is an orally available small molecule with potential antineoplastic activity. Class III receptor tyrosine kinase inhibitor AC220 selectively inhibits class III receptor tyrosine kinases, including FMS-related tyrosine kinase 3 (FLT3/STK1), colony-stimulating factor 1 receptor (CSF1R/FMS), stem cell factor receptor (SCFR/KIT), and platelet derived growth factor receptors (PDGFRs), resulting in inhibition of ligand-independent leukemic cell proliferation and apoptosis.
Sunitinib (Sutent) is a multi-targeted receptor tyrosine kinase (RTK) inhibitor for the treatment of renal cell carcinoma (RCC) and imatinib-resistant gastrointestinal stromal tumor (GIST). Sunitinib was the first cancer drug simultaneously approved for two different indications. Sunitinib inhibits cellular signaling by targeting multiple receptor tyrosine kinases (RTKs). These include all PDGF-Rs and VEGFRs, which play a role in both tumor angiogenesis and tumor cell proliferation.
Receptor Tyrosine Kinase animation. Binding of insulin ligand will cause monomers to become dimers. Then, the (many) tyrosine(s) will auto-phosphorylate. This creates another conformational change that allows it to interact with an "adapter protein" which then indirectly binds with a G-protein. The tyrosine kinase can lead to multiple cellular responses from just ONE signal.
A schematic shows how the binding of a ligand to receptor tyrosine kinases (RTKs) results in the activation of the RTKs. The RTKs are in a horizontal plasma membrane. Four different stages are shown: the RTKs before ligand binding, the dimerization of the RTKs after ligand binding, the phosphorylation of the RTKs, and the binding of various cytoplasmic proteins to the RTKs.