Sunitinib: Difference between revisions
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===Mechanism of Action=== | ===Mechanism of Action=== | ||
Sunitinib inhibits cellular signaling by targeting several different receptor tyrosine kinases (RTKs) including receptors for platelet-derived growth factor (PDGFRs) and [[VEGFR|vascular endothelial growth factor receptors]] (VEGFR). PDGFR and VEGFR play crucial roles in both tumor angiogenesis and cellular proliferation. Inhibition of PDGFR and VEGFR results in reduced tumor vascularization and cancer cell death. Sunitinib is also an inhibitor of KIT, a cytokine receptor inhibitor. KIT binds to stem cell factor, upon which KIT dimerizes and transmit second messenger signals ultimately resulting in cell survival and proliferation. Mutations of the KIT gene are associated with most gastrointestinal stromal [[cancer|tumors]]. <ref>PMID: 12072198</ref> | Sunitinib inhibits cellular signaling by targeting several different receptor tyrosine kinases (RTKs) including receptors for platelet-derived growth factor (PDGFRs) and [[VEGFR|vascular endothelial growth factor receptors]] (VEGFR). PDGFR and VEGFR play crucial roles in both tumor angiogenesis and cellular proliferation. Inhibition of PDGFR and VEGFR results in reduced tumor vascularization and cancer cell death. Sunitinib is also an inhibitor of KIT, a cytokine receptor inhibitor. KIT binds to stem cell factor, upon which KIT dimerizes and transmit second messenger signals ultimately resulting in cell survival and proliferation. Mutations of the KIT gene are associated with most gastrointestinal stromal [[cancer|tumors]].<ref>PMID: 12072198</ref> | ||
===Pharmacokinetics=== | ===Pharmacokinetics=== | ||