Gefitinib: Difference between revisions
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* The following is a list of Pharmacokinetic Parameters. See: [[Pharmaceutical Drugs]] for more information | * The following is a list of Pharmacokinetic Parameters. See: [[Pharmaceutical Drugs]] for more information | ||
===Mechanism of Action=== | ===Mechanism of Action=== | ||
[[EGFR|Epidermal Growth Factor Receptors]] are overexpressed in many types of human [[Cancer|carcinomas]] including lung, pancreatic, and breast cancer. This overexpression leads to excessive activation of the anti-apoptotic [[Ras]] signalling cascade. | [[EGFR|Epidermal Growth Factor Receptors]] are overexpressed in many types of human [[Cancer|carcinomas]] including lung, pancreatic, and breast cancer. This overexpression leads to excessive activation of the anti-apoptotic [[Ras]] signalling cascade, resulting in uncontrolled DNA synthesis and cell proliferation. Studies have revealed that the EGFR tyrosine kinase domain is responsible for activating this Ras signaling cascade. Upon binding ligands like Epidermal Growth Factor, EGFR dimerizes and autophosphorylates several tyrosine residues at its C-terminal domain. It is these phosphorylated tyrosine residues which elicit downstream activation of other signaling proteins. This signal transduction ultimately leads to activation of the MAPK, Akt and JNK pathways, in addition | ||
Gefitinib inhibits the EGFR tyrosine kinase by binding to the ATP-Binding site located within the kinase domain. Unable to bind ATP, EGFR is unable to | |||
===Pharmacokinetics=== | ===Pharmacokinetics=== | ||
