Indications
Axitinib is primarily indicated for the treatment of renal cell carcinoma (RCC). Ongoing research is exploring its potential utility in the management of pancreatic and thyroid cancers, broadening its therapeutic applications.
Pharmacodynamics
The mechanism of action of Axitinib involves the inhibition of angiogenesis, a critical process in tumor growth. By targeting specific pathways, Axitinib effectively impedes the vascularization necessary for tumor proliferation, thereby restricting cancer progression.
Absorption
Upon administration of a single 5 mg dose of Axitinib, the drug reaches its maximum plasma concentration within approximately 2.5 to 4.1 hours. This pharmacokinetic profile is crucial for determining the appropriate dosing schedule to maintain therapeutic efficacy.
Metabolism
Axitinib is primarily metabolized in the liver, with the enzymes CYP3A4 and CYP3A5 playing the principal roles in its biotransformation. Additional metabolism occurs via secondary enzymes, including CYP1A2, CYP2C19, and UGT1A1.
Mechanism of Action
Axitinib operates as a selective inhibitor targeting the tyrosine kinase receptors VEGFR-1, VEGFR-2, and VEGFR-3. By blocking these receptors, axitinib effectively disrupts the signaling pathways associated with vascular endothelial growth factor, which plays a crucial role in angiogenesis. This inhibition impedes the formation of new blood vessels, thereby restricting the delivery of oxygen and nutrients necessary for tumor growth and progression.
