Description
Alecinix (Alectinib) 150mg Online
Alecinix (Alectinib) 150mg by Beacon Pharmaceuticals is used to treat Non-Small Cell Lung Cancer (NSCLC). Alectinib is a highly selective and potent ALK and RET tyrosine kinase inhibitor. In nonclinical studies, inhibition of ALK tyrosine kinase activity led to blockage of downstream signaling pathways including STAT 3 and PI3K/AKT, and induced tumor cell death (apoptosis).
The recommended dose of Alecensa is 600 mg (four 150 mg capsules) given orally, twice daily (total daily dose of 1200 mg). Patients with underlying severe hepatic impairment should receive a dose of 450 mg given orally twice daily (total daily dose of 900 mg).
Alecensa hard capsules should be taken with food, swallowed whole, and must not be opened or dissolved.
Alectinib demonstrated in Vitro and in vivo activity against mutant forms of the ALK enzyme, including mutations responsible for resistance to crizotinib. The major metabolite of alectinib (M4) has shown similarly in vitropotency and activity. In vitro studies indicate that neither Alecensa nor its major active metabolite (M4) inhibits CYP1A2, CYP2B6, CYP2C9, CYP2C19, or CYP2D6 at clinically relevant concentrations. Alectinib and M4 show weak time-dependent inhibition of CYP3A4. Results from a clinical drug-drug interaction study in ALK-positive NSCLC patients demonstrated that multiple doses of Alecensa had no influence on the exposure of midazolam, a sensitive CYP3A substrate. Therefore, no dose adjustment is required for co-administered CYP3A substrates. Although in vitro studies indicate that Alecensa is an inhibitor of CYP2C8, physiologically based pharmacokinetic (PBPK) modeling supports that at clinically relevant concentrations alectinib does not have the potential to increase plasma Contraindications. Alectinib is contraindicated in patients with a known hypersensitivity to Alecensa or any of the excipients.
The substance potently and selectively blocks two receptor tyrosine kinase enzymes: anaplastic lymphoma kinase (ALK) and the RET proto-oncogene. The active metabolite M4 has similar activity against ALK. Inhibition of ALK subsequently blocks cell signaling pathways, including STAT3 and the PI3K/AKT/mTOR pathway, and induces death (apoptosis) of tumour cells.
