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Tab 200 mg


Sorafenib is a kinase inhibitor that decreases tumor cell proliferation in vitro. Sorafenib was shown to inhibit multiple intracellular (c-CRAF, BRAF and mutant BRAF) and cell surface kinases (KIT, FLT-3, RET, RET/PTC, VEGFR-1, VEGFR-2, VEGFR-3, and PDGFR-ß).

Several of these kinases are thought to be involved in tumor cell signaling, angiogenesis and apoptosis. Sorafenib inhibited tumor growth of HCC, RCC, and DTC human tumor xenografts in immunocompromised mice.

Reductions in tumor angiogenesis were seen in models of HCC and RCC upon sorafenib treatment, and increases in tumor apoptosis were observed in models of HCC, RCC, and DTC

    Unresectable hepatocellular carcinoma
    Advanced renal cell carcinoma
    Locally recurrent or metastatic, progressive, differentiated thyroid carcinoma refractory to radioactive iodine treatment
    400 mg (2 tablets) orally twice daily without food.
    Treatment interruption and/or dose reduction may be needed to manage suspected adverse drug reactions
    GI perforation: GI perforation has been reported (rare); monitor patients for signs/symptoms (abdominal pain, constipation, or vomiting); discontinue treatment if gastrointestinal perforation occurs
    Bleeding: Increased risk of bleeding may occur; consider permanently discontinuing with serious bleeding events (eg, requires medical intervention). Fatal bleeding events have been reported. Thyroid cancer patients with tracheal, bronchial, and esophageal infiltration should be treated with local therapy prior to administering sorafenib due to the potential bleeding risk.
    Cardiovascular events: May cause cardiac ischemia or infarction; consider discontinuation (temporary or permanent) in patients who develop these conditions. Use in patients with unstable coronary artery disease or recent myocardial infarction has not been studied. Heart failure has been reported in multiple clinical studies. In a scientific statement from the American Heart Association, sorafenib has been determined to be an agent that may exacerbate underlying myocardial dysfunction (magnitude: minor)
    Dermatologic toxicity: Hand-foot skin reaction and rash (generally grades 1 or 2) are the most common drug-related adverse events, and typically appear within the first 6 weeks of treatment; usually managed with topical treatment, treatment delays, and/or dose reductions. Consider permanently discontinuing with severe or persistent dermatological toxicities.
    Hepatotoxicity: Sorafenib-induced hepatitis (characterized by a hepatocellular pattern of liver damage with significant increases of transaminases) which may result in hepatic failure and death has been observed. Bilirubin elevations and INR increases may also occur. Severe drug-induced liver injury (transaminase elevations >20 times ULN or with significant clinical sequelae [eg, elevated INR, ascites, transplantation or fatality]) occurred rarely. Monitor liver function tests regularly. Discontinue sorafenib if significantly increased transaminases occur without alternative explanation (eg, viral hepatitis or progressing underlying malignancy).
    Hypertension: May cause hypertension (generally mild-to-moderate), especially in the first 6 weeks of treatment; monitor. Use caution in patients with underlying or poorly-controlled hypertension. Consider discontinuing (temporary or permanent) in patients who develop severe or persistent hypertension while on appropriate antihypertensive therapy.
    QT prolongation: QT prolongation has been observed; may increase the risk for ventricular arrhythmia. Avoid use in patients with congenital long QT syndrome. Monitor electrolytes and ECG in patients with heart failure, bradyarrhythmias, and concurrent medications know to prolong the QT interval. Correct electrolyte (calcium, magnesium, potassium) imbalances. Interrupt treatment for QTc interval >500 msec or for ≥60 msec increase from baseline.
    Thyroid impairment: Sorafenib impairs exogenous thyroid suppression. TSH level elevations were commonly observed in the thyroid cancer study; monitor TSH levels monthly and as clinically necessary, and adjust thyroid replacement as needed.
    Wound healing complications: May complicate wound healing; temporarily withhold treatment for patients undergoing major surgical procedures. The appropriate timing to resume sorafenib after major surgery has not been determined.

CYP3A4 Inducers

Continuous co-administration of sorafenib and rifampicin resulted in an average 37% reduction of sorafenib AUC. Other inducers of CYP3A4 activity (for example, St. John’s wort, phenytoin, carbamazepine, phenobarbital, and dexamethasone) may also increase metabolism of sorafenib and thus decrease sorafenib concentrations.

CYP3A4 Inhibitors and CYP Isoform Substrates

In vitro and in vivo data suggest that: 1) sorafenib is unlikely to be altered by CYP3A inhibitors, and 2) sorafenib is unlikely to alter the metabolism of substrates of CYP2C19, CYP2D6, and CYP3A4
Sorafenib prolongs the QT interval, hence, concomitant administration with patients taking certain anti-arrhythmic medicines or other medicinal products that lead to QT prolongation, e.g. certain anti-arrhythmic drugs, should be used with caution

Sorafenib and Neoplastic Agents

When used concomitantly with carboplatin and paclitaxel, sorafenib has been observed to increase the AUC of paclitaxel, and the AUC of sorafenib also increased. Sorafenib can also cause increases in plasma concentrations of doxorubicin, irinotecan, docetaxel, fluorouracil, and paclitaxel.1,2,5 Sorafenib is contraindicated in patients with squamous cell lung cancer, as a result of observed increased mortality with the addition of sorafenib.

Sorafenib and CYP Inhibitors and Substrates

Sorafenib inhibits CYP2B6 and CYP2C8 in vitro. Systemic exposure to substrates of CYP2B6 and CYP2C8 is therefore expected to increase when co-administered with sorafenib.