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Regonib®(Regorafenib)

Regonib®(Regorafenib)

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Tablet 40 mg

 

Regorafenib is a small molecule inhibitor of multiple membrane-bound and intracellular kinases involved in normal cellular functions and in pathologic processes such as oncogenesis, tumor angiogenesis, metastasis and tumor immunity.

In in vitro biochemical or cellular assays, regorafenib or its major human active metabolites M-2 and M-5 inhibited the activity of RET, VEGFR1, VEGFR2, VEGFR3, KIT, PDGFR-alpha, PDGFR-beta, FGFR1, FGFR2, TIE2, DDR2, TrkA, Eph2A, RAF-1, BRAF, BRAF V600E, SAPK2, PTK5, Abl and CSF1R at concentrations of regorafenib that have been achieved clinically. In in vivo models, regorafenib demonstrated anti-angiogenic activity in a rat tumor model and inhibition of tumor growth in several mouse xenograft models including some for human colorectal carcinoma, gastrointestinal stromal and hepatocellular carcinoma. Regorafenib also demonstrated anti-metastatic activity in a mouse xenograft model and two mouse orthotopic models of human colorectal carcinoma.




INDICATIONS

REGONIB is a kinase inhibitor indicated for the treatment of patients with:

• Metastatic colorectal cancer (CRC) who have been previously treated with fluoropyrimidine-, oxaliplatin- and irinotecan-based chemotherapy, an anti VEGF therapy, and, if RAS wild-type, an anti-EGFR therapy

• Locally advanced, unresectable or metastatic gastrointestinal stromal tumor (GIST) who have been previously treated with imatinib mesylate and sunitinib malate.

• Hepatocellular carcinoma (HCC) who have been previously treated with sorafenib.

DOSAGE AND ADMINISTRATION

Recommended dose: 160 mg orally, once daily for the first 21 days of each 28-day cycle.

-Take REGONIB after a low-fat meal.

WARNINGS AND PRECAUTIONS

• Hepatotoxicity

Monitor liver function tests.

• Infections

• Hemorrhage

• Gastrointestinal perforation or fistula

• Dermatologic toxicity

• Hypertension

• Cardiac ischemia and infarction

• Reversible posterior leukoencephalopathy syndrome (RPLS)

• Risk of impaired wound healing

• Embryo-fetal toxicity

DRUG INTERACTIONS

 Effect of Strong CYP3A4 Inducers on Effect of Strong CYP3A4 Inhibitors on Regorafenib Co-administration of a strong CYP3A4 inhibitor with STIVARGA increased the plasma concentrations of regorafenib and decreased the plasma concentrations of the active metabolites M-2 and M-5 [see Clinical Pharmacology (12.3)], and may lead to increased toxicity. Avoid concomitant use of STIVARGA with strong CYP3A4 inhibitors (e.g. clarithromycin, grapefruit juice, itraconazole, ketoconazole, nefazodone, posaconazole, telithromycin, and voriconazole).  

Co-administration of a strong CYP3A4 inducer with REGONIB decreased the plasma concentrations of regorafenib, increased the plasma concentrations of the active metabolite M-5, and resulted in no change in the plasma concentrations of the active metabolite M-2 , and may lead to decreased efficacy. Avoid concomitant use of STIVARGA with strong CYP3A4 inducers (e.g. rifampin, phenytoin, carbamazepine, phenobarbital, and St. John’s 

Effect of Strong CYP3A4 Inhibitors on Regorafenib :  Co-administration of a strong CYP3A4 inhibitor with REGONIB increased the plasma concentrations of regorafenib and decreased the plasma concentrations of the active metabolites M-2 and M-5 , and may lead to increased toxicity. Avoid concomitant use of STIVARGA with strong CYP3A4 inhibitors (e.g. clarithromycin, grapefruit juice, itraconazole, ketoconazole, nefazodone, posaconazole, telithromycin, and voriconazole). 

Effect of Regorafenib on Breast Cancer Resistance Protein (BCRP) Substrates

Co-administration of REGONIB with a BCRP substrate increased the plasma concentrations of the BCRP substrate. Monitor patients closely for signs and symptoms of exposure related toxicity to the BCRP substrate (e.g. methotrexate, fluvastatin, atorvastatin). Consult the concomitant BCRP substrate product information when considering administration of such products together with REGONIB 

Regonib

Regonib