Nexavar

The main ingredient of this product is sorafenib tosylate.

CYP3A4 inducers: There is no clinical data on the effect of CYP3A4 inducers on the metabolism of sorafenib. CYP3A4 inducers (such as rifampicin, Hypericum perforatum (or Hypericum perforatum, commonly known as St. John's wort), phenytoin, carbamazepine, phenobarbital and dexamethasone) may accelerate the metabolism of sorafenib, thereby reducing the drug concentration of sorafenib. CYP3A4 inhibitors: Ketoconazole is a strong inhibitor of CYP3A4. Healthy male volunteers used ketoconazole once a day for 7 consecutive days and combined with a single dose of sorafenib 50mg. The average blood concentration of sorafenib did not change. Therefore, it is unlikely that there is a drug metabolism interaction between sorafenib and CYP3A4 inhibitors. CYP2C9 substrate: Warfarin is a substrate of CYP2C9. The effect of sorafenib on warfarin metabolism was evaluated by comparing patients taking sorafenib and placebo. The mean PT-INR value of patients treated with warfarin in combination with sorafenib did not change compared with the placebo group. However, INR values should be monitored regularly when patients are treated with warfarin. CYP isomer-selective substrate: Sorafenib is neither an inhibitor nor an inducer of cytochrome P450 isoenzymes. Interactions with other anti-cancer drugs: In clinical trials, sorafenib was used in combination with other conventional doses of anti-cancer drugs, including gemcitabine, oxaliplatin, doxorubicin and irinotecan. Sorafenib did not affect the drug metabolism of gemcitabine and oxaliplatin. When paclitaxel (225 mg/m2) and carboplatin (AUC=6) were used concomitantly with this product (twice daily, 0.1g, 0.2g or 0.4g each time), stopping this product for 3 days before and after the use of paclitaxel/carboplatin did not significantly affect the pharmacokinetics of paclitaxel or carboplatin. When sorafenib and doxorubicin are used together, the average AUC value of doxorubicin in patients with liver cancer can increase by 21%. When sorafenib and irinotecan are used together, the AUC of irinotecan's active metabolite SN-38 (metabolized by UGTIAI enzyme) increases by 67%-120%, and the AUC value of irinotecan increases by 26%-42%. The clinical significance of this is unknown (see [Precautions]). Docetaxel (75mg/m2 or 100mg/m2, 0.2g or 0.4g twice daily from day 2 to day 19 in every 21-day treatment cycle), there is a three-day medication interval between this product and docetaxel, and the AUC of docetaxel increases by 36-80%, and Cmax increases by 16-32%. It is recommended to be cautious when this product is used in combination with docetaxel (see [Precautions]).

The main ingredient of this product is sorafenib tosylate.

CYP3A4 inducers: There is no clinical data on the effect of CYP3A4 inducers on the drug metabolism of sorafenib. CYP3A4 inducers (such as rifampicin, Hypericum perforatum (or Hypericum perforatum, commonly known as St. John's wort), phenytoin, carbamazepine, phenobarbital and dexamethasone) may accelerate the metabolism of sorafenib, thereby reducing the drug concentration of sorafenib. CYP3A4 inhibitors: Ketoconazole is a strong inhibitor of CYP3A4. Healthy male volunteers used ketoconazole once a day for 7 consecutive days and combined with a single dose of sorafenib 50 mg. The average blood concentration of sorafenib did not change. Therefore, there is no possibility of drug metabolism interaction between sorafenib and CYP3A4 inhibitors. CYP2C9 substrate: Warfarin is a substrate of CYP2C9. The effect of sorafenib on warfarin metabolism was evaluated by comparing patients taking sorafenib and placebo. Compared with the placebo group, the mean PT-INR value of patients treated with sorafenib combined with warfarin did not change. However, INR values should be monitored regularly when patients are treated with warfarin. CYP isomer selective substrates: Sorafenib is neither an inhibitor nor an inducer for these cytochrome P450 isoenzymes. Interactions with other anti-cancer drugs: In clinical trials, sorafenib was used in combination with other conventional doses of anti-cancer drugs, including gemcitabine, oxaliplatin, doxorubicin and irinotecan. Sorafenib did not affect the drug metabolism of gemcitabine and oxaliplatin. When sorafenib and doxorubicin were used in combination, the mean AUC value of doxorubicin in patients with liver cancer increased by 21%. When sorafenib and irinotecan were used in combination, the AUC of irinotecan's active metabolite SN-38 (metabolized by the UGTIA1 enzyme) increased by 67%-120%, and the AUC value of irinotecan increased by 26-42%. The clinical significance of this is unknown.