Примери за използване на Midostaurin на Английски и техните преводи на Български
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Rydapt 25 mg capsules midostaurin.
Midostaurin is not an inhibitor of CYP3A4 in vivo.
Rydapt 25 mg soft capsules midostaurin.
Responses to midostaurin are shown in Table 7.
Each soft capsule contains 25 mg midostaurin.
Midostaurin is a compound with good absorption and poor solubility.
Table 5 Efficacy of midostaurin in AML.
Midostaurin is metabolised by CYP3A4 mainly via oxidative pathways.
Rydapt contains the active substance midostaurin.
No midostaurin dose adjustment is required based on gender.
Renal elimination is a minor route of elimination for midostaurin.
The active substance in Rydapt, midostaurin, is a‘tyrosine kinase inhibitor'.
Midostaurin can cause foetal harm when administered to a pregnant woman.
Strong CYP3A4 inhibitors may increase midostaurin blood concentrations.
Midostaurin inhibits multiple receptor tyrosine kinases, including FLT3 and KIT kinase.
CGP52421 concentrations do not appear to decline as significantly as for midostaurin and CGP62221.
Midostaurin and its metabolites are distributed mainly in plasma rather than red blood cells.
Strong CYP3A4 inducers decrease exposure of midostaurin and its active metabolites(CGP52421 and CGP62221).
In vitro, midostaurin did not inhibit hERG channel activity up to the limit of solubility of 12 µM.
All animal findings described below were observed at midostaurin exposure significantly lower than therapeutic levels.
Peak midostaurin concentration(Cmax) was reduced by 20% with a standard meal and by 27% with a high-fat meal versus on an empty stomach(see section 5.2).
Available animal data have shown that midostaurin and its active metabolites pass into the milk of lactating rats.
In addition, in patients who achieved complete remission during induction,the cumulative incidence of relapse at 12 months was 26% in the midostaurin arm versus 41% in the placebo arm.
The median terminal half-lives of midostaurin, CGP62221 and CGP52421 in plasma are approximately 20.9, 32.3 and 471 hours.
Due to the limited pharmacokineticdata in paediatric patients, no comparison with midostaurin pharmacokinetics in adults can be made.
In vitro data showed midostaurin is more than 98% bound to plasma proteins, such as albumin, α1-acid glycoprotein(AGP) and lipoprotein.
In AML and ASM, SM-AHN and MCL patients,population pharmacokinetic estimates for clearance of midostaurin at steady state were 5.9 l/h and 4.4 l/h, respectively.
Tmax was delayed for all entities, midostaurin median Tmax was 3 h, and for CGP52421 and CGP62221 Tmax was delayed to 6 and 7 hours respectively.
For EFS, considering complete remissions within 60 days of study treatment start, the HR was 0.602(95% CI: 0.372, 0.974) for patients with SCT and 0.827(95% CI: 0.689, 0.993)for patients without SCT, favouring midostaurin.
Safety pharmacology studies indicate that midostaurin is unlikely to interfere with vital functions of the central nervous system.