Примери за използване на Niraparib на Английски и техните преводи на Български
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The active substance is niraparib.
Effect of niraparib on other medicinal products.
Zejula contains the active substance niraparib.
Oxidative metabolism of niraparib is minimal in vivo.
Carcinogenicity studies have not been conducted with niraparib.
Niraparib is not a substrate of bile salt export pump(BSEP).
Pancytopenia has been observed in<1% of patients receiving niraparib.
Niraparib is a type of anti-cancer medicine called a PARP inhibitor.
Reproductive and developmental toxicity studies have not been conducted with niraparib.
Niraparib is not a substrate of MATE 1 or 2, while M1 is a substrate of both.
Each hard capsule contains niraparib tosylate monohydrate equivalent to 100 mg niraparib.
Niraparib is eliminated primarily through the hepatobiliary and renal routes.
The absolute bioavailability of niraparib is approximately 73%, indicating minimal first pass effect.
Niraparib is an inhibitor of MATE1 and -2 with IC50 of 0.18 µM and≤ 0.14 µM, respectively.
Paediatric population No studies have been conducted to investigate the pharmacokinetics of niraparib in paediatric patients.
It is unknown whether niraparib or its metabolites are excreted in human milk.
The white opaque capsule body is printed with‘100 mg' in black ink, andthe purple capsule cap is printed with‘Niraparib' in white ink.
Niraparib can cause haematological toxicity that includes febrile neutropenia.
Hard capsule of approximately 22 mm× 8 mm; white body with“100 mg” printedin black ink and purple cap with“Niraparib” printed in white ink.
Niraparib as a substrate of hepatic uptake transporters(OATP1B1, OATP1B3, and OCT1).
A concomitant high-fat meal did not significantly affect the pharmacokinetics of niraparib after administration of 300 mg of niraparib. .
The combination of niraparib with vaccines or immunosuppressant agents has not been studied.
Even though inhibition of CYP3A4 in the liver is not expected,the potential to inhibit CYP3A4 at the intestinal level has not been established at relevant niraparib concentrations.
The data on niraparib in combination with cytotoxic medicinal products are limited.
In pooled samples collected over 6 days, 40.0% of the dose was recovered in the urine primarily as metabolites and31.6% of the dose was recovered in the feces primarily as unchanged niraparib.
In vitro, niraparib inhibits P-gp very weakly and BCRP with an IC50= 161 µM and 5.8 µM, respectively.
Demographics, baseline disease characteristics, andprior treatment history were generally well balanced between the niraparib and placebo arms in the gBRCAmut(n= 203) and the non-gBRCAmut cohorts(n= 350).
In vitro, niraparib weakly inhibits the organic cation transporter 1(OCT1) with an IC50= 34.4 µM.
The safety and efficacy of niraparib in children and adolescents below 18 years of age have not yet been established.
Niraparib is metabolised primarily by carboxylesterases(CEs) to form a major inactive metabolite, M1.