Примери за използване на To imatinib на Английски и техните преводи на Български
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(Applicable to imatinib, dasatinib and nilotinib).
Poor compliance is the predominant reason for inadequate molecular response to imatinib.
If you are allergic to imatinib or any of the other ingredients of this medicine listed in.
An open-label, single-arm, multicenter study was conducted in patients intolerant or resistant to imatinib.
Were randomised to dasatinib and 49 to imatinib(all imatinib-resistant).
A total of 519 patients were randomised to a treatment group:259 to SPRYCEL and 260 to imatinib.
If you are allergic(hypersensitive) to imatinib or any of the other ingredients of Glivec listed at.
The first study included a total of 320 patients whose disease was in the‘ chronic phase',three quarters of whom had stopped responding to imatinib.
Prior complete haematologic response(CHR) to imatinib was achieved in 93% of the overall patient population.
In addition to imatinib, 35% of patients had received prior cytotoxic chemotherapy, 65% had received prior interferon, and 10% had received a prior stem cell transplant.
Glivec must not be used in people who are hypersensitive(allergic) to imatinib or any of the other ingredients.
A prior MCyR to imatinib was achieved in 28% and 29% of the patients in the dasatinib and imatinib arms, respectively.
Fifty-five percent of the imatinib-resistant patients with no prior MCyR to imatinib(n= 288) achieved a MCyR with dasatinib.
Because 90% of the combination group had switched to imatinib by 18 months(mostly because of intolerance of side effects), a survival difference may never be observed.
The duration of imatinib therapy can vary with the treatment program selected, butgenerally longer exposures to imatinib have yielded better results.
Do not take Glivec:- if you are allergic to imatinib or any of the other ingredients of this medicine(listed in section 6).
Four single-arm, uncontrolled, open-label Phase II clinical studies were conducted to determine the safety and efficacy of dasatinib in patients with CML in chronic, accelerated, ormyeloid blast phase, who were either resistant or intolerant to imatinib.
However, since the effects of low-dose exposure of the infant to imatinib are unknown, women taking imatinib should not breast-feed.
Separate treatment arms were also included in the Phase II study to investigate Tasigna in a group of CP andAP patients who had been extensively pre-treated with multiple therapies including a tyrosine kinase inhibitor agent in addition to imatinib.
Among dasatinib-treated CML-CP paediatric patients previously exposed to imatinib, the mutations detected at the end of treatment were: T315A, E255K and F317L.
Resistance to imatinib included failure to achieve a complete haematological response(by 3 months), cytogenetic response(by 6 months) or major cytogenetic response(by 12 months) or progression of disease after a previous cytogenetic or haematological response.
Two clinical studies were conducted in patients resistant or intolerant to imatinib; the primary efficacy endpoint in these studies was Major Cytogenetic Response(MCyR).
Continuous daily exposure to imatinib early in the course of treatment in combination with chemotherapy in cohort 5-patients(n=50) improved the 4-year event-free survival(EFS) compared to historical controls(n=120), who received standard chemotherapy without imatinib 69.6% vs.
Although the results of pharmacokinetic analysis showed that there is considerable inter-subject variation,the mean exposure to imatinib did not increase in patients with varying degrees of liver dysfunction as compared to patients with normal liver function(see sections 4.2, 4.4 and 4.8).
Substances that are inducers of CYP3A4 activity(e.g. dexamethasone, phenytoin, carbamazepine, rifampicin, phenobarbital, fosphenytoin, primidone or Hypericum perforatum, also known as St. John's Wort)may significantly reduce exposure to imatinib, potentially increasing the risk of therapeutic failure.
There was a significant increase in exposure to imatinib(the mean Cmax and AUC of imatinib rose by 26% and 40%, respectively) in healthy subjects when it was co-administered with a single dose of ketoconazole(a CYP3A4 inhibitor).
Concomitant use of imatinib and medicinal products that induce CYP3A4(e.g. dexamethasone, phenytoin, carbamazepine, rifampicin, phenobarbital or Hypericum perforatum, also known as St. John's Wort)may significantly reduce exposure to imatinib, potentially increasing the risk of therapeutic failure.
The clinical safety andefficacy of sunitinib has been studied in the treatment of patients with GIST who were resistant to imatinib(i.e., those who experienced disease progression during or following treatment with imatinib) or intolerant to imatinib(i.e., those who experienced significant toxicity during treatment with imatinib that precluded further treatment), the treatment of patients with MRCC, and the treatment of patients with unresectable pNET.
Active substances that may decrease imatinib plasma concentrations Substances that are inducers of CYP3A4 activity(e.g. dexamethasone, phenytoin, carbamazepine, rifampicin, phenobarbital, fosphenytoin, primidone or Hypericum perforatum, also known as St. John's Wort)may significantly reduce exposure to imatinib, potentially increasing the risk of therapeutic failure.
Active substances that may decrease imatinib plasma concentrations Substances that are inducers of CYP3A4 activity(e.g. dexamethasone, phenytoin, carbamazepine, rifampicin, phenobarbital, fosphenytoin, primidone or Hypericum perforatum, also known as St. John's Wort)may significantly reduce exposure to imatinib, potentially increasing the risk of therapeutic failure.