The Pharmaceutical Journal
Vol 269 No 7229 p879
21/28 December 2002

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American Society of Hematology (www.hematology.org)

Imatinib proves effective in chronic phase of CML

More patients with newly diagnosed chronic-phase chronic myeloid leukaemia (CML) respond to treatment with imatinib (Glivec) than to standard treatment, a new study shows.

The trial, which was presented at an American Society of Hematology meeting earlier this month in Philadelphia, is the first head-to-head trial comparing the two treatment regimens in this group of patients.

The trial involved 1,106 patients with CML aged 18–70 years who were randomly assigned to receive imatinib 400mg daily or to interferon alfa plus cytarabine. The target dose for interferon alfa was 5 mega units/m² body area daily and for cytarabine was 20mg/m² body area, given subcutaneously for 10 days every month. The data for 18-months' follow-up revealed that more patients randomised to imatinib than interferon alfa plus cytarabine achieved a normal blood count (97 per cent versus 69 per cent).

In addition, more than twice as many patients treated with imatinib than interferon alfa plus cytarabine showed major cytogenetic response — elimination of cells containing the Philadelphia chromosome, the genetic abnormality that characterises most cases of CML (87 per cent versus 35 per cent). Complete cytogenetic response occurred in 87 per cent of the imatinib group, compared with only 14 per cent of the interferon alfa plus cytarabine patients (P<0.001). Progression-free survival at 18 months was greater with imatinib (92 per cent versus 73 per cent, P<0.001).

Presenting the findings, Dr Richard Larson, University of Chigaco, said: "The use of imatinib resulted in a significantly higher response rate and a longer period before the disease progressed. This should be viewed as a positive step forward in the treatment of CML."

Further data reported at the meeting showed that in patients who achieved complete cytogenetic remission, levels of BCR-ABL — the protein that activates signal transduction pathways, resulting in uncontrolled cell growth — continued to fall in patients treated with imatinib.