Latest research on Imatinib

Imatinib is a small molecule kinase inhibitor used to treat certain types of cancer. It is currently marketed by Novartis as Gleevec (USA) or Glivec (Europe/Australia) as its mesylate salt, imatinib mesilate (INN). It is occasionally referred to as CGP57148B or STI571 (especially in older publications). It is used in treating chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies. It is the first member of a new class of agents that act by inhibiting particular tyrosine kinase enzymes, instead of non-specifically inhibiting rapidly dividing cells.

Imatinib indications

To explore whether, and to what extent, therapeutic treatment would be reflected in the different lung biomarkers and particularly in total lung volume changes, we quantified the effect of Imatinib, demonstrated previously to have a modest beneficial effect on bleomycin-induced lung disease as quantified by the aerated lung volume (De Langhe et al., 2012). [source, 2016]
Based on the results of this meta-analysis, adjuvant Imatinib treatment is proved to be effective for GIST patients with R1 resection. [source, 2016]
Besides, this study proves that adjuvant Imatinib treatment is effective in reducing the recurrence rate by the analysis of all patients with R1 resection. [source, 2016]
Patients with typical BCR-ABL1 transcripts (that is, b2a2 and/or b3a2) and ⩽3 months of prior Imatinib treatment were included in the molecular analysis population for evaluating molecular response rates (patients with atypical BCR-ABL1 transcripts were excluded because standard RQ-PCR methodology was not optimized for detection of atypical BCR-ABL1 transcripts; patients with >3 months of Imatinib therapy (a protocol violation) were excluded to be as conservative as possible in analyzing the efficacy of frontline nilotinib by avoiding potential confounding effects of prior Imatinib). [source, 2016]
Using the same carrier, the antifibrotic drugs PTX, a drug that has an antiproliferative effect on HSCs and blocks their activation in vitro (Gonzalo et al., 2006), DOX, which also potently impairs proliferation of HSCs in vitro (Greupink et al., 2006), 15-deoxy-Δ12,14-prostaglandin J2 (15dPGJ2), an apoptosis-inducing drug (Hagens et al., 2007), as well as 4-chloro-N-[4-methyl-3-(4-pyridin-3-yl-pyrimidin-2-ylamino)-phenyl]-benzamide (PAP19), a TYROSINE kinase inhibitor and a derivative of Imatinib (Gonzalo et al., 2007) and 18β-glycyrrhetinic acid (18β-GA) also known as enoxolone (Luk et al., 2007) could all be successfully delivered to HSCs to selectively unfold their respective activity. [source, 2016]
However, as is the case with Imatinib, the clinical effectiveness of Sunitinib is influenced by mutations in the KIT and PDGFRA genes. [source, 2016]
Key eligibility criteria included: age ≥18 years (however, protocol amendments also allowed younger patients to enroll), histologically confirmed metastatic and/or unresectable GIST not amenable to standard therapy, failed prior treatment with Imatinib (indicated by disease progression or intolerance), potential to derive clinical benefit from Sunitinib treatment, and resolution of all acute toxic effects of any prior therapy/surgery to grade ≤1. [source, 2016]
Although effective in the vast majority of patients, the eventual evolution of resistance to Imatinib is common in patients with GIST, with resistance observed in more than 80 % of evaluable patients during long-term follow-up in a phase III trial [30]. [source, 2016]
For patients receiving long-term Imatinib treatment, maintaining the continued administration at a sufficient dose is critical for maintaining the clinical effectiveness of Imatinib [11,12]. [source, 2016]
The continuation of therapeutic doses of Imatinib has important implications regarding the efficacy of Imatinib. [source, 2016]