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Competitor Analysis: Bcr-Abl and Src Kinase Inhibitors
La Merie Publishing, July 2009, Pages: 20
The present Competitive Intelligence Report about Bcr-Abl and Src Kinase Inhibitors provides a competitor evaluation in the field of novel molecular entities inhibiting Bcr-Abl and/or Src kinase for treatment of cancer as of July 2009. Purchase of the downloadable pdf report includes a 6-month online access to the data of the report and any updates since the publication date. Credentials to access the database will be sent by e-mail and allow online work with the project data to print or export an individual report.
Chronic myeloid leukemia (CML) is characterized by the presence of the Philadelphia (Ph) chromosome, which results from a reciprocal translocation between the long arms of the chromosomes 9 and 22 t(9;22)(q34;q11). This translocation creates two new genes, BCR-ABL on the 22q- (Ph chromosome) and the reciprocal ABL-BCR on 9q-. The “breakpoint cluster region/Abelson” (BCR-ABL) gene encodes for a 210-kD protein with deregulated tyrosine kinase (TK) activity, which is crucial for malignant transformation in CML. The recognition of the BCR-ABL gene and corresponding protein led to the synthesis of small-molecule drugs, designed to interfere with BCR-ABL tyrosine kinase activation by competitive binding at the ATP-binding site. The first tyrosine kinase inhibitor (TKI), introduced into clinical practice in 1998, was imatinib mesylate.
The advent of imatinib, a selective inhibitor of the ABL tyrosine kinase, has revolutionized the treatment of Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL). Combined with chemotherapy, imatinib exerts remarkable efficacy in patients with newly diagnosed disease. Despite such improvement, however, relapse does occur, mainly owing to acquisition of resistance.
Growing comprehension of the molecular mechanisms of resistance to imatinib has led to the development of novel BCR-ABL inhibitors that yield higher affinity for BCR-ABL and/or potent inhibitory activity against other target molecules such as SRC family kinases. The second-generation ABL kinase inhibitors, namely dasatinib and nilotinib, are already showing clinical activity in patients with imatinib-resistant Ph+ ALL, and other novel agents are undergoing preclinical and early clinical evaluation.
The c-Src protein is a 60-kDa nonreceptor tyrosine kinase that is emerging as a potential target for cancer therapy. c-Src regulates signals from multiple cell surface molecules, including integrins, growth factors , and G protein–coupled receptors. Elevated c-Src protein levels and/or kinase activity has been reported in a variety of cancers, including HNSCC. The activation of c-Src has been reported to mediate several aspects of tumor growth and progression, including proliferation, migration, invasion, survival, and angiogenesis.
The report includes a compilation of current active projects in research and development of Bcr-Abl and Src kinase inhibitors in oncology and other indications. In addition, the report lists company-specific R&D pipelines of Bcr-Abl and Src kinase inhibitors. Competitor projects are listed in a tabular format providing information on:
- Drug Codes,
- Target / Mechanism of Action,
- Class of Compound,
- Company,
- Product Category,
- Indication,
- R&D Stage and
- additional comments with a hyperlink leading to the source of information.
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