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Clinical Trials

Date: 2014-10-17

Type of information: Presentation of results at a congress

phase: preclinical

Announcement: presentation of results the annual meeting of the Connective Tissue Oncology Society, held October 15-18 in Berlin, Germany

Company: Epizyme (USA - MA)

Product: EPZ-6438 (E7438)

Action mechanism:

Epizyme and Eisai are developing EPZ-6438 (E7438), a small molecule inhibitor of EZH2 for the treatment of non-Hodgkin lymphoma patients. In many human cancers, misregulated EZH2 enzyme activity results in misregulation of genes that control cell proliferation — without these control mechanisms, cancer cells are free to grow rapidly.
Epizyme granted Eisai a worldwide license to EPZ-6438 (E7438), subject to Epizyme\'s right to opt in for co-development, co-commercialization and profit share arrangement with Eisai in the United States. Epizyme is working with Roche and Eisai to develop a companion diagnostic to identify patients with non-wild type EZH2, where EZH2 contains point mutations. 

Disease:

synovial sarcoma

Therapeutic area: Cancer - Oncology

Country:

Trial details:

Latest news:

* On October 17, 2014, Epizyme, a clinical stage biopharmaceutical company creating innovative personalized therapeutics for patients with genetically defined cancers, presented pre-clinical data on EPZ-6438 (E7438), its oral, small molecule inhibitor of EZH2, in models of synovial sarcoma, a soft tissue sarcoma that typically affects young adults. Synovial sarcomas are characterized by a translocation of chromosomes X and 18, generating an SS18-SSX fusion protein that creates a state of deficiency of the INI1 protein. The data were presented by Heike Keilhack, Ph.D., Director of Biological Sciences, Epizyme, during the annual meeting of the Connective Tissue Oncology Society, held October 15-18 in Berlin, Germany. In the study, synovial sarcoma cell lines and patient-derived xenograft models were evaluated for their sensitivity to EZH2 inhibition in vitro and in vivo. Histone methylation, changes in gene expression and histology endpoints were also assessed. The data showed that EPZ-6438 induced dose-dependent inhibition of cell growth and cell death specifically in SS18-SSX fusion-positive cells in vitro. Treatment of mice with either a cell line xenograft or two patient-derived xenograft models led to dose-dependent tumor growth inhibition, while treatment in a fourth xenograft model did not reflect such results. The poster is available on the Epizyme website.

Is general: Yes