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TG02 Potently Inhibits the Proliferation and Survival of Multiple Myeloma Cell Lines through Depletion of the Key Survival Protein MCL-1
Date:4/5/2013

San Diego (PRWEB) April 05, 2013

Tragara Pharmaceuticals, Inc. today announced that profiling biological data on TG02, the Company's unique oral kinase inhibitor, has been published in Clinical Cancer Research. Researchers from the Instituto de Biologia Molecular y Celular del Cancer, University of Salamanca, utilized in vivo models and patient-derived ex vivo samples to evaluate the antitumor activity and mechanism of action of TG02 in multiple myeloma. The data show that TG02 potently and consistently inhibited proliferation and survival of multiple myeloma cell lines, even under protective bone marrow niche conditions, and selectively induced apoptosis of primary patient-derived malignant plasma cells. The study also reported that that TG02 induced robust activation of the intrinsic pathways of apoptosis via its ability to deplete the key survival protein Mcl-1.

In this study, TG02 displayed significant single agent activity in two multiple myeloma xenograft models. Additionally, TG02 enhanced the in vivo activity of bortezomib and lenalidomide, two currently approved treatments for myeloma. As most of the treatment regimens for myeloma patients are based upon drug combinations, TG02’s demonstrated ability to augment the antitumor activity of other agents is a clinically important observation. The researchers also reported that the studied TG02 combinations were well tolerated by the animals.

TG02 is currently in phase I clinical testing in patients with multiple myeloma in the United States. An additional phase I clinical study in patients with chronic lymphocytic leukemia is also underway and a phase I study in acute leukemia has been completed.

1. Álvarez-Fernández, Stela, et al. "Potent antimyeloma activity of a novel ERK5/CDK inhibitor." Clinical Cancer Research (2013).

About TG02
TG02 is a unique, oral multi-kinase inhibitor which combines the benefits
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