SGI-1776 Causes Tumor Regression In AML Xenograft Models

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SuperGen announced that its lead, oral PIM kinase inhibitor, SGI-1776, causes tumor regression in acute myologenous leukemia (AML) xenograft models.

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In a poster presentation entitled "A potent small molecule PIM kinase inhibitor with in vivo oral availability and activity in cell lines from hematological malignancies," Dr. Gregory Berk, SuperGen's Chief Medical Officer, detailed how scientists used SuperGen's CLIMB technology to build a model that allowed for the creation of small molecule PIM kinase inhibitors.

SGI-1776 was identified as an orally available, potent and selective inhibitor of the PIM kinases. SGI-1776 induces cell cycle arrest, dose dependent apoptosis and a reduction in phospho-BAD levels in leukemia and lymphoma cell lines. Phospho-BAD is a direct substrate for PIM, and may serve as a useful in vivo biomarker for future clinical trials. Most notably, SGI-1776 induced significant tumor regression in MOLM-13 and MV-4-11 (AML) xenograft models.

"Our PIM kinase inhibitor, SGI-1776, has the potential to be an effective treatment for AML and other malignancies that over-express PIM kinase," said Dr. James Manuso, SuperGen's President and Chief Executive Officer. "The data also provide support for the use of our CLIMB technology to identify and rapidly advance candidates into the clinic. We plan to initiate Phase 1 clinical trials with SGI-1776 in solid tumors and leukemias later this year. SGI-1776 may become the first drug in this class of inhibitors to enter the clinic."

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