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news.EntreMed has reported that preclincal results of its lead aurora kinase-angiogenesis inhibitor, ENMD-981693, have demonstrated tumor regression and significant growth inhibition in multiple myeloma xenografts, including tumors that have high levels of constitutively active FGFR3, a mutation found in a subset of multiple myeloma patients that promotes disease progression.
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In addition, ENMD-981693 exhibited antiangiogenic activity in animal models by both inducing regression of formed blood vessels and preventing the formation of new blood vessels at well-tolerated doses.
ENMD-981693 has been shown to inhibit a distinct profile of angiogenic tyrosine kinase targets in addition to Aurora A kinase and other oncogenic proteins. Aurora kinases are key regulators of mitosis (cell division), and are often over-expressed in human cancers. Inhibition of Aurora A has been shown to induce cell death in multiple myeloma tumor cells preclinically. ENMD-981693 is selective for the Aurora A isoform in comparison to Aurora B.
Mark Bray, vice president of research at EntreMed, said: “ENMD-981693 has robust antitumor activity. In multiple preclinical models, ENMD-981693 induces tumor regression demonstrating the activity and tolerability of the molecule. Further characterization of the unique target profile of ENMD-981693 will direct the clinical development program. These data support EntreMed’s clinical rationale for this compound and provide further validation for its potential clinical utility in hematological cancers.”