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ChemGenex Reports Oral Bioavailability of Omacetaxine and Expands on Mechanism of Action
15 / 04 / 2008
ChemGenex Pharmaceuticals Limited (ASX:CXS and NASDAQ:CXSP) announced today that pre-clinical data characterizing the bioavailability and mechanism of action of omacetaxine mepesuccinate (formerly known as Ceflatoninr) were presented on Monday local time at the American Association of Cancer Research (AACR) 99th Annual Meeting in San Diego, California.
Data from ChemGenex researchers and collaborators were presented across three sessions. Highlights include:
Omacetaxine can be delivered orally in animals with oral bioavailability of approximately 75% compared with subcutaneous administration. (Abstract 2275).
Omacetaxine reduced the number of leukemic stem cells in the bone marrow by more than 80% in an animal model of chronic myeloid leukemia (CML). Significantly, the tyrosine kinase inhibitor (TKI) imatinib mesylate did not reduce leukemic stem cell number. (Abstract 2275).
Omacetaxine causes a rapid and dose-dependent reduction in the level of the key regulatory protein Mcl-1 in a cell model of CML. Mcl-1 is a key target protein in several types of leukemias and other cancers. Mcl-1 levels were not reduced in the short term by imatinib mesylate. (Abstract 2350).
"Following the clinical update presented last week showing hematologic and/or cytogenetic responses in 86% of chronic phase patients on trial, this is a timely confirmation of the significant advances we have made in understanding the mechanism of action of omacetaxine," said Dr. Greg Collier, ChemGenex's Managing Director and Chief Executive Officer. "In addition, we now have independent confirmation that omacetaxine has excellent oral bioavailability, opening a range of development and potential commercialization opportunities into the future."
Dr. Collier confirmed that the strategic positioning of omacetaxine is strongly supported by the new mechanism of action data emerging from the laboratories of ChemGenex, its collaborators and independent researchers. "We can reiterate that Mcl-1 is down-regulated by omacetaxine in CML, and that in an animal model the drug acts directly on leukemic stem cells in the bone marrow. We are seeing a range of biological effects of omacetaxine that clearly differentiate it from the TKIs, supporting its clinical development both in CML patients who fail TKI therapy and in other forms of leukemia."
Data from ChemGenex researchers and collaborators were presented across three sessions. Highlights include:
Omacetaxine can be delivered orally in animals with oral bioavailability of approximately 75% compared with subcutaneous administration. (Abstract 2275).
Omacetaxine reduced the number of leukemic stem cells in the bone marrow by more than 80% in an animal model of chronic myeloid leukemia (CML). Significantly, the tyrosine kinase inhibitor (TKI) imatinib mesylate did not reduce leukemic stem cell number. (Abstract 2275).
Omacetaxine causes a rapid and dose-dependent reduction in the level of the key regulatory protein Mcl-1 in a cell model of CML. Mcl-1 is a key target protein in several types of leukemias and other cancers. Mcl-1 levels were not reduced in the short term by imatinib mesylate. (Abstract 2350).
"Following the clinical update presented last week showing hematologic and/or cytogenetic responses in 86% of chronic phase patients on trial, this is a timely confirmation of the significant advances we have made in understanding the mechanism of action of omacetaxine," said Dr. Greg Collier, ChemGenex's Managing Director and Chief Executive Officer. "In addition, we now have independent confirmation that omacetaxine has excellent oral bioavailability, opening a range of development and potential commercialization opportunities into the future."
Dr. Collier confirmed that the strategic positioning of omacetaxine is strongly supported by the new mechanism of action data emerging from the laboratories of ChemGenex, its collaborators and independent researchers. "We can reiterate that Mcl-1 is down-regulated by omacetaxine in CML, and that in an animal model the drug acts directly on leukemic stem cells in the bone marrow. We are seeing a range of biological effects of omacetaxine that clearly differentiate it from the TKIs, supporting its clinical development both in CML patients who fail TKI therapy and in other forms of leukemia."