ChemGenex Pharmaceuticals has announced that the United States Patent and Trademark Office has granted a patent that protects the semisynthetic production of homoharringtonine and its analogs and the use of these compounds in a treatment of leukaemia.

The US 7,169,774 B2 patent, entitled "Cephalotaxane Derivatives and their processes of preparation and purification" provides ChemGenex and its partner, Stragen Pharma, with a proprietary position until 2019 in the United States.

"This is another very positive step in the Ceflatonin development programme that further consolidates our patent position," said Greg Collier, Ph.D., CEO and managing director. "In addition to the strong regulatory position obtained through patents and orphan drug status in major jurisdictions, the Ceflatonin clinical development programme is progressing very well. We now have 11 centres in the USA and Europe recruiting patients for our registration-directed trial of Ceflatonin in chronic myeloid leukaemia (CML) patients with the T315I mutation who have failed Gleevec therapy, and have a group of outstanding clinicians working with us.

Following the granting of Fast Track status in November 2006, we are in ongoing discussion with the FDA concerning aspects of the development program and have the goal of completing enrolment in H2 2007."

Ceflatonin (HHT) is a potent inducer of apoptosis (programmed cell death) in myeloid cells and inhibits angiogenesis (blood vessel formation). In Phase 2 studies, Ceflatonin has demonstrated clinical activity in patients with CML, both as a single agent and in combination with other chemotherapeutic drugs. ChemGenex is developing Ceflatonin for the treatment of CML, and pilot studies are underway in myelodysplastic syndrome (MDS) and in acute myeloid leukaemia (AML).

Ceflatonin has a different mechanism of action than tyrosine kinase inhibitors (TKI's), and ongoing and proposed clinical studies will seek to determine.

Efficacy in treatment of CML patients who have developed resistance to tyrosine kinase inhibitor (TKI) therapy due to development of the T315I bcr-abl kinase domain point mutation. The T315I bcr-abl mutation, which develops in some CML patients treated with TKI's, is associated with resistance to Gleevec and Sprycel.