Summary of Clinical Trials

Our lead product, Cloretazine® (VNP40101M), is an alkylating (DNA-damaging) agent. Our primary registration strategy for this compound is for the treatment of acute myelogenous leukemia (AML). A pivotal Phase 2 trial in elderly patients with de novo poor-risk AML commenced in 2006 and in August 2007 it was announced that 85 patients had been accrued to this trial. The Company plans to file a New Drug Application (NDA) for Cloretazine® (VNP40101M), based on this pivotal Phase 2 trial, with the U.S. Food and Drug Administration (FDA) in 2008. In addition, clinical trials of Cloretazine® (VNP40101M) are underway elderly AML and myelodysplastic syndromes in combination with cytarabine, in brain tumors in combination with temozolomide, and in advanced hematologic malignancies in combination with hematopoietic cell transplantation. Cloretazine® (VNP40101M) has received two fast track designations from the U.S. Food and Drug Administration (FDA) for the treatment of: (i) relapsed AML and (ii) elderly poor-risk AML. Cloretazine® (VNP40101M) has also received orphan drug designation for the treatment of AML in the United States and the European Union. A Phase 3 trial of Cloretazine® (VNP40101M) in combination with cytosine arabinoside (Ara-C) in relapsed AML commenced in 2005 and was put on clinical hold by the U.S. Food and Drug Administration (FDA) in May 2007 pending a complete medical review of all data on the trial. In January 2008, the FDA agreed to lift the clinical hold on this trial. The Company now plans to file a Special Protocol Assessment (SPA) for a new trial of Cloretazine® (VNP40101M) and cytarabine in relapsed acute myelogenous leukemia (AML).

Preclinical data on Cloretazine® (VNP40101M) demonstrated broad antitumor activity in in vivo models. It was curative in certain preclinical leukemia models, including mice bearing certain derivatives of a leukemia cell line that was resistant to standard alkylating agents. Cloretazine® (VNP40101M) was also active against solid tumor models, including lung, colon, and brain cancer, and melanoma. It was curative in mouse models in which a human glioma (brain tumor) or a mouse colon cancer was implanted and growing under the skin. The drug has been shown in preclinical studies to be capable of crossing the blood-brain barrier, a common obstacle in achieving active concentrations of most drugs within the brain.

Our second clinical compound, Triapine®, is a small molecule that in preclinical models inhibits the enzyme ribonucleotide reductase, and therefore prevents the replication of tumor cells by blocking a critical step in DNA synthesis. Triapine® is being evaluated in clinical trials sponsored by the National Cancer Institute (NCI).

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