Abstract: Disclosed are methods are of treating acute myeloid leukemia (AML) comprising administering an effective amount of a first AML therapeutic and an effective amount of a second AML therapeutic. Also disclosed are methods of treating AML comprising administering an effective amount of a first AML therapeutic conjugated to N-(2-hydroxypropyl)methacrylamide (HPMA) copolymer. Also disclosed are methods of treating AML comprising administering an effective amount of a first AML therapeutic conjugated to HPMA copolymer, wherein the first AML therapeutic conjugated to HPMA copolymer comprises a HPMA copolymer backbone comprising at least two HPMA copolymer segments connected by a degradable peptide sequence.

Abstract: The present invention provides for a method of simultaneously treating both cancer and the Multidrug Resistance Phenotype via inhibition of cellular thiols, such as Glutathione S-Transferase (GST). This enzyme is overproduced in leukemia and solid tumor cells and is one of the main pathways involved in the Multidrug Resistance phenotype. The treatment provides for the administration of a chemically inert pro-drug, designed to be a specific substrate for the GST enzyme that, once cleaved, liberates the bioactive toxin Nitric Oxide (NO) intracellularly at the site of a malignant growth. NO then acts to inhibit the growth of the malignant cells and to induce cellular differentiation and apoptosis therein, effectively treating an existing cancerous condition. Additionally, once NO is liberated from the pro-drug, the remaining structure acts to inhibit further GST activity, providing a treatment for the Multidrug Resistant phenotype.

Abstract: The present invention provides for a method of simultaneously treating both cancer and the Multidrug Resistance Phenotype via inhibition of cellular thiols, such as Glutathione S-Transferase (GST). This enzyme is overproduced in leukemia and solid tumor cells and is one of the main pathways involved in the Multidrug Resistance phenotype. The treatment provides for the administration of a chemically inert pro-drug, designed to be a specific substrate for the GST enzyme that, once cleaved, liberates the bioactive toxin Nitric Oxide (NO) intracellularly at the site of a malignant growth. NO then acts to inhibit the growth of the malignant cells and to induce cellular differentiation and apoptosis therein, effectively treating an existing cancerous condition. Additionally, once NO is liberated from the pro-drug, the remaining structure acts to inhibit further GST activity, providing a treatment for the Multidrug Resistant phenotype.