Synergism between clofarabine and decitabine through p53R2: A pharmacodynamic drug–drug interaction modeling
Copyright policy )Synergism between clofarabine and decitabine through p53R2: A pharmacodynamic drug–drug interaction modeling
Clofarabine (CLO), a purine nucleoside analog with promising efficacy in acute myeloid leukemia (AML), inhibits the ribonucleotidereductase, p53R2. We have shown that p53R2 mRNA is up-regulated by decitabine (DEC), another drug with promising activity in AML. We developed a pharmacodynamic model to characterize the interaction between CLO and DEC on an AML cell line and down-regulated p53R2 protein to understand its role. These results confirm a role for p53R2 in both CLO and DEC mechanism of action, demonstrate synergism between these two drugs in this AML model and support the use of this combination in a future clinical trial.
- State University of New York at Potsdam United States
- Roswell Park Cancer Institute United States
- University at Buffalo, State University of New York United States
- D'Youville College United States
Adenine Nucleotides, Cell Survival, Blotting, Western, Cell Cycle Proteins, Drug Synergism, Decitabine, Cell Line, Tumor, Protein Biosynthesis, Ribonucleotide Reductases, Azacitidine, Humans, Arabinonucleosides, Clofarabine
Adenine Nucleotides, Cell Survival, Blotting, Western, Cell Cycle Proteins, Drug Synergism, Decitabine, Cell Line, Tumor, Protein Biosynthesis, Ribonucleotide Reductases, Azacitidine, Humans, Arabinonucleosides, Clofarabine
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