Acute myeloid leukemia is characterized by an arrest in differentiation and uncontrolled proliferation of myeloid precursors in the bone marrow. This approach leads to hematopoietic deficit, and when undifferentiated cells escape the marrow, to major leukocytosis, with often devastating and life threatening sequelae. Even though majority of people under age 60 achieve a complete remission with traditional anthracycline and cytarabine based induction sessions, the CHK1 inhibitor long haul survival rates continue to be poor at around 30 C40%. The prognosis is even poorer for those with high risk AML, including those who are older, who had previous myelodysplastic syndromes or myeloproliferative disorders, or those with secondary AML from environmental exposures or prior chemotherapy. In such cases, a complete remission is attained in less than 40% of cases, with survival rates of less than 10% 2, 3. Novel solutions to improve these poor outcomes are targeted at those which affect DNA repair and reproduction, as well as developing agents which target cell signaling and cycling. Some of these endeavors are in early phases of study and development, while others demonstrate promise in preclinical and clinical investigation. The greatest goal is to broaden the therapeutic potential of old-fashioned induction programs in AML by the incorporation of mechanistically novel Plastid agents. In the present evaluation, we’ve selected these promising approaches to discuss below. Flavopiridol Flavopiridol is just a semi-synthetic flavone derived from the stem bark of Amoora rohituka and Dysoxylum binectariferum, plants utilized in India as herbal medicine 4. It’s been proven to have strong activity against numerous cyclin dependent kinases, and arrests the cell cycle at the G2/M phase and delays the G1 to S phase progression 5. Flavopiridol also inactivates ALK inhibitor the cdk 9/cyclin T complex, also known as PTEF b, causing inhibition of RNA polymerase II, and suppression of RNA and polypeptide synthesis. That transcriptional inhibition results in a decline in quantities of proteins, such as cyclin D1, VEGF, MCL 1, and STAT 3, required for cell cycling and survival 6 C8. In addition, flavopiridol is effective to a lesser degree on tyrosine kinases, such as the epidermal growth factor receptor, protein kinase C and Erk 5. In pre-clinical studies, flavopiridol was active in various hematopoietic cell lines. When administered concomitantly with cytarabine and topotecan, S period dependent providers, antagonistic effects are produced by it through its tendency to induce cell cycle arrest. However, it had been noted that after flavopiridol administration and withdrawal preceded cytarabine and topotecan, dormant surviving cells were permitted to re enter the cell cycle and were thus further sensitized to the latter agents. Clinical trials on the basis of the in vitro model studies are in progress.