This is likely through the inhibition of Etk and down regulation of Myc and BCL2. The more detailed signaling pathways between the link remains to be further investigated. In summary, we have identified an Etk and Src dual inhibitor, CTA095, with good selectivity toward prostate cancer cells. This inhibitor could overcome Src inhibitor resistance and induce apoptosis in Src inhibitor-resistant prostate cancer cells. This study indicates that Etk and Src dual inhibition holds exceptional promise as a novel treatment strategy for prostate cancer. Acute myeloid leukemiais the most common hematologic malignancy in adults with a high incidence rate and low survival probability. AML progresses rapidly due to the rapid growth of abnormal white blood cells that accumulate in the bone marrow and interfere with the production of red blood cells, platelets, and normal white blood cells. If left untreated, AML is usually fatal within weeks or months after diagnosis. FLT3, a cell surface receptor belonging to the class III receptor tyrosine kinase family, plays a pivotal role in the differentiation and survival of the hematopoietic stem cells in bone marrow. FLT3 is one of the most commonly mutated genes in AML. Activating FLT3 mutations, FLT3-ITDand FLT3-TKD, are frequently observed in approximately 30% of adult AML patients. FLT3-activating mutantions critically regulate leukemic transformation by accelerating proliferation and suppressing apoptosis and are significantly associated with poor prognosis. These findings highlight FLT3-ITD and FLT3-TKD as highly attractive therapeutic targets for drug development in human AML. There are now several NVP-BKM120 distributor classes of small molecule FLT3 inhibitors that have entered clinical trials. However, effective drugs have not yet been identified in clinics. Although these inhibitors have demonstrated promising anti-cancer activity in in vitro and in vivo preclinical models, clinically positive responses in AML patients receiving single-agent FLT3 inhibitors are limited due to the transient reduction of peripheral blasts but not bone marrow blasts or the occurrence of inhibitor-resistant FLT3 mutations in patients. Therefore, combinatorial strategies of FLT3 inhibitors and other chemotherapeutic agents may be beneficial approaches to improve FLT3 inhibitor therapy and to overcome treatment failures. The FLT3 inhibitor CEP701combined with standard AML chemotherapeutic agents has the potential to improve clinical outcomes in AML patients. In addition, histone deacetylase inhibitors, a class of compounds that can induce cancer cell growth arrest and cell death by altering the acetylation status of both histone and non-histone proteins, can enhance the activity of FLT3 inhibitors on AML cell apoptosis. The HDACi vorinostatexhibits clinical activity in AML; however, its efficacy as a single agent is only WY 14643 moderate. In this study, we report data characterizing the pharmacological profile of a new FLT3 kinase inhibitor, BPR1J-340, and elucidate the possible molecular mechanism of the strongly synergistic effects in combination with SAHA in FLT3-ITD + cells. These results highlight the therapeutic potential of BPR1J-340 and SAHA in AML and support its preclinical or clinical development. Given that the abnormal expression of FLT3 kinase, including amplified or aberrantly activated FLT3, is frequently observed in the blast cells of AML patients, FLT3 represents an attractive therapeutic target of choice for drugs development in AML. To date, several potential FLT3 inhibitors have been developed and examined in AML patients, including lestaurtiniband midostaurinin phase III clinical trials and sunitinib malate, sorafenib, quizartinib, and crenolanibin phase II trials.