الفهرس 
1 IntroductionOnly 14 pages are availabe for public view
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Abstract
Abstract
Cancer is a genetic disorder distinguished by two primary attributes: uncontrolled cellular proliferation and the capability to infiltrate surrounding tissues, a phenomenon known as metastasis. It can be conceived as the consequence of a series of genetic alterations wherein a once-healthy cell undergoes a transformation into a malignant form.
In case of acute myeloid leukemia (AML), it represents a hematological malignancy marked by the rapid proliferation of aberrant myeloid blood cell precursors within the bone marrow. These atypical cells, often referred to as blasts, disrupt the regular production of normal blood cells as they accumulate excessively.
FMS-like tyrosine kinase 3 (FLT3) is a receptor tyrosine kinase that normally functions to regulate the growth and development of blood cells. Within the realm of AML, FLT3 has emerged as a pivotal player. In a significant proportion of AML cases, FLT3 is either overexpressed or harbors mutations that lead to its constant activation. This aberrant signaling can result in the uncontrolled proliferation of immature blood cells within the bone marrow. Moreover, these genetic alterations are associated with a higher risk of disease relapse and, consequently, with poorer treatment outcomes.
Several small molecule FLT3 inhibitors have been approved for the treatment of AML. Our research objective is to design and synthesize novel inhibitors targeting FLT3 with promising anti-leukemic activity. Building on the already known inhibitors, profound literature survey, SAR studies, and molecular modeling, a series of novel benzimidazole-based compounds were designed, synthesized, purified, and structurally confirmed by different analytical and spectral techniques.