Myeloid lineage Inhibitors

The chemical class designated as Myeloid lineage Inhibitors encompasses a diverse array of compounds that interfere with various cellular processes and signaling pathways critical for the function and survival of myeloid lineage cells. These inhibitors operate through distinct mechanisms to modulate the activity of enzymes, receptors, kinases, and other proteins that are pivotal in myeloid cell proliferation, differentiation, and survival. Compounds such as Imatinib Mesylate and Dasatinib act on tyrosine kinases, which are essential for signal transduction in cellular processes. Imatinib Mesylate specifically targets the aberrant BCR-ABL tyrosine kinase, which is active in specific myeloid cell conditions, leading to a decrease in abnormal cell proliferation. Dasatinib extends its inhibition to a broader spectrum of tyrosine kinases, including BCR-ABL and SRC family kinases, thereby influencing both growth and differentiation of myeloid cells. Similarly, Midostaurin obstructs the action of FLT3, a receptor tyrosine kinase that is crucial for myeloid cell development. On the other hand, Enasidenib specifically inhibits the mutant IDH2 enzyme, which results in the accumulation of oncometabolites and impacts myeloid cell differentiation.

Other inhibitors target different aspects of myeloid cell biology. For instance, Tretinoin modulates retinoic acid receptors, promoting the differentiation of myeloid cells, whereas Cytarabine and 5-Azacytidine interfere with nucleic acid metabolism. Cytarabine mimics a nucleoside, impeding DNA synthesis, whereas 5-Azacytidine and Decitabine inhibit DNA methyltransferases, enzymes that add methyl groups to the DNA molecule, thus influencing gene expression patterns critical for the fate of myeloid cells. A different class of inhibitors, including Sorafenib, Sunitinib Malate, and Ruxolitinib, impacts the cellular microenvironment of myeloid cells. These inhibitors obstruct various receptor tyrosine kinases like VEGFR and PDGFR or inhibit JAK kinases, thereby modulating signaling pathways that contribute to the regulation of myeloid cells, including the JAK-STAT pathway.