It is not clear when the compounds it were tested were enantiomerical

Lenalidomide As a means of improving the immunomodulatory effects and beating the nonhematological adverse events of thalidomide, analogs such as lenalidomide have already been created. Like thalidomide, lenalidomide exerts pleiotropic effects, which include immunomodulatory, antiangiogenic, and antineoplastic activities. Decitabine In pre-clinical studies, lenalidomide has demonstrated more potent anti MM action than its parent compound and its toxicity profile is more favorable. After extensive phase I and phase II trials in advanced MM, followed by two pivotal phase III trials, lenalidomide was approved by the US FDA and by the European Medicines Agency in June 200770 to be used in conjunction with dexamethasone in the treatment of MM in patients who have received at least one prior therapy. Mechanism of action in MM The molecular mechanisms connected with disease progression Infectious causes of cancer in MM are determined by the interaction between the bone marrow microenvironment and MM cells. Briefly, the adhesion of MM cells to bone marrow stromal cells triggers the release of cytokines that mediate separate paths of MM cell growth and success, including proliferation, antiapoptosis, cell cycle progression, and migration. Stromal cell derived IL 6, tumefaction necrosis factor alpha and vascular endothelial growth factor, for example, take part in the activation of several MM cell signaling pathways, including phosphatidylinositol 3 kinase /Akt, Janus kinase /signal transducer and activator of transcription 3, Raf/Mek/ mitogen-activated protein kinase, and NF T, together with their downstream targets. Lenalidomide has been proven to influence Avagacestat many of the relationships central to myeloma growth by both direct and indirect systems. The immediate effects of lenalidomide contain induction of apoptosis or cell cycle arrest of the tumor cell and indirect effects involving modification of the tumor microenvironment and augmentation of the innate and acquired immune responses. Combined, these effects end in effective tumefaction cell reduction and suppression. This duality of action might be essential in the treatment of MM. The development of lenalidomide as an anticancer agent followed the success of thalidomide, a potent inhibitor of TNF with antiangiogenesis activity and T cell costimulatory activity. Compared with its parent compound, lenalidomide is a stronger inhibitor of TNFsecretion by activated monocytes. In addition to TNF, lenalidomide also inhibits transforming growth factor beta and the proinflammatory cytokines, IL 1, IL 6, and IL 12, although release of the antiinflammatory cytokine IL 10 appears to be increased by lenalidomide.