Table 2.
Years | Milestone | Description | Significance | References |
---|---|---|---|---|
2006 | Initial Discovery and Preclinical Studies | Identification of HHT’s cytotoxic properties against lymphoid and myeloid cells | Foundation for the clinical potential of HHT | [52] |
2007 | Confirmation of Apoptotic Efficacy | HHT shown effective in various tumors, including primary leukemic cells from AML patients | Broadened therapeutic scope of HHT | [54] |
2011 | Regulatory Approval of Omacetaxine (OM) | OM, a semi-synthetic HHT derivative, approved by EMA and FDA for CML treatment | Marked HHT's entry into clinical use for CML | [53] |
2011–2016 | Advanced Efficacy Studies | Studies highlighted OM’s mechanism in rapid protein degradation and the up-regulation of myosin-9 | Reinforced HHT’s effectiveness in hematologic malignancies | [55, 56] |
2014 | Elucidation of Mechanism of Action | Detailed understanding of how HHT and OM inhibit protein translation in cancer cells | Clarified the molecular basis of HHT's anticancer action | [53] |
AML: Acute Myeloid Leukemia; CML: Chronic Myeloid Leukemia; EMA: European Medicines Agency; FDA: Food and Drug Administration; HHT: Homoharringtonine; OM: Omacetaxine Mepesuccinate