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Homoharringtonine, omacetaxine mepesuccinate, and chronic myeloid leukemia circa 2009
Author(s) -
QuintásCardama Alfonso,
Kantarjian Hagop,
Cortes Jorge
Publication year - 2009
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/cncr.24601
Subject(s) - homoharringtonine , medicine , myeloid leukemia , imatinib , imatinib mesylate , tyrosine kinase , chronic myelogenous leukemia , pharmacology , tyrosine kinase inhibitor , philadelphia chromosome , leukemia , cancer research , immunology , cancer , chromosomal translocation , receptor , genetics , biology , gene
Homoharringtonine (HHT) is a natural alkaloid that is obtained from various Cephalotaxus species. The mechanism of action by which HHT exerts its antitumor activity is through inhibition of protein synthesis and promotion of apoptosis. In the 1990s, HHT proved to be significantly active as salvage therapy for patients with chronic myeloid leukemia (CML) after failure on interferon‒α therapy. However, the remarkable success of imatinib mesylate in the treatment of CML relegated HHT to oblivion. The development of omacetaxine mepesuccinate, a subcutaneously bioavailable semisynthetic form of HHT, and its activity in imatinib‐resistant CML has established this agent for the second time as a valuable option in the management of this disease. Preliminary results appear to support the use of this agent for patients who have imatinib‐resistant CML, including those who carry the tyrosine kinase inhibitor‐insensitive mutation that exchanges the amino acids threonine and isoleucine at position 315 (the T315I mutation). In this article, the authors discuss the current data on omacetaxine and the prospects of this agent to be integrated into the state‐of‐the‐art treatment algorithms for CML. Cancer 2009. © 2009 American Cancer Society.