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Revisiting the role of cladribine in acute myeloid leukemia: An improvement on past accomplishments or more old news?
Author(s) -
Freyer Craig W.,
Gupta Neha,
Wetzler Meir,
Wang Eunice S.
Publication year - 2015
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.23862
Subject(s) - cladribine , medicine , myeloid leukemia , cytarabine , myeloid , oncology , pharmacology , adenosine deaminase , leukemia , immunology , adenosine
Originally studied in lymphoid diseases, cladribine (CdA) is an adenosine deaminase resistant analog of adenosine that was later discovered to induce myeloid cell apoptosis. The activity of CdA in myeloid malignancies was first reported in relapsed/refractory (RR) pediatric acute myeloid leukemia (AML) with complete response (CR) rates of up to 47%. Consequently, several studies have confirmed the efficacy of single agent CdA or CdA combination regimens in AML. Established CR rates for combination regimens in RR adults are approximately 50%, while CR rates for newly diagnosed (ND) adults are approximately 70% and show similar toxicity profiles to previously used regimens. Despite these promising data, many centers have yet to adopt CdA combination regimens for these difficult to treat populations. We review the pharmacology, pharmacokinetics, clinical data, and safety of CdA monotherapy and combination regimens for the management of pediatric and adult ND and RR‐AML. Am. J. Hematol. 90:62–72, 2015. © 2014 Wiley Periodicals, Inc.