BENITIONSClinical Trial Intelligence

05-001: Treatment of Acute Lymphoblastic Leukemia in Children

Phase 3 Completed NCT00400946

ConditionDrug/Agent Toxicity by Tissue/Organ, Leukemia
PhasePhase 3
SponsorDana-Farber Cancer Institute
StatusCompleted
Enrollment800 participants
Interventionsasparaginase, cyclophosphamide, cytarabine, dexamethasone, dexrazoxane hydrochloride
Start dateApr, 2005
Completion dateAug, 2014
Results postedJun 14, 2017

Summary

RATIONALE: L-asparaginase is an important component of treatment for childhood acute lymphoblastic leukemia, but is also associated with notable side-effects, including hypersensitivity, pancreatitis, and thrombosis. We have previously reported that patients with acute lymphoblastic leukemia in whom asparaginase treatment was discontinued because of intolerable side-effects had survival outcomes that were inferior to those who received all or nearly all of their intended doses. Two bacterial sources of asparaginase exist: Escherichia coli (E coli) and Erwinia chrysanthemia (Erwinia). Generally, the E coli-derived enzyme has been used as front-line therapy and the Erwinia-derived preparation has been reserved for patients who develop hypersensitivity reactions. Pegylated E coli asparaginase (PEG-asparaginase) has a longer half-life and is potentially less immunogenic than native E coli L-asparaginase, and has been used as the initial asparaginase preparation in some pediatric acute lymphoblastic leukemia treatment regimens. PURPOSE: Although the pharmacokinetics of each of these asparaginase preparations: intravenous PEG-asparaginase (IV-PEG) and intramuscular native E coli L-aspara

Asparaginase-Related Toxicity Rate

30-week post-induction asparaginase treatment period · percentage of participants

Intramuscular Native E Coli L-asparaginase (IM-EC)26 percentage of participants
Intravenous PEG-asparaginase (IV-PEG)28 percentage of participants
p-value.60

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