Erwinaze (asparaginase Erwinia chrysanthemi) contains an asparaginase specific enzyme derived from Erwinia chrysanthemi. The mechanism of action of Erwinaze thought to be based on the inability of leukemic cells to synthesize asparagine due to lack of asparagine synthetase activity, resulting in cytotoxicity specific for leukemic cells.
Erwinaze is specifically approved as a component of a multi-agent chemotherapeutic regimen for the treatment of patients with acute lymphoblastic leukemia who have developed hypersensitivity to E. coli-derived asparaginase.
Erwinaze is supplied as a solution for intramuscular administration. The recommended initial dose of the drug is as follows:
To substitute for a dose of pegaspargase: 25,000 International Units/m2 administered intramuscularly three times a week (Monday/Wednesday/Friday) for six doses for each planned dose of pegaspargase.
To substitute for a dose of native E. coli asparaginase: 25,000 International Units/m2 administered intramuscularly for each scheduled dose of native E. coli asparaginase within a treatment.
The FDA approval of Erwinaze was based on a single-arm, multi-center, open-label, safety and clinical pharmacology trial. This trial enrolled 58 subjects with ALL who were unable to continue to receive pegaspargase due to hypersensitivity reactions. The subjects received Erwinaze 25,000 International Units/m2 intramuscularly for two weeks (six total doses) as a replacement for each scheduled dose of pegaspargase remaining on their original treatment protocol.The main endpoint was determination of the proportion of patients who achieved a serum trough asparaginase level greater than or equal to 0.1 International Units/ mL. More than 50% of the subjects reached this endpoint at 48 or 72 hours following the third dose.
Adverse events associated with the use of Erwinaze may include, but are not limited to, the following:
Erwinaze (asparaginase Erwinia chrysanthemi) contains an asparaginase specific enzyme derived from Erwinia chrysanthemi. Asparaginase Erwinia chrysanthemi catalyzes the deamidation of asparagine to aspartic acid and ammonia, resulting in a reduction in circulating levels of asparagine. The mechanism of action of Erwinaze thought to be based on the inability of leukemic cells to synthesize asparagine due to lack of asparagine synthetase activity, resulting in cytotoxicity specific for leukemic cells that depend on an exogenous source of the amino acid asparagine for their protein metabolism and survival.
For additional information regarding Erwinaze or acute lymphoblastic leukemia, please visit the Erwinaze web page.
The Erwinaze drug information shown above is licensed from Thomson CenterWatch. The information provided here is for general educational purposes only and does not constitute medical or pharmaceutical advice which should be sought from qualified medical and pharmaceutical advisers.