BL22
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US National Guidelines Clearinghouse on BL22
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Phone:617-525-6884
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BL22, also called CAT-3888 or GCR-3888, is an immunotoxin which attaches to and, upon internalization, kills B cells. It has completed a Phase I clinical (human) trial and is currently in a Phase II clinical trial for the treatment of hairy cell leukemia at a Phase I clinical trial for pediatric acute lymphoblastic leukemia and non-Hodgkin's lymphoma[3] at the NIH in the U.S. It may be useful against any B cell leukemia or lymphoma.
Technically, BL22 is an anti-CD22 immunotoxin fusion protein between a murine anti-CD22 disulphide-linked Fv (dsFv) antibody fragment and an edited copy of bacterial Pseudomonas exotoxin PE38. The toxin is activated intracellularly, by the low pH of the lysosome into which the entire protein was internalized via the CD22 receptor. The toxin kills the targeted cell through ribosome inactivation.[4]
BL22 is very similar to the newer HA22, which changes one amino acid in the antibody fragment to increase the binding affinity for the target molecule. Both of these proteins are designed to bind to the CD22 receptor on the surface of B cells.
Business History
BL22 was initially designed and produced at the U.S. National Cancer Institute, one of the agencies which make up the NIH. Early development of BL22 was funded by California biotech Genencor.[5] The future drug was acquired by Cambridge Antibody Technology at the end of 2005; less than a year later, CAT was purchased by British pharmaceutical company AstraZeneca.[6]
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
