Thalidomide (Figure 1) was derived from alpha-phnthaloylisoglutamine, a derivative of glutamic acid1 by Chemie Grünenthal GmbH, a West German Company in 1954. Thalidomide has a low level of toxicity and no LD50 could be established. Indeed, high doses of thalidomide did not cause respiratory or cardiac failure, suggesting that accidental death or suicide with this compound was highly unlikely. As a matter of fact, 17 patients, including small children and one suicide attempt, survived ingestion of excessive amounts of thalidomide. In 1957, thalidomide was approved for commercial use in West Germany as a sedative and sold under the brand name Kevadon. About this time, the anti-emetic (anti-nausea) activity was discovered and the drug was prescribed to counteract morning sickness in pregnant women. Unfortunately, the teratological effects of thalidomide were not revealed through studies in rodents and approximately 12,000 children were born deformed before thalidomide was banned for clinical use in March 1962 by the Canadian Food and Drug Directorate2. In 1998, thalidomide was approved to treat erythema nodosum leprosum, a painful inflammatory dermatologic reaction of leprosy. In 2006, the FDA approved thalidomide under the brand name Thalomid (Celgene Corp) for treatment of newly diagnosed multiple myeloma As a result of these approvals, the interest in thalidomide as a chemotherapeutic agent for other cancers, including prostate cancer (Figure 2), has emerged.
Thalidomide and its analogues in prostate cancer therapy: A scientific update
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Carlton R. Cooper, Cliff Poindexter, Benjamin Rohe, Robert A. Sikes; Thalidomide and its analogues in prostate cancer therapy: A scientific update. Biochem (Lond) 1 October 2010; 32 (5): 36–39. doi: https://doi.org/10.1042/BIO03205036
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