Abstract

From 1956 through 1958, was released into the European and Canadian pharmaceutical markets as a rapid-acting, hangover-free sedative without danger of respiratory depression. In 1960, reports of peripheral neuropathy with chronic use began to surface. Growing evidence of severe infant limb defects (phocomelia) and internal organ deformities associated with maternal use of soon eclipsed this lesser concern. By late 1961, was withdrawn from the world market but not before more than 10,000 thalidomide babies were affected. Since that time, thalidomide’s ability to inhibit tumor necrosis factor-alpha (TNF-alpha) activity has been found to be beneficial for the treatment of erythema nodosum leprosum (ENL), chronic graft-vs-host disease (CGVHD), HIV-associated cachexia, oropharyngeal ulcers, and a variety of mucocutaneous disorders. Currently, is under study as an angiogenesis inhibitor, with the majority of human data in refractory multiple myeloma.

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