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Thalidomide was synthesised in 1954 and first marketed in Europe in October 1957 as an anti-emetic sedative and non-barbiturate hypnotic. In 1961 thalidomide was reported to have a major teratogenic effect given the frequent occurrence of a congenital defect that had been rare up to that point, phocomelia, in which the malformed children’s limbs resemble a seal’s flippers. It is estimated that between 5,000 and 6,000 cases of phocomelia were attributable to thalidomide during this period. The drug was then withdrawn from the market .
In 1965, its striking efficacy in treating erythema nodosum leprosum led to thalidomide use becoming increasingly widespread, though restricted; this resulted in reports that thalidomide was effective in treating numerous inflammatory pathologies of the skin and/or internal organs. Little by little, mechanisms of action were proposed and studied, rather than being wholly explained [2, 3]. Two main areas are currently being researched: thalidomide’s immunomodulatory effect caused by inhibiting tumour necrosis factor α (TNF-α) production in some inflammatory pathologies, and its antiangiogenic effect, which seems to be an avenue for the future in the fight against cancer.
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