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Transcript of Thalidomide Presentation
it was already tested on humans. Distribution and Effects Thalidomide spread to 46 different countries across Europe, Africa, Asia, Australia, and America from 1957-1961. It was prescribed to pregnant women as a sedative to alleviate morning sickness. About 12,000 babies were born with birth defects. Miscarriages tally that number up to 20,000. Children suffered from phocomelia (missing or shortened limbs) and brain damage. And 40% of babies with thalidomide-induced defects died before their first birthday. The chemistry behind it all Thalidomide contains 2 enantiomers (a.k.a. optical isomers), structures that are mirror images of each other but are not identical. (R) Thalidomide - sedative (S) Thalidomide - teratogenic; causes birth defects by blocking growth of blood vessels during limb formation Both enantiomers can racemize. In other words, either (R) or (S) Thalidomide can interconvert into the other. The once safe and mitigative drug will become teratogenic (and vice versa) regardless of which enantiomer is administered in the drug. Today 50 years later, Dr. Vargesson and Dr. Handa uncovered the cause of the phocomelia. A metabolite, a simpler form of Thalidomide broken down by enzymes, called CPS49 killed the blood vessels that were developing into limbs. The thalidomide binds itself to cereblon, a protein vital to limb formation, and deactivates it. Luckily, Dr. Frances Oldham Kelsey's skepticalness prevented the marketing of Thalidomide in the U.S. Dr. William McBride, an Australian obstetrician, and Dr. Widukind Lenz, a German pediatrician, discovered a link between Thalidomide and birth defects. Finally, Dr. Lenz proved that the drug was responsible and caused the termination of Thalidomide sales in 1961. The FDA approved the use of Thalidomide for reducing inflamation from leprosy in 1998 and for multiple myeloma, a cancer of the plasma cells, in 2006. However, the reappearance of Thalidomide still worries some scientists and doctors.