The medication famously associated with causing phocomelia and other severe limb defects in newborns when taken during pregnancy is Thalidomide.

- Thalidomide was originally marketed in the late 1950s as a sedative and treatment for morning sickness in pregnant women.
- However, it was soon discovered that exposure to thalidomide during the first trimester of pregnancy led to a dramatic increase in cases of severe congenital malformations, most notably phocomelia, a condition characterized by severely shortened or absent limbs.

Key points include:
- Thalidomide is a potent teratogen, particularly harmful during early embryonic development.
- Limb abnormalities such as phocomelia, amelia, and other skeletal deformities are classic examples of thalidomide embryopathy.
- Other defects can include ear, eye, and cardiac malformations, but limb defects remain the hallmark.
- Unlike other antiepileptic drugs such as carbamazepine, valproic acid, or phenytoin, which have different teratogenic profiles (e.g., neural tube defects or fetal hydantoin syndrome), thalidomide’s association with limb reduction defects is historically and clinically distinctive.

This tragic episode significantly changed the landscape of drug regulation and the study of teratology.

Reference: *Harrison's Principles of Internal Medicine, 20th Edition, Volume 2, Chapter 350*