Thalidomide was synthesized in 1953 by a West German company as a sedative. It became popular outside of the United States to help with morning sickness in the mid 1950s, but in 1961 it was discovered to cause birth defects. Its popular use was discontinued, but it is now used as a treatment for other diseases, such as leprosy and multiple myeloma. 
Thalidomide is a tasteless and odorless white crystalline compound. 
The chemical formula of thalidomide is C13H10N2O4, and it exists as a racemic mixture.
A two-step synthesis of thalidomide is presented in 2 scheme below requires no purifications. Reaction of L-glutamine with N-carbethoxyphthalimide produces N-phthaloyl-L-glutamine. Cyclization of N-phthaloyl-L-glutamine to produce thalidomide is accomplished by treatment with CDI in the presence of a catalytic amount of DMAP. 
Despite the widespread tragedy associated with thalidomide, it continues to be used in medical settings due to its usefulness in the treatment of a number of conditions and diseases, such as leprosy and cancer.
The aspects of thalidomide most applicable to treatments such as those for leprosy and multiple myeloma are its inhibition of angiogenesis, and the anti-inflammatory effects. In leprosy, thalidomide is particularly effective in suppressing painful related conditions.
In a study of patients with advanced multiple myeloma, thalidomide was shown to cause remission in 10% of the patients. This could be due to a number of factors, including angiogenesis inhibition, the ability of thalidomide to alter adhesion molecule expression, and its inhibiting effect on the growth of the tumor necrosis factor alpha. 
Thalidomide selectively inhibits the tumor necrosis factor alpha by degrading its mRNA, decreasing the half life of this molecule.  Inhibition of this factor, which causes fever and discomfort in cancer patients, can make quality of life much better. However, it may also weaken the immune system. 
Thalidomide can also help with the wasting caused by HIV, because it inhibits tumor necrosis factor alpha. .
Children whose mothers took thalidomide during pregnancy were often born with shortened or missing limbs.
The structure of thalidomide contributes to its teratogenic effects. Tests show that only the S enantiomer of thalidomide is teratogenic. Thalidomide was originally racemic, but cannot be made safe by isolating one enantiomer, as the R entantiomer will readily convert to the S enantiomer in the body. 
There have been various hypotheses regarding the mechanisms of thalidomide, particularly as it relates to teratogenicity. However, current research is mostly concerned with "(1) oxidative stress/damage, (2) DNA intercalation, (3) inhibition of angiogenesis, and (4) cereblon (CRBN) binding." .
- Thalidomide has been shown to encourage production of oxygen radicals in rats to whom it has been administered, which results in oxidative stress as fewer viable oxygens are biologically available, effecting a large number of organs that rely on oxygen.
- Thalidomide attaches to promoter sites that are GC-rich using DNA intercalation, decreasing transcription of IGF-1 and FGF-2, which both lead to angiogenesis and the proper growth of extremities and limbs.
- Thalidomide is an angiogenesis inhibitor, which means that it prevents the formation of new blood vessels. This is useful in the treatment of diabetic retinopathy, macular degeneration, and solid tumors 
- CRBN has been found to be a thalidomide-binding protein, and its mutant form, which binds poorly to thalidomide, may weaken thalidomide's tetatogenic limb affects when it is overexpressed.
It is likely that these mechanisms all contribute to some way in thalidomide's overall teratogenic effect.
When pregnant rabbits (thalidomide sensitive) and pregnant rats (thalidomide insensitive), green fluorescent protein expression in the cells of the limb buds of the rabbit embryos was decreased, while that the in the rats was unaffected. .
Exposure periods have been correlated to specific problems caused by thalidomide: http://toxsci.oxfordjournals.org/content/122/1/1/F3.large.jpg
Thalidomide originally underwent animal testing as well as clinical trials in humans. This included 98 children under the age of 1, 160 nursing mothers, and 81 women in the third trimester of pregnancy. No teratogenic effects were observed during the clinical trials.  Following the thousands of birth defects caused by thalidomide, it became mandatory to test drugs on pregnant animals, to detect teratogenic effects. 
- The Saga of Thalidomide
- A Concise Two-Step Synthesis of Thalidomide
- Thalidomide: The Tragedy of Birth Defects and the Effective Treatment of Disease
- Antitumor Activity of Thalidomide in Refractory Multiple Myeloma
- Moreira et. al.
- Sampaio et. al
- A Concise Two-Step Synthesis of Thalidomide
- Angiogenesis Inhibition