Apoptosis

(S)-Thalidomide treatment results in a reduction in cell viability in U266 cells with an IC ₅₀ of 362 μM.
(S)-Thalidomide treatment increased apoptosis in a dose-dependent manner in U266 cells.
There are changes in the expression profile of genes involved in angiogenesis and apoptosis, but the changes are most dramatic in the apoptotic genes. In particular, the expression of I-κB kinase is decreased by two-fold, which is associated with a four-fold decrease in NF-κB expression. (S)-Thalidomide increases the Bax:Bcl-2 ratio, also increases I-kB protein levels, and decreases NF-kB activity. A dramatic decrease in Bcl-2 expression with (S)-Thalidomide suggests a possible enhancement of cytotoxic effect if combined with other cytotoxic agents.

Thalidomide does cause limb reduction defects in chick embryos as long as the embryos are directly exposed to the drug. The most useful techniques are implanting Thalidomide-soaked beads into the embryo immediately adjacent to the limb territory or soaking presumptive chick limb territories in Thalidomide and then grafting the explants to a host embryo celom. Thalidomide affects the chick limb grafted to a host embryo in a dose response fashion. Furthermore, (S)-Thalidomide is more teratogenic than (R)-Thalidomide.