(R)-Thalidomide is a COX 1/2 inhibitor that induces apoptosis in MCF-7, IM-9, HS-Sultan, KB and other cancer cells.

With the affinity of (R)-Thalidomide by the MIP present surface capture, that is more strongly than the other forms. In the case of (R)-Thalidomide, it is found to bind to the selective sites of the MIP more strongly than the other which reflects their different biological entities[1]. The (S)-Thalidomide imprints MIP nanoparticles exerted a greater cytotoxic effect on the caco-2 cells than the (R)-Thalidomide imprinted MIPs[1].

Methods: Adult female F344 rats were implanted with 9L gliosarcoma tumors intracranially, subcutaneously (flank), or both. The efficacy of oral thalidomide alone and in combination with intraperitoneal BCNU or cisplatin was evaluated after several weeks of treatment. S- and (R)-Thalidomide were measured by chiral HPLC in presumed pseudo-steady-state serum, tumor, and other tissues collected after treatment.
Results: Serum and tissue concentrations of (R)-Thalidomide were 40-50% higher than those of (S)-Thalidomide. [1]