[Action mechanism of thalidomide in treatment of multiple myeloma].
Thalidomide, N-phtalidoglutamide, is a well-known teratogenic agent when given to pregnant women. It was first synthesized by CIBA in 1953, but put on market in Germany as a sedative, but Dr. Rentz reported first the relation with the teratogenicity. However, its clinical activity to erythema nodosum leprosum was accidentally found. In 1997, thalidomide was found active to multiple myeloma, but its clinical use is not authorized yet in Japan. The mechanisms which so far reported are as follows. 1) The inhibitory activity of angiogenesis 2) NF-kappaB suppression 3) Suppression of GVHD, and other activity to immunity (suppression or augmentation), suppression of TNFa 4) Suppression of intracellular adhesion molecule 5) Binding to DNA From these reports, the teratogenicity or the clinical activities have been somewhat understood. Recently clinical studies of the analogue, Lenalidomide, have been reported.
Tsukagoshi
Shigeru
S
The Tokyo Cooperative Oncology Group.
D020533:Angiogenesis Inhibitors; D015815:Cell Adhesion Molecules / Q000378:metabolism; D004247:DNA / Q000378:metabolism; D005260:Female; D006801:Humans; D007166:Immunosuppressive Agents; D000077269:Lenalidomide; D007917:Leprostatic Agents; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D011247:Pregnancy; D013723:Teratogens; D013792:Thalidomide / Q000009:adverse effects / Q000031:analogs & derivatives / Q000494:pharmacology*
D020533:Angiogenesis Inhibitors; D015815:Cell Adhesion Molecules; D007166:Immunosuppressive Agents; D007917:Leprostatic Agents; D016328:NF-kappa B; D013723:Teratogens; D013792:Thalidomide; D004247:DNA; D000077269:Lenalidomide