Reference

Rabbit sural nerve responses to chronic treatment with thalidomide and supidimide

Rabbit sural nerve responses to chronic treatment with thalidomide and supidimide. Schwab, Bradley W.; Arezzo, Joseph C.; Paldino, Albert M.; Flohe, Leopold; Matthiessen, Theo; Spencer, Peter S. (Inst. Neurotoxicol., Albert Einstein Coll. Med., Bronx, NY, USA). Muscle Nerve, 7(5), 362-8 (English) 1984. CODEN: MUNEDE. ISSN: 0148-639X. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Chronic treatment of rabbits with thalidomide (I) [50-35-1], but not supidimide (II) [49785-74-2], caused progressive decrements in sural nerve conduction velocity which were not accompanied by qual. or quant. morphol. changes of nervous tissue. These effects of I may have some relation to the sensory neuropathy reported in humans receiving this drug.

Teratogen metabolism: activation of thalidomide and thalidomide analogs to products that inhibit the attachment of cells to concanavalin A coated plastic surfaces

Teratogen metabolism: activation of thalidomide and thalidomide analogs to products that inhibit the attachment of cells to concanavalin A coated plastic surfaces. Braun, Andrew G.; Weinreb, Steven L. (Dep. Radiat. Ther., Harvard Med. Sch., Boston, MA 02115, USA). Biochem. Pharmacol., 33(9), 1471-7 (English) 1984. CODEN: BCPCA6. ISSN: 0006-2952. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Thalidomide (I) [50-35-1] metabolites inhibited the attachment of tumor cells to concanavalin A [11028-71-0]-coated polyethylene surfaces. I, itself, was noninhibitory. I activation to inhibitory products required hepatic microsomes, an NADPH-generating system, and O. Prodn. of inhibitory metabolites was unaffected by either epoxide hydrolase or 1,2-epoxy-3,3,3-trichloropropane, an inhibitor of epoxide hydrolase endogenous to hepatic S9 fraction. Therefore, the attachment inhibitor was probably not an arene oxide. Inhibition was not accompanied by cytotoxicity, as judged by trypan blue exclusion. Although uninduced hepatic microsomes from mice, rats, and dogs had similar abilities to activate I, microsomes from Aroclor 1254-induced rats were relatively inactive in the system. Inhibitory metabolites were generated from the I analogs EM8 [16477-31-9], EM12 [26581-81-7], EM16 [26581-91-9], EM87 [49785-74-2], EM136 [42472-96-8], EM255 [79458-80-3], E350 [303-31-1], phthalimide [85-41-6], phthalimidophthalimide [4388-29-8], indan [496-11-7], 1-indanone [83-33-0] and 1,3-indandione [606-23-5]. Glutarimide [1121-89-7], glutamic acid [56-86-0], and phthalic acid [88-99-3] did not activate to inhibitory products.