Incorporation of sodium channel blocking and free radical scavenging activities into a single drug, AM-36, results in profound inhibition of neuronal apoptosis

British Journal of Pharmacology

Volumn 132, Issue 8, 2001, Pages 1691-1698

  Callaway, J K ^a   Beart, P M ^a   Jarrott, B ^a   Giardina, S F ^a  

^a MONASH UNIVERSITY   (Australia)

Author keywords

AM 36; Antioxidants; Apoptosis; Cerebellar granule cells; Cerebral ischaemia; Sodium channel blockade; Veratridine

Indexed keywords

1 [2 (4 CHLOROPHENYL) 2 HYDROXY]ETHYL 4 [3,5 BIS(1,1 DIMETHYL) 4 HYDROXYPHENYL]METHYLPIPERAZINE; 2 [[4 [2,6 BIS(1 PYRROLIDINYL) 4 PYRIMIDINYL] 1 PIPERAZINYL]METHYL] 3,4 DIHYDRO 2,5,7,8 TETRAMETHYL 2H 1 BENZOPYRAN 6 OL; 21 [4 [5,6 BIS(DIETHYLAMINO) 2 PYRIDYL] 1 PIPERAZINYL] 16ALPHA METHYLPREGNA 1,4,9(11) TRIENE 3,20 DIONE; AM 36; CINCHOCAINE; REACTIVE OXYGEN METABOLITE; SCAVENGER; SODIUM CHANNEL; SODIUM CHANNEL BLOCKING AGENT; UNCLASSIFIED DRUG; VERATRIDINE;

ANIMAL CELL; ANTIOXIDANT ACTIVITY; APOPTOSIS; ARTICLE; BRAIN ISCHEMIA; CONCENTRATION RESPONSE; DRUG MECHANISM; GRANULE CELL; MOUSE; NERVE CELL NECROSIS; NEUROPROTECTION; NEUROTOXICITY; NONHUMAN; PRIORITY JOURNAL;

EID: 0035036830     PISSN: 00071188     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.bjp.0704018     Document Type: Article

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