| Stereochemistry | RACEMIC |
| Molecular Formula | C27H39ClN2O2 |
| Molecular Weight | 459.064 |
| Optical Activity | ( + / - ) |
| Defined Stereocenters | 0 / 1 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
CC(C)(C)C1=CC(CN2CCN(CC(O)C3=CC=C(Cl)C=C3)CC2)=CC(=C1O)C(C)(C)C
InChI
InChIKey=ZGSFWANJADAZQC-UHFFFAOYSA-N
InChI=1S/C27H39ClN2O2/c1-26(2,3)22-15-19(16-23(25(22)32)27(4,5)6)17-29-11-13-30(14-12-29)18-24(31)20-7-9-21(28)10-8-20/h7-10,15-16,24,31-32H,11-14,17-18H2,1-6H3
AM-36 is a novel arylalkylpiperazine with combined antioxidant and Na(+) channel blocking actions. This compound was discovered as a four-year Amrad-funded program with the Departments of Pharmacology and Chemistry at Monash University. In preclinical studies was shown, that AM-36 might have great promise in the acute treatment of human stroke. But these investigation were discontinued.
CNS Activity
Originator
Approval Year
PubMed
Sample Use Guides
in rats: nominal i.v. doses are: 0.2, 1 and 3 mg/kg
Route of Administration:
Intravenous
AM-36 inhibited batrachotoxinin (BTX)-sensitive Na+ channel binding in rat brain homogenates with an IC50 of 0.28 uM. Veratridine (100 uM)-induced neurotoxicity in murine cerebellar granule cells was completely inhibited by AM-36 (1.7 uM) compared to only partial inhibition by sipatrigine (26 uM). Veratridine-stimulated glutamate release, as measured through a microdialysis probe in the cortex of anesthetised rats, was inhibited by 90% by superfusion of AM-36 (1000 uM).
ACTIVE MOIETY
