Skip to main content
. Author manuscript; available in PMC: 2020 Nov 1.
Published in final edited form as: Mol Neurobiol. 2019 May 19;56(11):7719–7730. doi: 10.1007/s12035-019-1637-8

Table 2.

Pharmacology

MC65 HT22
Compounds MOA Activity EC50 Activity EC50
R-1 methanandamide CB1 agonist protects 3 μM protects 4 μM
2 AG CB1/2 agonist protects 0.05 μM potentiates 0.35 μM
Arvanil CB1 agonist protects 0.4 μM potentiates 0.1 μM
AEA Endocannabinoid protects 0.3 μM protects 0.35 μM
AM 404 AEA analogue protects 0.4 μM protects 10 μM
SLV319 CB1 antagonist no effect no effect
AM 281 CB1 antagonist potentiates 0.9 μM potentiates 1.5 μM
AM 251 CB1 antagonist potentiates 3.5 μM potentiates 1 μM
CP-55, 940 CB1 and 2 agonist protects 5 μM protects 6 μM
NADA CB1 and CB2 agonist protects 0.08 μM protects 1.1 μM
WIN-55, 212 CB2 agonist protects 1.5 μM no effect
JWH 133 CB2 agonist no effect >10 μM no effect
Q-3-Carboxamide CB2 agonist protects 0.09 μM no effect
AM 1241 CB2 agonist protects 0.3 μM protects 0.45 μM
AM 630 CB2 antagonist potentiates 0.01 μM potentiates 0.3 μM
UBR 597 Inhibits AEA degradation protects 1.1 μM protects 0.5 μM
RCS-8 CB1 agonist no effect no effect
MDA-19 CB2 agonist no effect no effect
MCBN Methyl ether of CBN no effect no effect
Hu210 CB1 agonist protects 0.95 μM protects 0.6 μM
Hu211 Inactive enantomer of Hu210 protects 1.5 μM protects 0.72 μM

MC65 cells were induced to make Aβ or HT22 cells were exposed to a toxic glutamate concentration in the presence of three-fold serial dilutions between 10 nM and 20 μM of the indicated compounds. Cell viability was monitored and the compounds either had no effect, potentiated, or inhibited toxicity. There was no direct toxicity to cells at the concentrations indicated. The EC50S are given for either protection or potentiation. NADA is N-arachidonoyl dopamine, Q-3-carboxamide is 4-quinolone-3 carboxamide, and AEA is arachidonyl ethanolamide, 2 AG is arachidonoylglycerol, and MCBN is methyl CBN. (—) means no value determined.