BML-190, a known inverse agonist of mammalian cannabinoid receptors. BML-190 likely targets the C. neoformans G-protein-coupled receptor Gpr4 and, via the cyclic AMP (cAMP)/protein kinase A (PKA) signaling pathway, contributes to an intracellular accumulation of cAMP that results in decreased chitosan[3]. In HEK-293 cells stably expressing the human CB(2) receptor, BML-190 and AM251 potentiated the forskolin-stimulated accumulation of cAMP. BML-190 and AM251 reduce the basal levels of inositol phosphate production in cells expressing the CB(2) receptor and 16z44[4]. The selective CB2 receptor ligands JWH-015 and indomethacin morpholinylamide (BML-190), when added to THP-1 cells before stimulation with lipopolysaccharide (LPS) and IFN-gamma, reduced the toxicity of their culture supernatants to SH-SY5Y cells[5].
BML-190/吲哚美辛吗啉代酰胺 细胞实验
Cell Line
Concentration
Treated Time
Description
References
THP-1 cells
10 μM
30 min
reduced the toxicity of THP-1 cell supernatants to SH-SY5Y cells
Br J Pharmacol. 2003 Jun;139(4):775-86.
Cryptococcus neoformans (KN99α strain)
10 μM
3 days
To verify the effect of BML-190 in reducing chitosan in different strains, results showed reduced chitosan production in all tested strains
mBio. 2019 Dec 17;10(6):e02264-19.
Cryptococcus neoformans (cda2Δ3Δ strain)
1 μM, 10 μM, 5 μg/ml, 50 μg/ml
3 days
To screen for small-molecule inhibitors that reduce chitosan production, BML-190 was confirmed as one of the compounds that reduced chitosan content
mBio. 2019 Dec 17;10(6):e02264-19.
rat liver microsomes
15 mM
0.5 to 4 h
To investigate the in vitro metabolic pathways of BML-190 and identify its metabolites
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