6 iodo 2 methyl 1 2 4 morpholinyl ethyl 1h indol 3 yl 4 methoxyphenyl methanone am 630

Manufactured by Bio-Techne

Sourced in United Kingdom

6-iodo-2-methyl-1-[2-(4-morpholinyl)ethyl]-1H-indol-3-yl](4-methoxyphenyl)methanone (AM-630) is a synthetic compound. It functions as a selective antagonist for the cannabinoid receptor 2 (CB2).

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Lab products found in correlation

Tetrodotoxin ttx, by Merck Group (1 mentions) N piperidin 1 yl 5 4 iodophenyl 1 2 4 dichlorophenyl 4 methyl 1h pyrazole 3 carboxamide am251, by Bio-Techne (1 mentions) Dss mw 40 000, by MP Biomedicals (1 mentions)

2 protocols using 6 iodo 2 methyl 1 2 4 morpholinyl ethyl 1h indol 3 yl 4 methoxyphenyl methanone am 630

Pharmacological Characterization of Detrusor

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The following drugs were used: acetylcholine (ACh), atropine, carbachol (CCh), N^G-nitro-L-arginine (L-Noarg) and tetrodotoxin (TTX), all from Sigma (USA). α,β-methylene-adenosine 5'-triphosphate (α,β-Met-ATP), arachidonyl-2'-chloroethyl amide (ACEA), N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (AM-251), 6-iodo-2-methyl-1-[2-(4-morpholinyl)ethyl]-1H-indol-3-yl](4-methoxyphenyl)methanone (AM-630) and N-(adamant-1-yl)-6-isopropyl-4-oxo-1-pentyl-1,4-dihydroquinoline-3-carboxamide (SER-601) from Tocris (UK). ACEA was dissolved in 96% ethanol. AM-251, AM-630 and SER-601 were dissolved in 10% dimethylsulphoxide (DMSO). The other drugs were dissolved in distilled water. The solvents, at the final concentration (< 0.05%) used in the bath, had no effect on the contractility of the detrusor preparations. The primary CB₁ and CB₂ antibodies were from Santa Cruz Biotechnology (Madrid, Spain) and PGP 9.5 was from Abcam (Cambridge, UK). The secondary antibodies were from Invitrogen (Paisley, UK).

Blaha I., Recio P., Martínez M.P., López-Oliva M.E., Ribeiro A.S., Agis-Torres Á., Martínez A.C., Benedito S., García-Sacristán A., Fernandes V.S, & Hernández M. (2016). Impaired Excitatory Neurotransmission in the Urinary Bladder from the Obese Zucker Rat: Role of Cannabinoid Receptors. PLoS ONE, 11(6), e0157424.

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Investigating Cannabinoid Modulation in Colitis

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All drugs and reagents, unless otherwise stated, were purchased from Sigma-Aldrich (Poznan, Poland). DSS (MW 40,000) was purchased from MP Biomedicals (Solon, OH, USA). N-3-Pyridinyl-4-[[3-[[5-(trifluoromethyl)-2-pyridinyl]oxy]phenyl]methyl]-1-piperidine-carboxamide (PF-3845) was prepared by TriMen Chemicals (Lodz, Poland). N-(Piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (AM251), and 6-Iodo-2-methyl-1-[2-(4-morpholinyl)ethyl]-1H-indol-3-yl](4-methoxyphenyl) methanone (AM630) were purchased from Tocris Bioscience (Bristol, UK).

Sałaga M., Mokrowiecka A., Zakrzewski P.K., Cygankiewicz A., Leishman E., Sobczak M., Zatorski H., Małecka-Panas E., Kordek R., Storr M., Krajewska W.M., Bradshaw H.B, & Fichna J. (2014). Experimental colitis in mice is attenuated by changes in the levels of endocannabinoid metabolites induced by selective inhibition of fatty acid amide hydrolase (FAAH). Journal of Crohn's & colitis, 8(9), 998-1009.

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