N-(2-methylphenyl)-4-(furan-3-yl)-2-methyl-5-oxo-1,4,5,6,7,8-hexahydro-quinoline-3-carboxamide (MQC)24 (link) was synthesized, purified and verified in Laboratory of Organic Chemistry, School of Pharmaceutical Sciences, University of Shizuoka, Japan. AR420626 was purchased from Cayman Chemical (Ann Arbor, MI, USA). AR420626 is a selective agonist of FFA3 (IC50 = 117 nM on cAMP content) that does not activate the related receptor FFA2 (GPR43) at concentrations up to 100 μM.25 (link) GR113808 and PTX were purchased from Tocris Bioscience (Pittsburgh, PA, USA). Atropine, bethanechol, hexamethonium, serotonin, TTX, IND, nicotine, L-NAME, ondansetron, granisetron, and other chemicals were purchased from Sigma-Aldrich (St. Louis, MO, USA). IND was dissolved in 100% ethyl alcohol; TTX, nicotine, bethanechol, PTX, and L-NAME were dissolved in distilled water, and other chemicals were dissolved in dimethyl sulfoxide.
Ar420626
Manufactured by Cayman Chemical
Sourced in United States
The AR420626 is a laboratory equipment product. It serves as a core function to perform specific tasks in a laboratory setting. A detailed description of its intended use or capabilities is not available at this time.
Automatically generated - may contain errors
Lab products found in correlation
Trichostatin a, by Merck Group (3 mentions)
Mk1903, by Bio-Techne (3 mentions)
Tiglic acid, by Merck Group (3 mentions)
Niacine, by Merck Group (3 mentions)
U73122, by Merck Group (2 mentions)
Mithramycin a, by Merck Group (2 mentions)
Tnf α, by Thermo Fisher Scientific (2 mentions)
Valproic acid, by Merck Group (2 mentions)
4 cmtb, by Bio-Techne (2 mentions)
Hexamethonium, by Merck Group (1 mentions)
Ondansetron, by Merck Group (1 mentions)
Granisetron, by Merck Group (1 mentions)
Serotonin, by Merck Group (1 mentions)
Bethanechol, by Merck Group (1 mentions)
L name, by Merck Group (1 mentions)
Gr113808, by Bio-Techne (1 mentions)
Nicotine, by Merck Group (1 mentions)
Ar c155858, by Bio-Techne (1 mentions)
Scfas, by Merck Group (1 mentions)
Il 1β, by Thermo Fisher Scientific (1 mentions)
5 protocols using ar420626
1
Synthesis and Characterization of MQC Compound
2
Modulation of GPR-mediated Signaling
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All agonists, drugs and inhibitors were dissolved in glycerol, DMSO or water following the manufacturer’s recommendations. SCFAs were from Sigma-Aldrich and used in a range of concentrations from 0.5 to 8 mM. GPRs agonists used were: GPR41: 4-CMTB (1 μM, Tocris 4642) and Tiglic acid (1–10 mM, Sigma); GPR43: AR420626 (1 μM, Cayman) and MCPC (1 mM, Sigma); GPR109a: Niacine (1 mM–10 mM, Sigma) and MK1903 (1 μM, Tocris). GPRs sub-unit inhibitors used were: Pertussis toxin (Ptx, 0.2 μg/ml, Sigma) and U73122 (Sigma 10 μM). MCT inhibitors used were: AR-C155858 (0.4 μM, Tocris), p-Chloromercuribenzoate acid (pCMB, 100 μM, Sigma). HDAC inhibitors used were: Trichostatin A (TSA, 1 μM, Sigma), SAHA (5 μM, Sigma). SP1 competitive inhibitor used was the Mithramycin A (0.1 μM) from Sigma. IL1β (10 ng/ml) and TNFα (10 ng/ml) were from Peprotech. Phorbol 12-myristate 13-acetate (PMA, 100 nM) was from Sigma.
3
Modulation of GPR Signaling Pathways
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All agonists, drugs and inhibitors were dissolved in glycerol, DMSO or water. Sodium salt of SCFAs were from Sigma and used in a range of concentrations from 0.5 to 8 mM. GPRs agonists: GPR41: 4-CMTB (1 μM Tocris) and Tiglic acid (1–10 mM Sigma); GPR43: AR420626 (1 μM Cayman) and 1-MCPC (1mM Sigma); GPR109a: Niacine (1–10 mM, Sigma) and MK1903 (1 μM Tocris). GPRs sub-unit inhibitors used were: Pertussis toxin (Ptx 0.2 μg/ml) and U73122 (10 μM) from Sigma. HDAC inhibitors: Trichostatin A (TSA 1 μM Sigma), SAHA (5 μM Sigma) and valproic acid (VPA 5 mM Sigma). SP1 inhibitor Mithramycin A (0.1 μM Sigma). PPARγ activators: Pioglitazone (5 μM), Roziglitazone (10 μM) and PPARγ inhibitor G9662 (100 μM), from Cayman. NF-kB inhibitor BAY 11-7082 (40 μM). AP-1 inhibitor SR-11302 (10 μM Tocris). STAT3/Jak2 inhibitor Cucurbitacin I (1 μM) from Tocris. IFNγ (100 U/ml) and TNFα (10 ng/ml) were from Peprotech. Final concentration of DMSO had no detectable effect on cells viability or responses.
4
Synthesis and Characterization of MQC Compounds
5
Investigating SCFA-mediated Cell Metabolic Regulation
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All agonists, antagonists and drugs tested were dissolved in a proper vehicle (DMSO, glycerol, water, PBS or ethanol) following the manufacturer’s recommendations. The final concentration used for vehicles had not detectable effect on metabolic activity of the cells. Sodium salts of tested SCFAs were from Sigma and used in a range of concentration from 0.125 to 8 mM (20 mM for acetate). AhR agonist: 2,3,7,8-Tetrachlorodibenzodioxin (TCDD 10 nM, Sigma). GPRs agonists: GPR41: 4-chloro-α-(1-methylethyl)-N-2-thiazolylbenzeneacetamide (4-CMTB 1 µM, Tocris) and Tiglic acid (1 mM, Sigma); GPR43: N-(2,5-Dichlorophenyl)-4-(furan-2-yl)-2-methyl-5-oxo-1,4,5,6,7,8-hexahydro-quinoline-3-carboxamide (AR420626 1 µM, Cayman) and 1-methylcyclopropane carboxylate (MCPC 1 mM, Sigma); GPR109a: Niacine (1 mM, Sigma) and (4aR, 5aR)-4,4a,5,5a-Tetrahydro-1H-cyclopropa[4,5]cyclopenta[1,2]pyrazole-3-carboxylic acid (MK1903 1 µM, Tocris). Pertussis toxin (Ptx at 0.2 µg/mL, Sigma) was used as Gαi-subunit inhibitor. MCT1 inhibitor used was p-Chloromercuribenzoate acid (pCMB 100 μM, Sigma). HDAC inhibitors: Trichostatin A (TSA 0.1 and 1 µM, Sigma), vorinostat (SAHA 5 µM, Sigma) and valproic acid (VPA 5 mM, Sigma). AhR antagonists: CH-22319 (1 µM, Millipore/Calbiochem), GNF-351 (1 µM, Millipore/Calbiochem), (−)Epigallocathechin gallate (20 µM, EGCG, Sigma).
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