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A 867744 is a positive allosteric modulator of α7 nAChRs (IC50 values are 0.98 and 1.12 μM for human and rat α7 receptor ACh-evoked currents respectively, in X. laevis oocytes). Displays no activity at 5-HT3A, α3β4 or α4β2 nAChRs. Brain penetrant.
|Storage||Store at +4°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
|ethanol||4.03||10 with gentle warming|
The following data is based on the product molecular weight 402.89. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||2.48 mL||12.41 mL||24.82 mL|
|5 mM||0.5 mL||2.48 mL||4.96 mL|
|10 mM||0.25 mL||1.24 mL||2.48 mL|
|50 mM||0.05 mL||0.25 mL||0.5 mL|
References are publications that support the biological activity of the product.
Malysz et al (2009) In vitro pharmacological characterization of a novel allosteric modulator of α 7 neuronal acetylcholine receptor, 4-(5-(4-chlorophenyl)-2-methyl-3-propionyl-1H-pyrrol-1-yl)benzenesulfonamide (A-867744), exhibiting J.Pharmacol.Exp.Ther. 330 257 PMID: 19389923
Faghih et al (2009) Discovery of 4-(5-(4-chlorophenyl)-2-methyl-3-propionyl-1H-pyrrol-1-yl)benzenesulfonamide (A-867744) as a novel positive allosteric modulator of the α7 nicotinic acetylcholine receptor. J.Med.Chem. 28 3377 PMID: 19419141
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Keywords: A 867744, A 867744 supplier, A867744, positive, allosteric, modulators, a7, alpha7, acetylcholine, nicotinic, receptors, nAChRs, selective, PAM, Nicotinic, (a7), Receptors, 4571, Tocris Bioscience
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Alzheimer's disease (AD) is a degenerative brain disease and the most common cause of dementia, affecting approximately 47 million people worldwide. Updated in 2015, this poster summarizes the structural and functional changes observed in the progression of this neurodegenerative disease, as well as classic AD drug targets.
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