Atropine sulfate salt monohydrate - CAS 5908-99-6
Catalog number: 5908-99-6
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
2(C17H23NO3).H2O.H2SO4
Molecular Weight:
694.83
COA:
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Targets:
mAChR
Description:
Atropine is a competitive muscarinic acetylcholine receptor antagonist with an IC50 of 2.5 nM.
Purity:
>98%
MSDS:
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InChIKey:
JPKKQJKQTPNWTR-BRYCGAMXSA-N
InChI:
InChI=1S/2C17H23NO3.H2O4S.H2O/c2*1-18-13-7-8-14(18)10-15(9-13)21-17(20)16(11-19)12-5-3-2-4-6-12;1-5(2,3)4;/h2*2-6,13-16,19H,7-11H2,1H3;(H2,1,2,3,4);1H2/t2*13-,14+,15?,16?;;
Canonical SMILES:
CN1C2CCC1CC(C2)OC(=O)C(CO)C3=CC=CC=C3.CN1C2CCC1CC(C2)OC(=O)C(CO)C3=CC=CC=C3.O.OS(=O)(=O)O
1.Determination of diphenoxylate hydrochloride and atropine sulfate in combination drug formulations by liquid chromatography.
Lehr GJ1. J AOAC Int. 1996 Nov-Dec;79(6):1288-93.
An isocratic, reversed-phase liquid chromatographic (LC) method was developed for simultaneous determination of diphenoxylate hydrochloride (I) and atropine sulfate (II) in pharmaceutical products. Analysis is conducted on a Spherisorb CN column (5 microns), with a mobile phase consisting of 47% 0.001M pentanesulfonic acid sodium salt monohydrate, 53% acetonitrile, and 0.1% phosphoric acid. The detection wavelength is 220 nm. Tablets are extracted with acetonitrile-water (50 + 50). Oral solutions are determined directly after dilution. The method is validated for linearity, precision, system reproducibility, and accuracy. Recoveries at 80-120% of label claim ranged from 98.7 to 101.0% and from 99.6 to 102.5% for I and II, respectively. Results were linear (r > 0.9999) in the ranges 125-375 micrograms/mL and 1.25-3.75 micrograms/mL for I and II, respectively. Assay and content uniformity results for each ingredient, in both innovator products and generic formulations, are reported.
2.Endothelium-dependent contraction induced by acetylcholine in isolated rat renal arteries.
Nishimura Y1, Usui H, Kurahashi K, Suzuki A. Eur J Pharmacol. 1995 Mar 6;275(2):217-21.
We investigated whether or not acetylcholine elicited an endothelium-dependent contraction and whether an arachidonic acid metabolite was involved in the acetylcholine-induced contraction in ring preparations of rat renal arteries. Acetylcholine (0.1-100 microM) caused a transient contraction in endothelium-intact arteries in a concentration-dependent manner. The contraction induced by acetylcholine (10 microM) was enhanced by pretreatment with NG-nitro-L-arginine (100 microM), a nitric oxide synthase inhibitor, and was abolished by mechanical removal of the endothelium. Atropine (0.1 microM), quinacrine (1 and 3 microM), manoalide (0.1 and 1 microM), aspirin (1 and 10 microM), indomethacin (30 and 300 nM), ONO-3708 (9,11-dimethyl-methane-11,12-methano-13,14-dihydro-13-aza-14- oxo-15(beta)-cyclophenyl-omega-pentenor-thromboxane A2 L-arginine salt) (10 nM), S-1452 (calcium (5Z)-1R,2S,3S,4S-7-[3-phenylsulphonyl-aminobicyclo[2.2.1]hep t-2yl]-5- heptenoate hydrate) (3 nM) and SQ29,548 ([1S- [1 alpha,2 beta(5Z),3 beta,4 alpha]]-7-[3-[[2-[(phenylamino) carbonyl]hydrazino]methyl]-7-oxabicyclo[2.
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CAS 5908-99-6 Atropine sulfate salt monohydrate

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