Quality Level
product line
ReagentPlus®
Assay
99%
bp
260 °C (lit.)
mp
125-127 °C (lit.)
SMILES string
OC(=O)c1cccs1
InChI
1S/C5H4O2S/c6-5(7)4-2-1-3-8-4/h1-3H,(H,6,7)
InChI key
QERYCTSHXKAMIS-UHFFFAOYSA-N
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Legal Information
ReagentPlus is a registered trademark of Merck KGaA, Darmstadt, Germany
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
Certificates of Analysis (COA)
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Bioorganic & medicinal chemistry letters, 14(3), 793-796 (2004-01-27)
The discovery of a novel class of HCV NS5B polymerase inhibitors, 3-arylsulfonylamino-5-phenyl-thiophene-2-carboxylic acids is described. SAR studies have yielded several potent inhibitors of HCV polymerase as well as of HCV subgenomic RNA replication in Huh-7 cells.
Chemistry (Weinheim an der Bergstrasse, Germany), 17(42), 11838-11843 (2011-09-08)
Herein, we describe our attempts to systematically prepare a series of oligo(2-thienyl)-substituted pyridine derivatives. The crucial starting material, a β-alkoxy-β-ketoenamide, is easily available on a large scale by the reaction of lithiated methoxyallene with thiophene-2-carbonitrile and thiophene-2-carboxylic acid. This three-component
Organic letters, 3(1), 91-93 (2001-06-30)
[figure: see text] A new methodology for the synthesis of substituted alkynes is described. In the presence of copper(I) thiophene-2-carboxylate (CuTC) or copper (I) 3-methylsalicylate (CuMeSal), the palladium-catalyzed cross-coupling of thioalkyne derivatives with boronic acids affords functionalized alkynes in yields
Journal of virology, 80(12), 6146-6154 (2006-05-30)
Multiple nonnucleoside inhibitor binding sites have been identified within the hepatitis C virus (HCV) polymerase, including in the palm and thumb domains. After a single treatment with a thumb site inhibitor (thiophene-2-carboxylic acid NNI-1), resistant HCV replicon variants emerged that
Antimicrobial agents and chemotherapy, 53(5), 2129-2132 (2009-03-11)
In vitro, telaprevir selects subtype-specific resistance pathways for hepatitis C virus GT-1a and GT-1b, as described to have occurred in patients. In GT-1a, the HCV-796 resistance mutation C316Y has low replication capacity (7%) that can be compensated for by the
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