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Key Documents

83000

Sigma-Aldrich

Potassium methanesulfonate

≥98.0% (dry substance, T)

Synonym(s):

Methanesulfonic acid potassium salt

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About This Item

Empirical Formula (Hill Notation):
CH3KO3S
CAS Number:
Molecular Weight:
134.20
Beilstein:
3914899
EC Number:
MDL number:
UNSPSC Code:
12352100
PubChem Substance ID:
NACRES:
NA.22

Assay

≥98.0% (dry substance, T)

form

crystals

loss

<10% loss on drying

SMILES string

[K+].CS([O-])(=O)=O

InChI

1S/CH4O3S.K/c1-5(2,3)4;/h1H3,(H,2,3,4);/q;+1/p-1

InChI key

XWIJIXWOZCRYEL-UHFFFAOYSA-M

Application

Potassium methanesulfonate can be employed as a cocatalyst in ruthenium-catalyzed C-H arylation of heteroarylbenzenes.

Pictograms

Exclamation mark

Signal Word

Warning

Hazard Statements

Hazard Classifications

Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3

Target Organs

Respiratory system

Storage Class Code

11 - Combustible Solids

WGK

WGK 2

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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Studies on the Cocatalyst in Ruthenium-Catalyzed C-H Arylation
Seki M, et al.
Synthesis, 47(10), 1423-1435 (2015)
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Human induced pluripotent stem cell derived cardiomyocytes (hiPSC-CMs) offer a unique in vitro platform to study cardiac diseases, as they recapitulate many disease phenotypes. The membrane potential (Vm) and intracellular calcium (Ca2+) transient (CaT) are usually investigated separately, because incorporating
R P Pölönen et al.
Molecular biology reports, 47(2), 1067-1077 (2019-12-02)
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited cardiac disease characterized by arrhythmias under adrenergic stress. Mutations in the cardiac ryanodine receptor (RYR2) are the leading cause for CPVT. We characterized electrophysiological properties of CPVT patient-specific induced pluripotent stem cell-derived
Benoit Labonté et al.
Nature medicine, 23(9), 1102-1111 (2017-08-22)
Major depressive disorder (MDD) is a leading cause of disease burden worldwide. While the incidence, symptoms and treatment of MDD all point toward major sex differences, the molecular mechanisms underlying this sexual dimorphism remain largely unknown. Here, combining differential expression

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