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Merck
CN

M81101

mono-Methyl hydrogen succinate

95%

Synonym(s):

Monomethyl succinate, Succinic acid monomethyl ester

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About This Item

Linear Formula:
CH3OCOCH2CH2COOH
CAS Number:
Molecular Weight:
132.11
Beilstein:
1722669
EC Number:
MDL number:
UNSPSC Code:
12352100
PubChem Substance ID:
NACRES:
NA.22
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Quality Level

Assay

95%

form

powder

bp

151 °C/20 mmHg (lit.)

mp

54-57 °C (lit.)

SMILES string

COC(=O)CCC(O)=O

InChI

1S/C5H8O4/c1-9-5(8)3-2-4(6)7/h2-3H2,1H3,(H,6,7)

InChI key

JDRMYOQETPMYQX-UHFFFAOYSA-N

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Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

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D L Eizirik et al.
Molecular and cellular endocrinology, 118(1-2), 71-83 (1996-04-19)
Nitric oxide (NO) has been proposed as a possible mediator of beta-cell damage in human IDDM. This hypothesis is based on in vitro studies with rodent pancreatic islets. In the present study we examined whether human beta-cells are affected by
Isabelle Briaud et al.
Diabetes, 51(3), 662-668 (2002-03-02)
Chronic elevations in plasma levels of fatty acids (FAs) adversely affect pancreatic beta-cell function in type 2 diabetes. In vitro, we have previously shown that deleterious effects of prolonged exposure of isolated islets to FAs were dependent on the presence
L Ladrière et al.
General pharmacology, 31(3), 377-383 (1998-08-14)
1. Selected esters of succinic acid are currently under investigation as potential insulinotropic tools in the treatment of non-insulin-dependent diabetes. At variance with the methyl esters of succinic acid used in most of the work so far conducted from this
Y P Zhou et al.
The American journal of physiology, 270(6 Pt 1), E988-E994 (1996-06-01)
Fasting inhibits glucose-induced insulin secretion. We investigated the role of a glucose fatty acid cycle for such inhibition and its molecular basis in pancreatic islets from 48-h fasted rats. The fasting-impaired insulin response to 27 mM glucose was restored by
S A Hinke et al.
British journal of pharmacology, 150(8), 1031-1043 (2007-03-07)
Two mechanisms have been proposed to explain the insulin-sensitising properties of metformin in peripheral tissues: (a) inhibition of electron transport chain complex I, and (b) activation of the AMP activated protein kinase (AMPK). However the relationship between these mechanisms and

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