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
UNSPSC Code:
12352100
NACRES:
NA.22
PubChem Substance ID:
EC Number:
223-408-2
Beilstein/REAXYS Number:
1722669
MDL number:
Assay:
95%
Form:
powder
InChI key
JDRMYOQETPMYQX-UHFFFAOYSA-N
InChI
1S/C5H8O4/c1-9-5(8)3-2-4(6)7/h2-3H2,1H3,(H,6,7)
SMILES string
COC(=O)CCC(O)=O
assay
95%
form
powder
bp
151 °C/20 mmHg (lit.)
mp
54-57 °C (lit.)
Quality Level
Related Categories
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, type N95 (US)
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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
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
L Ladrière et al.
Annals of nutrition & metabolism, 41(2), 118-125 (1997-01-01)
Rats were fasted for 48 h, but infused with either NaCl or the sodium salt of monoethyl succinic acid (EMS), both delivered at a rate of 80 mumol/g body weight per day. The infusion of EMS, as compared to NaCl
A D Lajoix et al.
Diabetes, 50(6), 1311-1323 (2001-05-26)
Evidence is presented showing that a neuronal isoform of nitric oxide synthase (NOS) is expressed in rat pancreatic islets and INS-1 cells. Sequencing of the coding region indicated a 99.8% homology with rat neuronal NOS (nNOS) with four mutations, three
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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