M81101
mono-Methyl hydrogen succinate
95%
Synonym(s):
Monomethyl succinate, Succinic acid monomethyl ester
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25 G
€74.00
100 G
€149.00
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25 G
€74.00
100 G
€149.00
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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Related Categories
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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Isabelle Briaud et al.
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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
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
K Capito et al.
Journal of molecular endocrinology, 17(2), 101-107 (1996-10-01)
The involvement of phosphatidylcholine (PC) hydrolysis in the regulation of insulin secretion was studied in mouse pancreatic islets prelabelled with [3H]choline. Phospholipase C (PLC) and phospholipase D (PLD) activities were demonstrated and also that of an enzyme that removes both
S A Hinke et al.
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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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