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Merck

M81101

Sigma-Aldrich

琥珀酸单甲酯

95%

别名:

丁二酸一甲酯, 丁二酸单甲酯

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About This Item

线性分子式:
CH3OCOCH2CH2COOH
CAS号:
分子量:
132.11
Beilstein:
1722669
EC號碼:
MDL號碼:
分類程式碼代碼:
12352100
PubChem物質ID:
NACRES:
NA.22

化驗

95%

形狀

powder

bp

151 °C/20 mmHg (lit.)

mp

54-57 °C (lit.)

SMILES 字串

COC(=O)CCC(O)=O

InChI

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

InChI 密鑰

JDRMYOQETPMYQX-UHFFFAOYSA-N

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儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable

個人防護裝備

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
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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