| CAS |
No.33342-05-1 |
| 中文名称 |
格列喹酮 |
| 英文名称 |
Gliquidone |
| 别名 |
AR-DF 26 |
| 分子式 |
C27H33N3O6S |
| 分子量 |
527.63 |
| 溶解性 |
Soluble in DMSO |
| 纯度 |
HPLC≥98% |
| 外观(性状) |
White to off-white Solid |
| 储存条件 |
Powder:2-8℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year |
| EC |
EINECS 251-463-2 |
| MDL |
MFCD00631870 |
| SMILES |
O=S(C1=CC=C(CCN(C(C(C)(C)C2=C3C=C(OC)C=C2)=O)C3=O)C=C1)(NC(NC4CCCCC4)=O)=O |
| InChIKey |
LLJFMFZYVVLQKT-UHFFFAOYSA-N |
| InChI |
InChI=1S/C27H33N3O6S/c1-27(2)23-14-11-20(36-3)17-22(23)24(31)30(25(27)32)16-15-18-9-12-21(13-10-18)37(34,35)29-26(33)28-19-7-5-4-6-8-19/h9-14,17,19H,4-8,15-16H2,1-3H3,(H2,28,29,33) |
| PubChem CID |
91610 |
| 靶点 |
Potassium Channel |
| 通路 |
Membrane Transporter&Ion Channel |
| 背景说明 |
Gliquidone具有降血糖活性。 此外,还具有过氧化物酶体增殖物激活受体(PPAR)γ激动作用。 |
| 生物活性 |
Gliquidone (AR-DF 26) is a potent， second-generation sulfonylurea with antihyperglycemic activity. Like other second-generation compounds， gliquidone exerts greater binding affinity to SUR1 and increased potency compared to first-generation compounds. In addition， this agent exerts peroxisome proliferator-activated receptor (PPAR) gamma agonistic activity.[1-6] |
| In Vitro |
The binding of the potent oral antidiabetic sulphonylurea [3H]glibenclamide was studied in rat cerebral cortex membranes. A single population of high affinity and saturable binding sites with equilibrium constants， Kd = 0.2 ± 0.06 nM and Bmax = 58.6 ± 6.2 fmol/mg protein was found. Specific [3H]glibenclamide binding to rat cerebral cortex membranes was inhibited by glibenclamide and other sulphonylureas， glibenclamide being the most potent drug and the sulphonylurea of the second generation chlorpropamide the least potent.This observation suggests that this site may be related to the hypoglycaemic properties of sulphonylureas and possibly to their interaction with ATP - sensitive K? - channel. Nevertheless， other non - selective K? - channel antagonists such as TEA， 4 - aminopyridine， quinine， quinidine or apamin failed to interact with this site (IC50 > 100 μM). Similarly， both non - selective K? - channel agonists such as cromakalim， pinacidil or minoxidil as well as the pancreatic ATP - sensitive K? - channel agonist diazoxide failed to interact with this site. It may thus be concluded that this site， under the present experimental conditions， represents a drug specific recognition site which may be coupled to the hypoglycaemic activity of sulphonylureas， possibly on a particulate ATP - dependent K? - channel.[1] |
| 数据来源文献 |
[1].Angel I， et al. Fundam Clin Pharmacol， 1991， 5(2)， 107-115.
[2].Galeotti N， et al. Neuropharmacology， 2001， 40(1)， 75-84.
[3].Ocana M， et al. Br J Pharmacol， 1995， 114(6)， 1296-1302.
[4].Galeotti N， et al. Br J Pharmacol， 1999， 126(5)， 1214-1220.
[5].Yarat A， et al. Free Radic Biol Med， 2001， 31(9)， 1038-1042.
[6].Capoci I R G， Faria D R， Sakita K M， et al. Repurposing approach identifies new treatment options for invasive fungal disease[J]. Bioorganic chemistry. 2019 Mar;84:87-97. |
| 规格 |
10mM*1mL in DMSO 50mg 100mg |
| 单位 |
瓶 |
中文
英语
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