Glibornuride
(Synonyms: 格列波脲) 目录号 : GC63568
Glibornuride 是一种对 ATP 敏感的 K+ 通道 (KATP 通道) 阻滞剂，pKi 值为 5.75。Glibornuride 是一种抗糖尿病剂。
Cas No.:26944-48-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Glibornuride is a blocker of ATP-sensitive K+ channels (KATP channel) with a pKi of 5.75[1]. Antidiabetic agent[2].
Administration of Glibornuride (5 mg/kg; gavage, daily for 28 days) for 28 days causes an increase in body weights in the diabetic groups in Swiss albino rats[2].Treatment with Glibornuride for 28 days decreases the serum uric acid levels in diabetic rats[2].Administration of Glibornuride for 28 days, insignificantly increases the liver lipid peroxidation levels in diabetic rats[2].
[1]. LÖffler C, et al. Pharmacological characterization of the sulphonylurea receptor in rat isolated aorta. Br J Pharmacol. 1997 Feb;120(3):476-80.
[2]. Ozsoy-Sacan O, et al. Effects of parsley (Petroselinum crispum) extract versus Glibornuride on the liver of streptozotocin-induced diabetic rats. J Ethnopharmacol. 2006 Mar 8;104(1-2):175-81.
| Cas No. | 26944-48-9 | SDF | |
| 别名 | 格列波脲 | ||
| 分子式 | C18H26N2O4S | 分子量 | 366.48 |
| 溶解度 | DMSO : 250 mg/mL (682.17 mM; Need ultrasonic) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.7287 mL | 13.6433 mL | 27.2866 mL |
| 5 mM | 0.5457 mL | 2.7287 mL | 5.4573 mL |
| 10 mM | 0.2729 mL | 1.3643 mL | 2.7287 mL |
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
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The morphological and biochemical effects of Glibornuride on rat liver in experimental diabetes
Hum Exp Toxicol 2004 May;23(5):257-64.PMID:15228018DOI:10.1191/0960327104ht444oa.
Glibornuride is a sulphonylurea derivative used as an oral hypoglycaemic drug in diabetics. The aim of this study was to examine the histological, ultrastructural and biochemical effects of Glibornuride in streptozotocin (STZ)-treated rats. The animals were rendered diabetic by intraperitoneal injection of 65 mg/kg STZ. Fourteen days later, Glibornuride was given at 5 mg/kg by gavage, daily for 28 days, to one STZ-diabetic and one control group. In the STZ-diabetic group, remarkable degenerative changes were observed. On the other hand, in the STZ-diabetic group given Glibornuride, the degenerative changes decreased. In the STZ-diabetic group, blood glucose levels, serum aspartate transaminase activity, and total lipid levels increased, whereas the blood glutathione levels decreased. In contrast, in the STZ-diabetic group given Glibornuride blood glucose levels, serum aspartate transaminase activity and total lipid levels decreased and blood glutathione levels increased. Significant changes in total protein levels in the serum were not observed in any group. As a conclusion, we can say that Glibornuride has a protective effect against the hepatotoxicity produced by STZ-diabetes.
Effects of Glibornuride versus metformin on eye lenses and skin in experimental diabetes
Arzneimittelforschung 2006;56(7):541-6.PMID:16927537DOI:10.1055/s-0031-1296749.
The aim of the study was to investigate the effect of Glibornuride (CAS 26944-48-9) and metformin (CAS 657-24-9) on eye lenses and skin of streptozotocin (STZ)-induced diabetic rats. The drugs were administered daily to one diabetic and one control group separately from day 14 to day 42. After 42 days, diabetes caused significant increases in blood glucose levels, non-enzymatic glycosylation (NEG) of skin and lens proteins and skin lipid peroxidation (LPO) levels as well as decreases in body weights and lens glutathione (GSH) levels. Metformin administration to the diabetic rats produced more significant reduction in blood glucose than Glibornuride. Metformin produced non-significant increase in NEG levels in lenses and skin. Unlike metformin, Glibornuride increased NEG levels significantly in lenses. Both drugs produced non-significant increase in lens GSH levels and decreases in skin LPO levels in diabetic rats. Sodium dodecyl sulphate (SDS) polyacrylamid gel electrophoresis revealed no significant difference in any of the protein bands between any of the groups. These observations suggest that metformin and Glibornuride as oral antidiabetics have similar protective effects on tissues in STZ induced diabetic rats.
Effects of parsley (Petroselinum crispum) extract versus Glibornuride on the liver of streptozotocin-induced diabetic rats
J Ethnopharmacol 2006 Mar 8;104(1-2):175-81.PMID:16223573DOI:10.1016/j.jep.2005.08.069.
Parsley (Petroselinum crispum) is one of the medicinal herbs used by diabetics in Turkey. The aim of this study is to investigate the effects of parsley (2g/kg) and Glibornuride (5mg/kg) on the liver tissue of streptozotocin-induced diabetic rats. Swiss albino rats were divided into six groups: control; control+parsley; control+Glibornuride; diabetic; diabetic+parsley; diabetic+Glibornuride. Diabetes was induced by intraperitoneal injection of 65 mg/kg streptozotocin (STZ). Parsley extract and Glibornuride were given daily to both diabetic and control rats separately, until the end of the experiment, at day 42. The drugs were administered to one diabetic and one control group from days 14 to 42. On day 42, liver tissues were taken from each rat. In STZ-diabetic group, blood glucose levels, serum alkaline phosphatase activity, uric acid, sialic acid, sodium and potassium levels, liver lipid peroxidation (LPO), and non-enzymatic glycosylation (NEG) levels increased, while liver glutathione (GSH) levels and body weight decreased. In the diabetic group given parsley, blood glucose, serum alkaline phosphatase activity, sialic acid, uric acid, potassium and sodium levels, and liver LPO and NEG levels decreased, but GSH levels increased. The diabetic group, given Glibornuride, blood glucose, serum alkaline phosphatase activity, serum sialic acid, uric acid, potassium, and liver NEG levels decreased, but liver LPO, GSH, serum sodium levels, and body weight increased. It was concluded that probably, due to its antioxidant property, parsley extract has a protective effect comparable to Glibornuride against hepatotoxicity caused by diabetes.
Clinical trial of Glibornuride in diabetes
Br Med J 1975 Aug 30;3(5982):514-5.PMID:126099DOI:10.1136/bmj.3.5982.514.
Glibornuride is an addition to the second-generation sulphonylureas, that has been shown in clinical trials to be effective and non-toxic. Twenty-three diabetics who were poorly controlled on other oral hypoglycaemic agents and seven newly diagnosed diabetics were treated with Glibornuride. The efficacy and lack of toxicity of this drug was confirmed, but there was no evidence to suggest that it is significantly more potent than other sulphonylureas. It does not seem to represent a significant therapeutic advance.
Lack of effect of tenoxicam on Glibornuride kinetics and response
Br J Clin Pharmacol 1985 Feb;19(2):249-54.PMID:3157397DOI:10.1111/j.1365-2125.1985.tb02638.x.
The pharmacokinetics of Glibornuride (25 mg i.v.) and the accompanying insulin and glucose responses were characterized in eight human subjects in the presence and absence of steady-state tenoxicam (20 mg p.o./day for 2 weeks). Tenoxicam affected neither the pharmacokinetic parameters of Glibornuride (systemic clearance, volume of distribution and biological half-life) nor the responses of plasma insulin and blood glucose to Glibornuride. The single i.v. dose of Glibornuride had no detectable effect on the kinetics of tenoxicam.