GLP-1(7-37) acetate
目录号 : GC34904
GLP-1(7-37)acetate是一种肠道胰岛素激素，可以增强葡萄糖诱导的胰岛素分泌。
Cas No.:1450806-98-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
GLP-1(7-37) acetate is an intestinal insulinotropic hormone that augments glucose induced insulin secretion[1].
GLP-1(7-37) (0.5, 5 or 50 pmol/min/kg) infused during the second hour of a 2-hour 11-mM hyperglycemic clamp produces a dose-related enhancement of the glucose-stimulated increase in plasma insulin concentration and an increased rate of glucose infusion in rats[2].Infusion of GLP-1(7-37) (5 pmol/min/kg) from 1 hour through 7 hours produces a sustained increase in plasma insulin concentration relative to levels in rats infused with vehicle in rats with maintained glucose concentration at 11 mM[2]. Animal Model: Male Sprague-Dawley rats weighing 300 to 350 g with glucose IV at a variablerate for 7 hours to maintain plasma glucose concentration at 11 mM[2].
[1]. Sarrauste de Menthiere, C. et al. Structural requirements of the N-terminal region of GLP-1-[7-37]-NH2 for receptor interaction and cAMP production. European journal of medicinal chemistry 39, 473-480, doi:10.1016/j.ejmech.2004.02.002 (2004). [2]. Hargrove DM, et al. Glucose-dependent action of glucagon-like peptide-1 (7-37) in vivo during short- or long-term administration. Metabolism. 1995 Sep;44(9):1231-7.
| Cas No. | 1450806-98-0 | SDF | |
| Canonical SMILES | OC(C)=O.[HAEGTFTSDVSSYLEGQAAKEFIAWLVKGRG] | ||
| 分子式 | C153H232N40O49 | 分子量 | 3415.72 |
| 溶解度 | Soluble in DMSO | 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 | 0.2928 mL | 1.4638 mL | 2.9276 mL |
| 5 mM | 0.0586 mL | 0.2928 mL | 0.5855 mL |
| 10 mM | 0.0293 mL | 0.1464 mL | 0.2928 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 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 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
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。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
The role of the free cytosolic calcium level in beta-cell signal transduction by gastric inhibitory polypeptide and glucagon-like peptide I(7-37)
Using the glucose-responsive hamster beta-cell line (hamster insulin tumor cells), we examined the cellular mechanisms by which gastric inhibitory polypeptide (GIP) and glucagon-like peptide I(7-37) (GLP-I) potentiate glucose-stimulated insulin secretion. Glucose alone increased insulin secretion and increased the free cytosolic calcium levels ([Ca2+]i) without altering cAMP content. When added to glucose-stimulated cells, GIP and GLP-I increased cAMP levels and further increased insulin secretion. At 4 mM but not 0.4 mM glucose, both peptides triggered a dose-dependent rise in [Ca2+]i with ED50s of 0.4 and 0.2 nM for GIP and GLP-I, respectively. The increase in [Ca2+]i was blocked by either chelation of extracellular Ca2+ with EGTA or nimodipine, the voltage-dependent Ca2+ channel blocker. Nimodipine also inhibited the potentiation of glucose-stimulated insulin secretion by GIP and GLP-I without inhibition of the stimulatory effect of these two peptides on cAMP accumulation. Neither peptide altered phosphoinositide metabolism, further underlining that the mobilization of intracellular Ca2+ from endoplasmic reticulum is not involved in the GIP and GLP-I signal transduction pathways. This study establishes that GIP and GLP-I potentiate glucose-stimulated insulin secretion by increasing extracellular Ca2+ influx through voltage-dependent Ca2+ channels.
Stability and stabilization of insulinotropin in a dextran formulation
The stability of insulinotropin in a formulation containing 23% dextran-75 is studied. The effects of temperature, excipients, dextran concentration, and drug concentration on the stability of insulinotropin are examined. The tryptophan residue is identified as the primary degradation site in the insulinotropin molecule by LC-MS. Different antioxidants are used to stabilize the peptide. The combination of cysteine and EDTA is found to be most effective in stabilizing insulinotropin in the dextran formulation.