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- 详细信息
- 文献和实验
- 技术资料
- 保存条件:
Powder:-20℃,2 years;Insolvent(母液):-20℃,6 months;-80℃,1 year
- 保质期:
Powder:-20℃,2 years;Insolvent(母液):-20℃,6 months;-80℃,1 year
- 英文名:
Lixisenatide
- 库存:
现询
- 供应商:
北京索莱宝科技有限公司
- CAS号:
320367-13-3
- 规格:
50mg/25mg/10mg/5mg/1mg
| 规格: | 50mg | 产品价格: | ¥5353.0 |
|---|---|---|---|
| 规格: | 25mg | 产品价格: | ¥3865.0 |
| 规格: | 10mg | 产品价格: | ¥2403.0 |
| 规格: | 5mg | 产品价格: | ¥1478.0 |
| 规格: | 1mg | 产品价格: | ¥738.0 |
是胰高血糖素样肽 1 受体 (GLP-1R) 的激动剂,可用于2 型糖尿病的相关研究。
| 基本信息 | |
| CAS | No.320367-13-3 |
| 中文名称 | 利西拉来 |
| 英文名称 | Lixisenatide |
| 别名 | Lyxumia;Adlyxin;ZP10A peptide;AVE0010 |
| 分子式 | C215H347N61O65S |
| 分子量 | 4858.49 |
| 溶解性 | Soluble in Water ≥10mg/mL |
| 纯度 | ≥98% |
| 外观(性状) | Solid |
| 储存条件 | Powder:-20℃,2 years;Insolvent(母液):-20℃,6 months;-80℃,1 year |
| MDL | MFCD13194768 |
| SMILES | CCC(C)C(C(=O)NC(CCC(=O)O)C(=O)NC(CC1=CNC2=CC=CC=C21)C(=O)NC(CC(C)C)C(=O)NC(CCCCN)C(=O)NC(CC(=O)N)C(=O)NCC(=O)NCC(=O)N3CCCC3C(=O)NC(CO)C(=O)NC(CO)C(=O)NCC(=O)NC(C)C(=O)N4CCCC4C(=O)N5CCCC5C(=O)NC(CO)C(=O)NC(CCCCN)C(=O)NC(CCCCN)C(=O)NC(CCCCN)C(=O)NC(CCCCN)C(=O)NC(CCCCN)C(=O)NC(CCCCN)C(=O)N)NC(=O)C(CC6=CC=CC=C6)NC(=O)C(CC(C)C)NC(=O)C(CCCNC(=N)N)NC(=O)C(C(C)C)NC(=O)C(C)NC(=O)C(CCC(=O)O)NC(=O)C(CCC(=O)O)NC(=O)C(CCC(=O)O)NC(=O)C(CCSC)NC(=O)C(CCC(=O)N)NC(=O)C(CCCCN)NC(=O)C(CO)NC(=O)C(CC(C)C)NC(=O)C(CC(=O)O)NC(=O)C(CO)NC(=O)C(C(C)O)NC(=O)C(CC7=CC=CC=C7)NC(=O)C(C(C)O)NC(=O)CNC(=O)C(CCC(=O)O)NC(=O)CNC(=O)C(CC8=CNC=N8)N |
| 靶点 | Glucagon Receptor |
| 通路 | GPCR & G Protein |
| 背景说明 | 是胰高血糖素样肽 1 受体 (GLP-1R) 的激动剂,可用于2 型糖尿病的相关研究。 |
| 生物活性 | Lixisenatide is a GLP-1 receptor agonist. Lixisenatide inhibits the inflammatory response through down regulation of proinflammatory cytokines, and blocks of cellular signaling pathways. Lixisenatide decreases atheroma plaque size and instability in Apoe?/? Irs2+/? mice by reprogramming macrophages towards an M2 phenotype, which leads to reduced inflammation[2][3][5]. |
| In Vitro | To our knowledge, this is the first study exploring the effects of agonism of the glucagon - like peptide - 1 (GLP - 1) receptor using lixisenatide, a licensed drug used for the treatment of type II diabetes, on the pathological characteristics of RA in human fibroblast - like synoviocytes. Our findings indicate that lixisenatide inhibited the inflammatory response through downregulation of proinflammatory cytokines, such as tumor necrosis factor α (TNF - α), interleukin - 6 (IL - 6), and interleukin - 8 (IL - 8); inhibition of matrix metalloproteinases (MMPs); and blockade of cellular signaling pathways, including the c - Jun N - terminal kinase (JNK), activator protein 1 (AP - 1), and nuclear factor κ B (NF - κB) pathways. Furthermore, lixisenatide improved oxidative stress, rescued mitochondrial membrane potential (ΔΨm), and prevented cell death in fibroblast - like synoviocytes.[3]Cell Viability Assay[1]:Cell Line:Hippocampal cells;Concentration:100 μM;Incubation Time:24 h;Result:Reversed Aβ25-35-triggered cytotoxicity on hippocampal cell cultures.Western Blot Analysis[3]:Cell Line:FLSs;Concentration:10 μM, 20 μM;Incubation Time:48 h;Result:Significantly reduced expression of MMP-1, MMP-3, and MMP-13 at both the mRNA and protein levels in a dose-dependent manner. |
| 细胞实验 | Atherosclerosis development was evaluated in Apoe -/- Irs2 +/- mice, a mouse model of insulin resistance, the metabolic syndrome and atherosclerosis, treated with the GLP - 1 analogues lixisenatide or liraglutide.Treatment of Apoe -/- Irs2 +/- mice with either lixisenatide or liraglutide improved glucose metabolism and blood pressure but this was independent of body weight loss. Both drugs significantly decreased atheroma plaque size. Compared with vehicle - treated control mice, lixisenatide treatment generated more stable atheromas, with fewer inflammatory infiltrates, reduced necrotic cores and thicker fibrous caps. Lixisenatide - treated mice also displayed diminished IL - 6 levels, proinflammatory Ly6Chigh monocytes and activated T cells.Furthermore, atheromas from lixisenatide - treated mice showed higher arginase I content and decreased expression of inducible nitric oxide synthase, indicating the prevalence of the M2 phenotype within plaques.[2]。Animal Model: Apoe?/? Irs2+/? mice [2];Dosage: 10 μg/kg;Administration:Subcutaneous injection (s.c.);Result:Exhibited smaller atheromas in the aortic arch region.Reduced the lesion size in cross-sections of hearts.Animal Model:Diabetic rats [4];Dosage:1 nmol/kg;Administration:Intraperitoneal injection (i.p.);Result:Showed a significant amelioration on the elevated renal parameters.Showed significant mitigation in renal MDA and total NOx? (by 50.3 and 79.9%, respectively) and 43.9% elevation in renal total antioxidant capacity.Averted the observed increments in iNOS and COX-2 expressions in the renal tissues of the diabetic group.Decreased the level of TGF-β protein expression. |
| 数据来源文献 | [1]. Cai H Y, et al. Lixisenatide attenuates the detrimental effects of amyloid β protein on spatial working memory and hippocampal neurons in rats [J]. Behavioural brain research, 2017, 318: 28-35. [2]. Vinué á, et al. The GLP-1 analogue lixisenatide decreases atherosclerosis in insulin-resistant mice by modulating macrophage phenotype [J]. Diabetologia, 2017, 60: 1801-1812. [3]. Du X, et al. The protective effects of lixisenatide against inflammatory response in human rheumatoid arthritis fibroblast-like synoviocytes [J]. International immunopharmacology, 2019, 75: 105732. [4]. Abdel-Latif R G, et al. Low-dose lixisenatide protects against early-onset nephropathy induced in diabetic rats [J]. Life Sciences, 2020, 263: 118592. [5]. Xiao M, et al. The protective effects of GLP-1 receptor agonist lixisenatide on oxygen-glucose deprivation/reperfusion (OGD/R)-induced deregulation of endothelial tube formation [J]. RSC advances, 2020, 10(17): 10245-10253. [6]. Ahrén B et al. Postprandial Glucagon Reductions Correlate to Reductions in Postprandial Glucose and Glycated Hemoglobin with Lixisenatide Treatment in Type 2 Diabetes Mellitus: A Post Hoc Analysis. Diabetes Ther. 2016 Jun 18 [7]. Ulrich Werner, et al. Pharmacological profile of lixisenatide: A new GLP-1 receptor agonist for the treatment of type 2 diabetes. Regul Pept. 2010 Sep 24;164(2-3):58-64. [8]. Lorenz M, et al. Effects of lixisenatide once daily on gastric emptying in type 2 diabetes--relationship to postprandial glycemia. Regul Pept. 2013 Aug 10;185:1-8. [9]. Mikkel Christensen, et al. Lixisenatide, a novel GLP-1 receptor agonist for the treatment of type 2 diabetes mellitus. IDrugs. 2009 Aug;12(8):503-13. [10]. D Tews, et al. Enhanced protection against cytokine- and fatty acid-induced apoptosis in pancreatic beta cells by combined treatment with glucagon-like peptide-1 receptor agonists and insulin analogues. Horm Metab Res. 2008 Mar;40(3):172-80. |
| 单位 | 瓶 |
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文献和实验删除突变的drs基因分析揭示,C末端区以及3个一致重复的N末端区都出现凋亡。Caspase-12、Caspase –9以及Caspase-3都继续被drs激活,Caspase--3,和Caspase-9的抑制剂都抑制drs引起的凋亡。在凋亡过程中没有看到因drs引起线粒体细胞色素C释放到细胞质去,这表明线粒体途径不是drs介导的凋亡,而且,研究人员发现,Drs蛋白能与定位在内质网的凋亡蛋白ASY/Nogo-B/RTN-x(S)结合,并且这些基因共同表达增加了凋亡的效果。这项研究结果提示,由ASY
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