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IL1640 利西拉来 抑制剂/拮抗剂/激动剂 索莱宝

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  • 北京
  • IL1640
  • 2025年07月23日
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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
    CASNo.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
    MDLMFCD13194768
    SMILESCCC(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 VitroTo 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.
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