Lixisenatide
(Synonyms: 利西拉来) 目录号 : GC31334
Lixisenatide是一种胰高血糖素样肽-1受体（GLP-1 receptor）激动剂，可用于治疗2型糖尿病。
Cas No.:320367-13-3
Sample solution is provided at 25 µL, 10mM.
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Lixisenatide is a glucagon-like peptide-1 receptor (GLP-1 receptor) agonist that can be used for the treatment of type 2 diabetes[1]. Lixisenatide enhances insulin secretion in a glucose-dependent manner, inhibits glucagon release, and delays gastric emptying to reduce food intake, thereby exerting hypoglycemic and weight-loss-promoting effects[2]. Lixisenatide can also inhibit inflammatory responses by downregulating pro-inflammatory cytokines and blocking cellular signaling pathways[3]. Lixisenatide can slow the progression of motor disorders in early Parkinson's disease patients[4].
In vitro, pretreatment of human umbilical vein endothelial cells (HUVECs) with Lixisenatide (5-20nM) for 6 hours, followed by oxygen-glucose deprivation/reperfusion (OGD/R) to simulate ischemia-reperfusion injury, significantly improved cell viability, inhibited the accumulation of reactive oxygen species (ROS), and alleviated the impairment of endothelial cell tube formation ability induced by OGD/R. Lixisenatide also enhanced eNOS phosphorylation and nitric oxide (NO) production by activating the PI3K/Akt pathway[5]. Pretreatment of HEK-293 cells stably expressing GFP-labeled α-synuclein A53T (α-Syn-HEK-293 cells) and SH-SY5Y cells with Lixisenatide (10-20nM) for 6 hours, followed by stimulation with α-synuclein preformed fibrils (α-Syn PFFs, 3μg/mL) for 48 hours, significantly inhibited the phosphorylation (pS129) and aggregation of α-synuclein, reduced cell apoptosis and mitochondrial dysfunction, and improved cell viability[6].
In vivo, continuous treatment of high-fat diet-induced obese insulin-resistant mice with Lixisenatide (50nmol/kg; subcutaneous injection twice daily) for 40 days significantly improved insulin sensitivity in the mice, enhanced glucose tolerance and insulin secretion, and significantly improved the mice's novel object recognition memory ability[7]. Treatment of rats that had experienced transient ischemia-reperfusion injury with Lixisenatide (10μg/kg/day; subcutaneous injection) for 10 weeks improved left ventricular end-diastolic pressure and relaxation time and prevented pulmonary congestion[8].
References:
[1] Nauck MA, Quast DR, Wefers J, et al. GLP-1 receptor agonists in the treatment of type 2 diabetes - state-of-the-art. Mol Metab. 2021 Apr;46:101102.
[2] Baker DE, Levien TL. Lixisenatide. Hosp Pharm. 2017 Jan;52(1):65-80.
[3] Pfeffer MA, Claggett B, Diaz R, et al. Lixisenatide in Patients with Type 2 Diabetes and Acute Coronary Syndrome. N Engl J Med. 2015 Dec 3;373(23):2247-57.
[4] Meissner WG, Remy P, Giordana C, et al. LIXIPARK Study Group. Trial of Lixisenatide in Early Parkinson's Disease. N Engl J Med. 2024 Apr 4;390(13):1176-1185.
[5] Xiao M, Lu D, Tian J, et al. The protective effects of GLP-1 receptor agonist lixisenatide on oxygen-glucose deprivation/reperfusion (OGD/R)-induced deregulation of endothelial tube formation. RSC Adv. 2020 Mar 10;10(17):10245-10253.
[6] Xu L, Chen G, Zhang L, et al. Lixisenatide ameliorated lipopolysaccharide (LPS)-induced expression of mucin and inflammation in bronchial epithelial cells. J Biochem Mol Toxicol. 2024 Jan;38(1):e23618.
[7] Lennox R, Flatt PR, Gault VA. Lixisenatide improves recognition memory and exerts neuroprotective actions in high-fat fed mice. Peptides. 2014 Nov;61:38-47.
[8] Wohlfart P, Linz W, Hübschle T, et al. Cardioprotective effects of lixisenatide in rat myocardial ischemia-reperfusion injury studies. J Transl Med. 2013 Mar 28;11:84. doi: 10.1186/1479-5876-11-84.
Lixisenatide是一种胰高血糖素样肽-1受体（GLP-1 receptor）激动剂，可用于治疗2型糖尿病[1]。Lixisenatide通过葡萄糖依赖的方式增强胰岛素分泌、抑制胰高血糖素释放，并能够延缓胃排空以减少食物摄入，从而发挥降血糖和促进体重减轻的作用[2]。Lixisenatide可通过下调促炎细胞因子和阻断细胞信号通路来抑制炎症反应[3]。Lixisenatide还能够减缓早期帕金森病患者的运动障碍进展[4]。
在体外，Lixisenatide（5-20nM）预处理人脐静脉内皮细胞（HUVECs）6小时，随后通过氧糖剥夺/再灌注（OGD/R）处理模拟缺血再灌注损伤，Lixisenatide显著改善细胞存活率，同时抑制活性氧（ROS）的积累，还缓解了OGD/R诱导的内皮细胞管形成能力受损，并通过激活PI3K/Akt通路增强eNOS磷酸化和一氧化氮（NO）的产生[5]。Lixisenatide（10-20nM）预处理稳定表达GFP标记α-突触核蛋白A53T的HEK-293细胞（α-Syn-HEK-293细胞）、SH-SY5Y细胞6小时，随后以α-突触核蛋白预制纤维（α-Syn PFFs，3μg/mL）刺激48小时，Lixisenatide显著抑制α-突触核蛋白的磷酸化（pS129）和聚集，同时减少细胞凋亡和线粒体功能障碍，并改善了细胞活力[6]。
在体内，Lixisenatide（50nmol/kg；每日两次皮下注射）持续40天处理高脂饮食诱导的肥胖胰岛素抵抗小鼠，Lixisenatide显著改善了小鼠的胰岛素敏感性，同时增强了葡萄糖耐量和胰岛素分泌，并显著改善了小鼠的新物体识别记忆能力[7]。Lixisenatide（10μg/kg/天；皮下注射）处理经历短暂缺血再灌注损伤的大鼠10周，Lixisenatide改善了左心室舒张末期压力和松弛时间，并预防了肺充血[8]。
| Cell experiment [1]: | |
Cell lines | HUVECs (Human Umbilical Vein Endothelial Cells) |
Preparation Method | HUVECs were maintained in EGM-2 medium supplemented with 2% fetal bovine serum (FBS) at 37°C, 5% CO₂. For pretreatment, HUVECs were treated with Lixisenatide (5, 10, 20nM) for 6 hours prior to Oxygen-Glucose Deprivation/Reperfusion (OGD/R) injury. OGD/R was induced by transferring cells to glucose-free medium and placing them in an anaerobic chamber (95% N₂/5% CO₂) for 6 hours, followed by reperfusion with complete medium for 24 hours. |
Reaction Conditions | 5-20mM; 6h pretreatment |
Applications | Lixisenatide pretreatment significantly protected HUVECs from OGD/R-induced cytotoxicity and improved cell viability. Lixisenatide ameliorated OGD/R-induced ROS accumulation and restored impaired endothelial tube formation. |
| Animal experiment [2]: | |
Animal models | High-fat fed Swiss NIH mice |
Preparation Method | Mice were fed a high-fat diet (45% fat) for 4 months to establish obesity, insulin resistance and impaired cognition. Animals then received twice-daily subcutaneous injections of Lixisenatide (50nmol/kg) or saline vehicle for 40 days. |
Dosage form | 50nmol/kg; s.c. |
Applications | Lixisenatide treatment significantly improved recognition memory during novel object recognition tasks, enhanced hippocampal progenitor cell proliferation, increased immature neuron numbers. Lixisenatide improved glycemic control, insulin sensitivity, and pancreatic insulin content without affecting body weight or food intake. |
References: | |
| Cas No. | 320367-13-3 | SDF | |
| 别名 | 利西拉来 | ||
| Canonical SMILES | His-Gly-Glu-Gly-Thr-Phe-Thr-Ser-Asp-Leu-Ser-Lys-Gln-Met-Glu-Glu-Glu-Ala-Val-Arg-Leu-Phe-Ile-Glu-Trp-Leu-Lys-Asn-Gly-Gly-Pro-Ser-Ser-Gly-Ala-Pro-Pro-Ser-Lys-Lys-Lys-Lys-Lys-Lys-NH2 | ||
| 分子式 | C215H347N61O65S | 分子量 | 4858.49 |
| 溶解度 | Water : 106 mg/mL (21.82 mM) | 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 | 205.8 μL | 1.0291 mL | 2.0583 mL |
| 5 mM | 41.2 μL | 205.8 μL | 411.7 μL |
| 10 mM | 20.6 μL | 102.9 μL | 205.8 μL |
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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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2.
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