2. GPCR/G Protein
  3. GLP Receptor
  4. LP-856866

LP-856866 是一种口服有效的 ACSL5 抑制剂，其对小鼠和人的 ACSL5 的 IC50 分别为 8 和 4 nM；对 小鼠和人 ACSL1 的 IC50 分别为 6 和 17 nM。LP-856866 可引发胃排空延迟、促进 GLP-1 释放、减少食物摄入、降低体重与体脂、保留瘦体重、改善葡萄糖稳态、增强胰岛素敏感性、减少肝脏脂肪堆积，并降低血清甘油三酯与总胆固醇水平。LP-856866 可用于饮食诱导肥胖的研究。

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LP-856866

LP-856866 Chemical Structure

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规格 价格 是否有货
1 mg ￥1394
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5 mg ￥3434
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10 mg ￥5474
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25 mg 询价 询问价格 & 货期
50 mg 询价 询问价格 & 货期

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Customer Review

LP-856866 相关抗体

Top Publications Citing Use of Products

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

LP-856866 is an orally active ACSL5 inhibitor, with IC50 values of 8 nM and 4 nM against mouse and human ACSL5, respectively, and IC50 values of 6 nM and 17 nM against mouse and human ACSL1, respectively. LP-856866 induces delayed gastric emptying, promotes GLP-1 release, reduces food intake, decreases body weight and body fat mass, preserves lean body mass, improves glucose homeostasis, enhances insulin sensitivity, reduces hepatic lipid accumulation, and lowers serum triglyceride and total cholesterol levels. LP-856866 is applicable to research on diet-induced obesity[1].

体内研究
(In Vivo)

LP-856866 (10-60 mg/kg/day; p.o.; 混饲; 共 28 天) 可在雄性饮食诱导肥胖小鼠中引发剂量依赖性的体重和体脂降低，同时保留瘦体重，并改善葡萄糖耐量和胰岛素敏感性[1]。
LP-856866 (p.o.; 混饲) 可减少野生型小鼠的高脂饮食摄入量，但对 Acsl5 敲除小鼠无此作用，证实其可靶向抑制 ACSL5[1]。
LP-856866 (75 mg/kg; p.o.; 混饲; 共 11 天) 会改变小鼠的饮食偏好，使其远离高脂饮食，减少总热量摄入，并阻止同时摄入低脂和高脂饮食的雄性小鼠体重增加[1]。
LP-856866 (60 mg/kg/day; p.o.; 混饲; 共 17 天) 可降低饲喂高脂饮食的小家鼠的肝脏甘油三酯水平[1]。
LP-856866 (60 mg/kg/day; p.o.; 混饲; 共 3 周) 可降低高脂饮食喂养小鼠的血清总胆固醇和甘油三酯水平[1]。
LP-856866 (60 mg/kg; p.o.; 单次给药) 可提高雄性小鼠餐后活性 GLP-1 水平[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6J-Tyrc−Brd X 129SvEvBrd hybrid (male; diet-induced obesity model, fed 45% high-fat diet from weaning for over 16 weeks)[1]
Dosage: 10 mg/kg/day; 30 mg/kg/day; 60 mg/kg/day
Administration: p.o.; continuous dietary admixture; 28 days
Result: Induced significant, dose-dependent body weight loss and body fat loss with reduced lean body mass loss compared to vehicle-treated mice at 28 days.
Lowered glucose excursions at 30 minutes significantly in 30 mg/kg/day and 60 mg/kg/day groups compared to vehicle-treated mice during OGTT.
Reduced insulin excursions at 30 and 60 minutes significantly in all treated groups compared to vehicle-treated mice during OGTT.
Improved Homeostatic Model Assessment Insulin Sensitivity Index (HOMA ISI) and Composite ISI significantly in all treated groups compared to vehicle-treated mice.
Animal Model: C57BL/6J-Tyrc−Brd X 129SvEvBrd hybrid (male; chow-fed, acclimated to 10% low-fat diet for 2 weeks)[1]
Dosage: 75 mg/kg/day
Administration: p.o.; continuous dietary admixture; 11 days
Result: Increased daily intake of 10% low-fat diet significantly and decreased daily intake of 60% high-fat diet significantly compared to vehicle-treated mice.
Lowered total caloric intake significantly on day 1 and throughout the study compared to vehicle-treated mice.
Reduced body weight change from day 0 significantly over the 11-day study compared to vehicle-treated mice.
Animal Model: C57BL/6J-Tyrc−Brd X 129SvEvBrd hybrid (male; fed Clinton 40% high-fat diet)[1]
Dosage: 60 mg/kg/day
Administration: p.o.; continuous dietary admixture; 17 days
Result: Reduced hepatic triglyceride levels (measured as mg/liver and mg/g liver) significantly compared to vehicle-treated mice.
Animal Model: C57BL/6J-Tyrc−Brd X 129SvEvBrd hybrid (male; fed 45% high-fat diet)[1]
Dosage: 60 mg/kg/day
Administration: p.o.; continuous dietary admixture; 3 weeks
Result: Reduced serum total cholesterol and serum triglyceride levels significantly compared to vehicle-treated mice.
Animal Model: C57BL/6J-Tyrc−Brd X 129SvEvBrd hybrid (male; fed 45% high-fat diet for at least 13 weeks)[1]
Dosage: 60 mg/kg
Administration: p.o.; single pretreatment dose; 30 minutes before HFD meal
Result: Increased plasma active glucagon-like peptide-1 (aGLP-1) levels compared to vehicle treatment, with peak levels at 5-10 minutes after HFD meal.
Produced a synergistic increase in plasma aGLP-1 levels when combined with sitagliptin, with significantly higher levels at 5, 10, 15, 30, 60, 120, and 240 minutes after HFD meal compared to vehicle, sitagliptin alone, or LP-856866 alone.
分子量

521.55

Formula

C26H26F3NO5S
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

LP-856866 相关分类

  • 摩尔计算器

  • 稀释计算器

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量   浓度   体积   分子量 *
= × ×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

浓度 (start) × 体积 (start) = 浓度 (final) × 体积 (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

LP-856866LP856866LP 856866GLP ReceptorAcsl5 knockout micehuman ACSL5glucose homeostasisaGLP-1ileal brakehuman ACSL3ACSL1diet-induced obesityACSL5mouseInhibitorinhibitorinhibit

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