Aldometanib (LXY-05-029) 是一种醛缩酶抑制剂。Aldometanib 可以激活溶酶体腺苷-磷酸活化蛋白激酶 AMPK 并降低血糖。Aldometanib 可用于代谢稳态的研究。
| 别名 | LXY-05-029 |
| 分子式 | C27H43Cl2IN2 |
| 分子量 | 593.45 |
| 储存条件 | 4°C, away from moisture |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. |
| Shipping Condition | Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request |
| 产品描述 | Aldometanib (LXY-05-029) is an orally activealdolaseinhibitor. Aldometanib can activate lysosomal adenosine monophosphate-activated protein kinase (AMPK) and decreases blood glucose. Aldometanib can be used for the research of metabolic homeostasis[1]. Aldometanib (0-1000 nM; 2 h) activates AMPK by preventing aldolase from binding to FBP to engender a pseudo-starvation signal[1].
Western Blot Analysis[1] | Cell Line: | Mouse primary hepatocytes, MEFs cells | | Concentration: | 0-1000 nM | | Incubation Time: | 2 h | | Result: | Activated AMPK in mouse embryonic fibroblasts (MEFs) and mouse primary hepatocytes cells. |
Immunofluorescence[1] | Cell Line: | MEFs cells | | Concentration: | 5 nM | | Incubation Time: | 2 h | | Result: | Inhibited TRPVs and induces AXIN lysosomal translocation. |
Aldometanib (oral; 0-10 mpk) reduces blood glucose in lean mice[1].
Aldometanib (oral; 2-10 mpk; twice daily; for a week) reduces blood glucose and alleviates fatty liver in obese hyperglycaemic mice[1].
Aldometanib alleviates fatty liver and nonalcoholic steatohepatitis[1].
Aldometanib (oral; 2mpk; twice-daily; for a month) alleviates liver fibrosis in NASH mice[1].
Aldometanib (oral; 0-50 μM; 0-50 days) extends lifespan inC. elegansvia the lysosomal pathway[1]. | Animal Model: | Lean mice[1] | | Dosage: | 0-10 mpk | | Administration: | Oral | | Result: | Decreased fasting blood glucose and improved glucose tolerance, promoted muscular TBC1D1 phosphorylation and glucose uptake. |
| Animal Model: | Obese hyperglycaemic mice[1] | | Dosage: | 2-10 mpk | | Administration: | Oral, twice daily, for a week | | Result: | Decreased blood glucose, lowered blood glucose in a muscular AMPK-dependent manner reduced hepatic TAG, improved insulin sensitivity, increased glucose disposal rates, inhibited TAG synthesis in liver and primary hepatocytes, decreased fat mass. |
| Animal Model: | NASH mice[1] | | Dosage: | 2 mpk | | Administration: | Oral, twice-daily, for a month | | Result: | Decreased histological scores used to describe the features of NASH, reduced apoptosis rate of hepatic cells, inhibited inflammatory responses in the liver of NASH mice and improved glucose tolerance of NASH mice. |
| Animal Model: | C. elegans[1] | | Dosage: | 0-50 μM | | Administration: | Oral, 0-50 days | | Result: | Promoted oxidative stress resistance and mitochondrial functions inC. elegans. |
| Animal Model: | C57BL/6 mice[1] | | Dosage: | 100 μg/mL | | Administration: | Oral | | Result: | Extended lifespan, elevated NAD＋levels and mitochondrial oxidative respiration, rejuvenated muscle function in aged mice. |
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