ZLN024CAS# 723249-01-2 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 723249-01-2 | SDF | Download SDF |
PubChem ID | 1825716 | Appearance | Powder |
Formula | C13H13BrN2OS | M.Wt | 325.22 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble in DMSO | ||
Chemical Name | 2-[2-(2-bromo-4-methylphenoxy)ethylsulfanyl]pyrimidine | ||
SMILES | CC1=CC(=C(C=C1)OCCSC2=NC=CC=N2)Br | ||
Standard InChIKey | KWJRSHZSULRJHE-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C13H13BrN2OS/c1-10-3-4-12(11(14)9-10)17-7-8-18-13-15-5-2-6-16-13/h2-6,9H,7-8H2,1H3 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
ZLN024 Dilution Calculator
ZLN024 Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 3.0748 mL | 15.3742 mL | 30.7484 mL | 61.4968 mL | 76.871 mL |
5 mM | 0.615 mL | 3.0748 mL | 6.1497 mL | 12.2994 mL | 15.3742 mL |
10 mM | 0.3075 mL | 1.5374 mL | 3.0748 mL | 6.1497 mL | 7.6871 mL |
50 mM | 0.0615 mL | 0.3075 mL | 0.615 mL | 1.2299 mL | 1.5374 mL |
100 mM | 0.0307 mL | 0.1537 mL | 0.3075 mL | 0.615 mL | 0.7687 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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ZLN024 is an AMPK allosteric activator. ZLN024 directly activates recombinant AMPK α1β1γ1, AMPK α2β1γ1, AMPK α1β2γ1 and AMPK α2β2γ1 heterotrimer with EC50s of 0.42 µM, 0.95 µM, 1.1 µM and 0.13 µM, respectively.
In Vitro:ZLN024 allosterically stimulates active AMPK heterotrimers and the inactive α1 subunit truncations α1 (1-394) and α1 (1-335) but not α1 (1-312). AMPK activation by ZLN024 requires the pre-phosphorylation of Thr-172 by at least one upstream kinase and protects AMPK Thr-172 against dephosphorylation by PP2Cα. ZLN024 activates AMPK in L6 myotubes and stimulates glucose uptake and fatty acid oxidation without increasing the ADP/ATP ratio. Using the established scintillation proximity assay (SPA) assay, random screening against the AMPK α1β1γ1 heterotrimer is performed and a new AMPK activator, ZLN024 is found. ZLN024 directly activates recombinant AMPK α1β1γ1 and its homologue α2β1γ1 in a concentration-dependent manner. ZLN024 increases the activity of α1β1γ1 by 1.5-fold and has an EC50 of 0.42 µM, and it increases the activity of α2β1γ1 by 1.7-fold with an EC50 of 0.95 µM. ZLN024 also directly activates recombinant AMPK α1β2γ1, by 1.7-fold with an EC50 of 1.1 µM; and AMPK α2β2γ1, by 1.6-fold with an EC50 of 0.13 µM[1].
In Vivo:C57BKS db/db mice are administered a 15 mg/kg/day dose of ZLN024 by daily gavage for 5 weeks; 250 mg/kg/day Metformin (Met) is used as a positive control. During the treatment period, there is no significant alteration in food intake and body weight compared with the vehicle group. After 4 weeks of treatment, ZLN024 improves glucose tolerance. ZLN024 reduces the fasting blood glucose by 15%. Liver tissue weight, triacylglycerol and the total cholesterol content are decreased[1].
References:
[1]. Zhang LN, et al. Novel small-molecule AMP-activated protein kinase allosteric activator with beneficial effects in db/db mice. PLoS One. 2013 Aug 20;8(8):e72092.
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The adenosine monophosphate-activated protein kinase-vacuolar adenosine triphosphatase-pH axis: A key regulator of the profibrogenic phenotype of human hepatic stellate cells.[Pubmed:29663481]
Hepatology. 2018 Sep;68(3):1140-1153.
Liver fibrosis and cirrhosis are characterized by activation of hepatic stellate cells (HSCs), which is associated with higher intracellular pH (pHi). The vacuolar H(+) adenosine-triphosphatase (v-ATPase) multisubunit complex is a key regulator of pHi homeostasis. The present work investigated the functional role of v-ATPase in primary human HSC (hHSC) activation and its modulation by specific adenosine monophosphate-activated protein kinase (AMPK) subunits. We demonstrate that the expression of different v-ATPase subunits was increased in in vivo and in vitro activated hHSCs compared to nonactivated hHSCs. Specific inhibition of v-ATPase with bafilomycin and KM91104 induced a down-regulation of the HSC fibrogenic gene profile, which coincided with increased lysosomal pH, decreased pHi, activation of AMPK, reduced proliferation, and lower metabolic activity. Similarly, pharmacological activation of AMPK by treatment with diflunisal, A769662, and ZLN024 reduced the expression of v-ATPase subunits and profibrogenic markers. v-ATPase expression was differently regulated by the AMPK alpha1 subunit (AMPKalpha1) and AMPKalpha2, as demonstrated in mouse embryo fibroblasts specifically deficient for AMPK alpha subunits. In addition, activation of v-ATPase in hHSCs was shown to be AMPKalpha1-dependent. Accordingly, pharmacological activation of AMPK in AMPKalpha1-depleted hHSCs prevented v-ATPase down-regulation. Finally, we showed that v-ATPase expression was increased in fibrotic livers from bile duct-ligated mice and in human cirrhotic livers. CONCLUSION: The down-regulation of v-ATPase might represent a promising target for the development of antifibrotic strategies. (Hepatology 2018).
Novel small-molecule AMP-activated protein kinase allosteric activator with beneficial effects in db/db mice.[Pubmed:23977216]
PLoS One. 2013 Aug 20;8(8):e72092.
AMP-activated protein kinase (AMPK) is an energy sensor of metabolism that is an attractive therapeutic target for type 2 diabetes mellitus and metabolic syndrome. Using a homogeneous scintillation proximity assay (SPA), we identified a new small-molecule AMPK activator, ZLN024, which allosterically stimulated active AMPK heterotrimers and the inactive alpha1 subunit truncations alpha1 (1-394) and alpha1 (1-335) but not alpha1 (1-312). AMPK activation by ZLN024 requires the pre-phosphorylation of Thr-172 by at least one upstream kinase and protects AMPK Thr-172 against dephosphorylation by PP2Calpha. ZLN024 activated AMPK in L6 myotubes and stimulated glucose uptake and fatty acid oxidation without increasing the ADP/ATP ratio. ZLN024 also activated AMPK in primary hepatocytes, decreased fatty acid synthesis and glucose output. Treatment of db/db mice with 15 mg/kg/day ZLN024 improved glucose tolerance; liver tissue weight, triacylglycerol and the total cholesterol content were decreased. The hepatic transcriptional level of G6Pase, FAS and mtGPAT were reduced. The transcription of genes involved in fatty acid oxidation and the mitochondrial biogenesis of muscle tissue were elevated. The ACC phosphorylation was increased in muscle and liver. This study provides a novel allosteric AMPK activator for functional study in vitro and in vivo and demonstrates that AMPK allosteric activators could be a promising therapeutic approach for type 2 diabetes mellitus and metabolic syndrome.