CGP 53353CAS# 145915-60-2 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 145915-60-2 | SDF | Download SDF |
PubChem ID | 6711154 | Appearance | Powder |
Formula | C20H13F2N3O2 | M.Wt | 365.34 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 100 mM in DMSO and to 20 mM in ethanol | ||
Chemical Name | 5,6-bis(4-fluoroanilino)isoindole-1,3-dione | ||
SMILES | C1=CC(=CC=C1NC2=C(C=C3C(=C2)C(=O)NC3=O)NC4=CC=C(C=C4)F)F | ||
Standard InChIKey | RONQPWQYDRPRGG-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C20H13F2N3O2/c21-11-1-5-13(6-2-11)23-17-9-15-16(20(27)25-19(15)26)10-18(17)24-14-7-3-12(22)4-8-14/h1-10,23-24H,(H,25,26,27) | ||
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. |
Description | Selective inhibitor of PKCβII (IC50 values are 0.41 and 3.8 μM for PKCβII and PKCβI respectively). Also inhibits prionogenic Sup35 fibrillization (IC50 ~ 3.4 μM) and inhibits de novo Aβ42 assembly in vitro. |
CGP 53353 Dilution Calculator
CGP 53353 Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.7372 mL | 13.6859 mL | 27.3718 mL | 54.7435 mL | 68.4294 mL |
5 mM | 0.5474 mL | 2.7372 mL | 5.4744 mL | 10.9487 mL | 13.6859 mL |
10 mM | 0.2737 mL | 1.3686 mL | 2.7372 mL | 5.4744 mL | 6.8429 mL |
50 mM | 0.0547 mL | 0.2737 mL | 0.5474 mL | 1.0949 mL | 1.3686 mL |
100 mM | 0.0274 mL | 0.1369 mL | 0.2737 mL | 0.5474 mL | 0.6843 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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Effect of GABAB receptor antagonists (CGP 35348 and CGP 55845) on serum interleukin 6 and 18 concentrations in albino mice following neonatal hypoxia ischemia insult.[Pubmed:27731803]
Pak J Pharm Sci. 2016 Sep;29(5):1503-1508.
Interleukin (IL) 6 and 18 plays an important role in inflammatory response following hypoxia ischemia encephalopathy (HIE). Present study was designed to demonstrate the effect of two GABAB receptor antagonists (CGP 35348 and 55845), respectively, on the serum IL6 and IL 18 concentrations in albino mice. Albino mice pups (of both genders) were subjected to Murine model of hypoxia-ischemia encephalopathy on postnatal day 10 (right common carotid artery was ligated followed by 8% hypoxia for 25 minutes). After neonatal brain damage and following weaning, mice were divided in three groups, in gender specific manner, and fed on normal rodent diet till they were 13 week old. At this time point, group 1 received intraperitonial saline solution (control group), group 2 was supplemented with CGP 35348 (1mg/ml solvent/Kg body weight) and group 3 with CGP 55845 (1mg/ml solvent/Kg body weight), intraperitonially, for 12 days and IL 6 and 18 concentrations were determined in serum by ELISA. It was observed that CGP 35348 supplementation resulted in reduced interlukin-6 and interlukin-18 concentrations in male albino mice. While CGP 55845 supplementation increased IL-6 and IL-18 concentrations in female albino mice following HIE. Our results are indicating that GABAB receptor antagonist's supplementation affects IL concentrations in albino mice in a gender specific manner following neonatal brain damage and can be further explored for the treatments of hypoxia ischemia associated neurological ailments.
Comprehensive genomic profiling (CGP) of ovarian clear cell carcinomas (OCCC) identifies clinically relevant genomic alterations (CRGA) and targeted therapy options.[Pubmed:28349114]
Gynecol Oncol Rep. 2017 Mar 1;20:62-66.
*MTOR pathway genes are often mutated in ovarian clear cell carcinomas (OCCC).*11.2% of OCCC have targetable alterations only in the mTOR pathway.*MTOR pathway mutations in OCCC can underlie robust, lasting responses to everolimus.
Gender-specific effects of CGP 55845, GABAB receptor antagonist, on neuromuscular coordination, learning and memory formation in albino mouse following neonatal hypoxia-ischemia insult.[Pubmed:25847084]
Neurol Sci. 2015 Jun;36(6):961-9.
GABAB receptor antagonists are experimentally proved as spatial memory enhancers in mouse models but their role has not been described following hypoxic-ischemic insult. 10-day-old albino mice were subjected to Murine model of hypoxia and ischemia. Following brain damage, mice were fed on normal rodent diet till they were 13 weeks old. At this time point, mice were divided into two groups. Group 1 received saline and group 2 received intraperitoneally CGP 55845 (1 mg/ml solvent/Kg body weight) for 12 days. Behavioural observations were made during rota rod, open field and Morris water maze test along with brain infarct measurement in both CGP 55845 treated and untreated groups. It was observed that application of GABAB receptor antagonist improved the over all motor function in male and female albino mice but effects were more pronounced in males. In open field, CGP 55845-treated female mice showed poor performance. CGP 55845 had no significant effect on learning and memory formation during Morris water maze test and also on brain infract size in both genders following hypoxia ischemia encephalopathy. Effects of CGP 55845 can be further explored in a dose and duration dependent manner to improve the learning and memory in albino mice following neonatal brain damage.
Selective inhibition of protein kinase Cbeta2 prevents acute effects of high glucose on vascular cell adhesion molecule-1 expression in human endothelial cells.[Pubmed:15210597]
Circulation. 2004 Jul 6;110(1):91-6.
BACKGROUND: Enhanced expression of adhesion molecules by the endothelium may account for vascular damage in diabetics and nondiabetic patients who develop stress hyperglycemia during acute myocardial infarction. We analyzed the phosphorylation of protein kinase Cbeta2 (PKCbeta2) at serine/threonine residues, which may contribute to the endothelial dysfunction during acute hyperglycemia. Furthermore, this study was designed to investigate whether selective blockade of this regulatory mechanism may prevent the development of endothelial hyperadhesiveness. METHODS AND RESULTS: Incubation of the human aortic endothelial cells with high glucose (22.2 mmol/L) resulted in significant increase of vascular cell adhesion molecule (VCAM)-1 protein expression (172+/-15% versus control; P<0.01). Phorbol 12-myristate 13-acetate, a potent activator of PKC, mimicked the effect of high glucose on VCAM-1 expression. High glucose led to a rapid increase (181+/-22% versus control; P<0.01) of membrane-bound PKCbeta, reflecting activation of this enzyme. The nonselective inhibitor of PKCbeta1 and PKCbeta2 isoforms LY379196, as well as CGP53353, a highly selective inhibitor of PKCbeta2, prevented in a dose-dependent manner upregulation of VCAM-1. Incubation with high glucose was associated with increased PKCbeta2 phosphorylation at the Ser-660 residue, and both LY379196 and CGP53353 prevented this event. Exposure of the cells to high glucose also reduced the protein level of the inhibitory subunit of nuclear factor-kappaB, IkappaBalpha, leading to its enhanced binding activity. Selective inhibition of PKCbeta abolished IkappaBalpha degradation. CONCLUSIONS: Our findings demonstrate for the first time that phosphorylation of Ser-660 represents a selective regulatory mechanism for glucose-induced upregulation of VCAM-1. Therefore, PKCbeta2-selective inhibitors may be promising drugs for treatment of endothelial dysfunction during acute hyperglycemia and possibly in diabetes.