Carbenoxolone disodium11β-HSD inhibitor CAS# 7421-40-1 |
- GAP-134
Catalog No.:BCC1588
CAS No.:943134-39-2
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 7421-40-1 | SDF | Download SDF |
PubChem ID | 636402 | Appearance | Powder |
Formula | C34H48Na2O7 | M.Wt | 614.72 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 100 mM in water | ||
Chemical Name | disodium;(2S,4aS,6aR,6aS,6bR,8aR,10S,12aS,14bR)-10-(3-carboxylatopropanoyloxy)-2,4a,6a,6b,9,9,12a-heptamethyl-13-oxo-3,4,5,6,6a,7,8,8a,10,11,12,14b-dodecahydro-1H-picene-2-carboxylate | ||
SMILES | CC1(C2CCC3(C(C2(CCC1OC(=O)CCC(=O)[O-])C)C(=O)C=C4C3(CCC5(C4CC(CC5)(C)C(=O)[O-])C)C)C)C.[Na+].[Na+] | ||
Standard InChIKey | BQENDLAVTKRQMS-SBBGFIFASA-L | ||
Standard InChI | InChI=1S/C34H50O7.2Na/c1-29(2)23-10-13-34(7)27(32(23,5)12-11-24(29)41-26(38)9-8-25(36)37)22(35)18-20-21-19-31(4,28(39)40)15-14-30(21,3)16-17-33(20,34)6;;/h18,21,23-24,27H,8-17,19H2,1-7H3,(H,36,37)(H,39,40);;/q;2*+1/p-2/t21-,23-,24-,27+,30+,31-,32-,33+,34+;;/m0../s1 | ||
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 | Glucocorticoid that inhibits 11β-hydroxysteroid dehydrogenase (11-HSD) and blocks gap junction communication. |
Carbenoxolone disodium Dilution Calculator
Carbenoxolone disodium Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 1.6268 mL | 8.1338 mL | 16.2676 mL | 32.5351 mL | 40.6689 mL |
5 mM | 0.3254 mL | 1.6268 mL | 3.2535 mL | 6.507 mL | 8.1338 mL |
10 mM | 0.1627 mL | 0.8134 mL | 1.6268 mL | 3.2535 mL | 4.0669 mL |
50 mM | 0.0325 mL | 0.1627 mL | 0.3254 mL | 0.6507 mL | 0.8134 mL |
100 mM | 0.0163 mL | 0.0813 mL | 0.1627 mL | 0.3254 mL | 0.4067 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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Carbenoxolone disodium is an inhibitor of 11β-hydroxysteroid dehydrogenase (11β-HSD) [1].
11β-HSD is a family of enzymes that regulating the access of glucocorticoids to the steroid receptors.
In bovine aortic endothelial cells (BAEC), carbenoxolone disodium can block gap junction communication (GJC) and modulates Cx43 expression, which based on junctional patency [2].
Carbenoxolone disodium is an inhibitor of 11β-HSD and causes hypokalemia and hypernatremia. In male rats, 11β-HSD was inhibited in the liver, kidney, pituitary, hippocampus, hypothalamus and amygdala 1h after intraperitoneal administration of CX (100 mg/kg). Injection of CX (1.5mg/kg) into the 3rd ventricle inhibited corticosterone to 11-dehydrocorticosterone by 11-HSD in the hippocampus and pituitary and produced behavioral hyperactivity, while had no effect in the liver or kidney. Injection of CX (10-50ug/rat) into intracerebroventricularly inhibited 11β-HSD differentially in the hypothalamus and hippocampus [1]. These results show that low doses of CX can alter the activity of 11β-HSD in specific brain regions without affecting its activity in peripheral tissues, and only marginally in the pituitary, provides a method to study the central role of this enzyme.
References:
[1]. Jellinck PH, Monder C, McEwen BS, et al. Differential inhibition of 11 beta-hydroxysteroid dehydrogenase by carbenoxolone in rat brain regions and peripheral tissues. J Steroid Biochem Mol Biol, 1993, 46(2): 209-213.
[2]. Sagar GD, Larson DM. Carbenoxolone inhibits junctional trasnfer and upregulates connexin43 expression by a protein kinase A-dependent pathway. J Cell Biochem, 2006, 98(6): 1543-1551.
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Carbenoxolone Disodium Treatment for Canine Pituitary-Dependent Hyperadrenocorticism.[Pubmed:27824928]
PLoS One. 2016 Nov 8;11(11):e0166267.
Pituitary-dependent hyperadrenocorticism (PDH) is mainly caused by pituitary corticotroph tumors in dogs. A characteristic feature of corticotroph tumors is their resistance to negative feedback by glucocorticoids. In some animal species, including dogs, the aberrant expression of 11beta-hydroxysteroid dehydrogenase (11HSD), a cortisol metabolic enzyme, is observed in corticotroph tumors. We previously reported that carbenoxolone (CBX), an inhibitor of 11HSD, suppressed ACTH secretion from the pituitary gland, and decreased cortisol concentrations in healthy dogs. Therefore, the aim of this study was to investigate the therapeutic effects of CBX on dogs with PDH. Six dogs with PDH were treated with 60 to 80 mg/kg/day of CBX for 6 weeks, followed by trilostane, which is a commonly used agent for canine PDH. CBX treatment led to a gradual decrease in both basal and in corticotropic releasing hormone (CRH)-stimulated plasma ACTH concentrations and CRH-stimulated serum cortisol concentrations, without side effects. However, basal and stimulated ACTH and cortisol concentrations remained higher than those of healthy dogs, and clinical symptoms such as polydipsia and polyuria were not ameliorated. After a 2-week wash-out interval, trilostane was administered for 2 weeks. Although basal plasma ACTH concentrations were higher after trilostane treatment than CBX treatment, polydipsia and polyuria resolved in all six dogs. The reason for the lack of improvement in polydipsia and polyuria with CBX treatment is unclear. Other mechanisms, in addition to a partial decrease in ACTH secretion, are likely to be involved. In conclusion, this is the first study to report the in vivo effects of CBX in dogs with PDH. The findings suggest that CBX inhibits ACTH secretion from canine pituitary tumors, resulting in lower cortisol concentrations.
Antiviral activity of Carbenoxolone disodium against dengue virus infection.[Pubmed:27155198]
J Med Virol. 2017 Apr;89(4):571-581.
As one of the most important mosquito-borne viral diseases, dengue infection is now becoming a global concern due to its rapid spread and rise in incidence. Currently, there is no approved vaccine or effective antiviral drug for dengue virus (DENV) infection. Glycyrrhetinic acid (GNa) and its related derivatives have been reported to inhibit a broad spectrum of viruses. However, it is unknown whether Carbenoxolone disodium (CBX), one of the GNa derivatives, affects DENV infection. Here, we found that the production of infectious DENV particles was significantly decreased by CBX treatment in DENV-permissive cells, while the viral RNA and viral protein synthesis were not affected. Moreover, results from time-of-addition study showed that the inhibitory effect of CBX on DENV was exhibited by targeting the virus itself, not the host cells. Directly incubating DENV with CBX resulted in a remarkable reduction of virus titer and virus infectivity. Furthermore, DENV RNA from progeny virions in the supernatants was significantly decreased by CBX treatment in a dose-dependent manner. Taken together, these data indicate that the antiviral activity of CBX against DENV may be mainly due to a virucidal effect exerted by the compound itself. Our work, for the first time, demonstrates that CBX has antiviral activity against DENV infection, providing useful information for development of potential therapeutic interventions against dengue. J. Med. Virol. 89:571-581, 2017. (c) 2016 Wiley Periodicals, Inc.
Carbenoxolone inhibits junctional transfer and upregulates Connexin43 expression by a protein kinase A-dependent pathway.[Pubmed:16552723]
J Cell Biochem. 2006 Aug 15;98(6):1543-51.
We have been investigating the function and gene expression of connexins by vascular wall cells, especially Connexin43 (Cx43) in bovine aortic endothelial cells (BAEC). In this study, we tested the effects of carbenoxolone (CBN), a gap junction communication (GJC) blocker on the junctional transfer of Lucifer yellow in BAEC. CBN is a water-soluble derivative of the liquorice-root extract 18-alpha-glycyrrhetinic acid. CBN rapidly abolished dye-transfer in the scrape-load transfer assay (a measure of GJC) in a reversible and dose-dependent fashion. We then asked whether the BAEC might somehow compensate for the loss of junctional communication by altering the expression of connexins. Thus, we treated BAEC with 100 microM CBN in serum free medium and determined the total Cx43 cellular distribution (immunostaining) and protein content (immunoblotting). Besides changes in distribution, by 6 h, Cx43 content levels increased to 166% +/- 22% (P < 0.0001) of controls. RNA blot data showed two-three fold increases in Cx43 message in BAEC after 6 h of CBN treatment, suggesting transcriptional control. Since CBN has structural similarities to corticosteroids, we tested both aldosterone and prednisolone but neither drug increased Cx43 levels, suggesting that the CBN response was not due to a generalized steroid effect. Staurosporine inhibited the CBN-induced increase in Cx43 content, suggesting a role for kinases in the signaling pathway. Further studies with inhibitors indicated that PKA but not PKC was implicated. In summary, CBN blocks junctional communication and modulates Cx43 expression in BAEC. These results suggest a feedback mechanism for control of connexin expression based on junctional patency.
Differential inhibition of 11 beta-hydroxysteroid dehydrogenase by carbenoxolone in rat brain regions and peripheral tissues.[Pubmed:8664169]
J Steroid Biochem Mol Biol. 1993 Aug;46(2):209-13.
Carbenoxolone (CX), the succinyl ester of glycyrrhetinic acid, causes hypokalemia and hypernatremia. Its pharmacological effects are believed to be due to its inhibition of 11 beta-hydroxysteroid dehydrogenase (11-HSD). There was a marked inhibition of this enzyme in the liver, kidney, pituitary, hippocampus, hypothalamus and amygdala 1 h after intraperitoneal administration of CX (100 mg kg-1) to intact male rats. Intracerebral injection of CX (1.5 mg kg-1) into the 3rd ventricle inhibited the oxidation of corticosterone to 11-dehydrocorticosterone by 11-HSD in the pituitary and hippocampus and produced marked behavioral hyperactivity but had no effect in the liver or kidney. Lower amounts of CX (10-50 micrograms/rat) given intracerebroventricularly (i.c.v) were without significant effect on 11-HSD in the pituitary or amygdala 1 h after infusion but inhibited this enzyme differentially in the hippocampus and hypothalamus. Inhibition of 11-HSD activity in the hippocampus and hypothalamus was observed up to 6 h after i.c.v. administration of CX (50 micrograms/rat) together with some decrease in activity of this enzyme in the pituitary at 3 h. The findings that low doses of CX given i.c.v. can alter the activity of 11-HSD in specific brain regions without affecting its activity in peripheral tissues, and only marginally in the pituitary, provides a method to study the central role of this enzyme independently of systemic effects.