NVP 231CerK inhibitor CAS# 362003-83-6 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 362003-83-6 | SDF | Download SDF |
PubChem ID | 4096211 | Appearance | Powder |
Formula | C25H25N3O2S | M.Wt | 431.55 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 100 mM in DMSO and to 5 mM in ethanol | ||
Chemical Name | N-(2-benzamido-1,3-benzothiazol-6-yl)adamantane-1-carboxamide | ||
SMILES | C1C2CC3CC1CC(C2)(C3)C(=O)NC4=CC5=C(C=C4)N=C(S5)NC(=O)C6=CC=CC=C6 | ||
Standard InChIKey | MVSSJPGNLQPWSW-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C25H25N3O2S/c29-22(18-4-2-1-3-5-18)28-24-27-20-7-6-19(11-21(20)31-24)26-23(30)25-12-15-8-16(13-25)10-17(9-15)14-25/h1-7,11,15-17H,8-10,12-14H2,(H,26,30)(H,27,28,29) | ||
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 | Potent, selective and reversible ceramide kinase (CerK) inhibitor (IC50 = 12 nM in vitro). Displays selectivity for CerK over sphingosine kinases (IC50 ≥100 μM) and other lipid kinases. |
NVP 231 Dilution Calculator
NVP 231 Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.3172 mL | 11.5861 mL | 23.1723 mL | 46.3446 mL | 57.9307 mL |
5 mM | 0.4634 mL | 2.3172 mL | 4.6345 mL | 9.2689 mL | 11.5861 mL |
10 mM | 0.2317 mL | 1.1586 mL | 2.3172 mL | 4.6345 mL | 5.7931 mL |
50 mM | 0.0463 mL | 0.2317 mL | 0.4634 mL | 0.9269 mL | 1.1586 mL |
100 mM | 0.0232 mL | 0.1159 mL | 0.2317 mL | 0.4634 mL | 0.5793 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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NVP 231 is a potent, reversible and specific inhibitor of ceramide kinase(CerK) with the IC50 value of 12±2nM in radio assay [1].
NVP 231 has been noted to inhibit CerK with the IC50 value of 12±2nM and have the 90% inhibition at 100 nM in the radio assay. In addition, NVP 231 has been reported to compete with ceramide with the Ki value of 7.4 nM. Furthermore, NVP 231 has been revealed to achieve complete inhibition of CIP at 100nM. NVP 231 in an assay based on human CerK-overexpressing COS-cells (COS-CerK). And the study has been exhibited that NVP 231 is a more potent inhibitor of mouse CerK. Apart from these, NVP 231 has been shown the specificity to CerK with the IC50 values of 0.01 μM, 100 μM, >100 μM, 5 μM, >25 μM, >25 μM, >10 μM, >10 μM and >10 μM for hCerK, hSphK1, hSphK2, hDAGKα, hPI3Kα, hVps34, hGCS, hSMS-1 and CERT, respectively [1].
References:
[1]Graf C1, Klumpp M, Habig M, Rovina P, Billich A, Baumruker T, Oberhauser B, Bornancin F. Targeting ceramide metabolism with a potent and specific ceramide kinase inhibitor. Mol Pharmacol. 2008 Oct;74(4):925-32.
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The ceramide kinase inhibitor NVP-231 inhibits breast and lung cancer cell proliferation by inducing M phase arrest and subsequent cell death.[Pubmed:25134723]
Br J Pharmacol. 2014 Dec;171(24):5829-44.
BACKGROUND AND PURPOSE: Ceramide kinase (CerK) catalyzes the generation of ceramide-1-phosphate which may regulate various cellular functions, including inflammatory reactions and cell growth. Here, we studied the effect of a recently developed CerK inhibitor, NVP-231, on cancer cell proliferation and viability and investigated the role of cell cycle regulators implicated in these responses. EXPERIMENTAL APPROACH: The breast and lung cancer cell lines MCF-7 and NCI-H358 were treated with increasing concentrations of NVP-231 and DNA synthesis, colony formation and cell death were determined. Flow cytometry was performed to analyse cell cycle distribution of cells and Western blot analysis was used to detect changes in cell cycle regulator expression and activation. KEY RESULTS: In both cell lines, NVP-231 concentration-dependently reduced cell viability, DNA synthesis and colony formation. Moreover it induced apoptosis, as measured by increased DNA fragmentation and caspase-3 and caspase-9 cleavage. Cell cycle analysis revealed that NVP-231 decreased the number of cells in S phase and induced M phase arrest with an increased mitotic index, as determined by increased histone H3 phosphorylation. The effect on the cell cycle was even more pronounced when NVP-231 treatment was combined with staurosporine. Finally, overexpression of CerK protected, whereas down-regulation of CerK with siRNA sensitized, cells for staurosporine-induced apoptosis. CONCLUSIONS AND IMPLICATIONS: Our data demonstrate for the first time a crucial role for CerK in the M phase control in cancer cells and suggest its targeted inhibition, using drugs such as NVP-231, in combination with conventional pro-apoptotic chemotherapy.
A secondary assay for ceramide kinase inhibitors based on cell growth inhibition by short-chain ceramides.[Pubmed:18831956]
Anal Biochem. 2009 Jan 1;384(1):166-9.
We recently reported that ectopic expression of ceramide kinase (CerK) in various cell lines increases their sensitivity to cell death induced by the exogenous addition of short-chain (e.g., C2) ceramides (Cer). Here we show that this higher sensitivity results from CerK catalytic activity and production of C2-ceramide 1-phosphate (C2-C1P). If CerK activity is inhibited by the potent inhibitor NVP-231, C2-C1P is not produced and viability returns to control levels. The EC(50) of NVP-231 in this assay is in the low nanomolar range, consistent with the IC(50) determined in activity assays in vitro using purified CerK. NVP-995, a structurally related but inactive compound, does not protect against C2-Cer-induced cell death. This assay is robust and easy to implement and scale up, thereby providing a valuable secondary screen assay for CerK inhibitors.
Ceramide kinase deficiency impairs microendothelial cell angiogenesis in vitro.[Pubmed:19323974]
Microvasc Res. 2009 May;77(3):389-93.
The recent generation of ceramide kinase (CerK)-deficient (Cerk (-/-)) mice as well as the identification of the potent CerK inhibitor NVP-231 have provided unprecedented opportunities to better understand CerK biology. Here we used skin dermal microendothelial cells (DMECs) and we show that CerK activity regulates their neovascularization in a matrigel environment in vitro. Capillary-like tube formation was significantly impaired in CerK-deficient cells or in wild-type (WT) cells treated with NVP-231 as compared with untreated WT cells. This was not the result of compromised proliferation or survival because Cerk (-/-) endothelial cells were able to migrate out of dermal fragments and grow in monolayer culture as well as their WT counterpart. Vascular endothelial growth factor, fibroblast growth factor or tumor necrosis factor could not rescue the angiogenesis defect observed in Cerk (-/-) DMEMs. Moreover, CerK ablation increased serum ceramide levels at the expense of dihydroceramide levels without affecting sphingosine, dihydrosphingosine, sphingosine-1-phosphate or dihydrosphingosine-1-phosphate levels. These observations collectively suggest that CerK-catalyzed formation of C1P may regulate angiogenesis by a novel mechanism that is independent of S1P formation and signaling.