CKI 7 dihydrochlorideCK1 inhibitor; induces retinal cell differentiation from human ESCs and iPSCs CAS# 1177141-67-1 |
- Narciclasine
Catalog No.:BCN4732
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 1177141-67-1 | SDF | Download SDF |
PubChem ID | 16078955 | Appearance | Powder |
Formula | C11H14Cl3N3O2S | M.Wt | 358.67 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 20 mM in water and to 50 mM in DMSO | ||
Chemical Name | N-(2-aminoethyl)-5-chloroisoquinoline-8-sulfonamide;dihydrochloride | ||
SMILES | C1=CC(=C2C=CN=CC2=C1S(=O)(=O)NCCN)Cl.Cl.Cl | ||
Standard InChIKey | JUAVTXYOCISSSL-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C11H12ClN3O2S.2ClH/c12-10-1-2-11(18(16,17)15-6-4-13)9-7-14-5-3-8(9)10;;/h1-3,5,7,15H,4,6,13H2;2*1H | ||
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 | Casein kinase 1 (CK1) inhibitor. Also inhibits SGK, S6K1 and MSK1. Induces retinal cell differentiation from human ESCs and iPSCs in combination with SB 431542 and Y-27632. |
CKI 7 dihydrochloride Dilution Calculator
CKI 7 dihydrochloride Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.7881 mL | 13.9404 mL | 27.8808 mL | 55.7616 mL | 69.702 mL |
5 mM | 0.5576 mL | 2.7881 mL | 5.5762 mL | 11.1523 mL | 13.9404 mL |
10 mM | 0.2788 mL | 1.394 mL | 2.7881 mL | 5.5762 mL | 6.9702 mL |
50 mM | 0.0558 mL | 0.2788 mL | 0.5576 mL | 1.1152 mL | 1.394 mL |
100 mM | 0.0279 mL | 0.1394 mL | 0.2788 mL | 0.5576 mL | 0.697 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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In vitro differentiation of retinal cells from human pluripotent stem cells by small-molecule induction.[Pubmed:19671662]
J Cell Sci. 2009 Sep 1;122(Pt 17):3169-79.
The use of stem-cell therapy to treat retinal degeneration holds great promise. However, definitive methods of retinal differentiation that do not depend on recombinant proteins produced in animal or Escherichia coli cells have not been devised. Here, we report a defined culture method using low-molecular-mass compounds that induce differentiation of human embryonic stem (ES) cells and induced pluripotent stem (iPS) cells into retinal progenitors, retinal pigment epithelium cells and photoreceptors. The casein kinase I inhibitor CKI-7, the ALK4 inhibitor SB-431542 and the Rho-associated kinase inhibitor Y-27632 in serum-free and feeder-free floating aggregate culture induce retinal progenitors positive for RX, MITF, PAX6 and CHX10. The treatment induces hexagonal pigmented cells that express RPE65 and CRALBP, form ZO1-positive tight junctions and exhibit phagocytic functions. Subsequent treatment with retinoic acid and taurine induces photoreceptors that express recoverin, rhodopsin and genes involved in phototransduction. Both three-factor (OCT3/4, SOX2 and KLF4) and four-factor (OCT3/4, SOX2, KLF4 and MYC) human iPS cells could be successfully differentiated into retinal cells by small-molecule induction. This method provides a solution to the problem of cross-species antigenic contamination in cell-replacement therapy, and is also useful for in vitro modeling of development, disease and drug screening.
3,4-Diaryl-isoxazoles and -imidazoles as potent dual inhibitors of p38alpha mitogen activated protein kinase and casein kinase 1delta.[Pubmed:19591487]
J Med Chem. 2009 Dec 10;52(23):7618-30.
In this study, we report on the discovery of isoxazole 1 as a potent dual inhibitor of p38alpha (IC(50) = 0.45 microM) and CK1delta (IC(50) = 0.23 microM). Because only a few effective small molecule inhibitors of CK1 have been described so far, we aimed to develop this structural class toward specific agents. Molecular modeling studies comparing p38alpha/CK1delta suggested an optimization strategy leading to design, synthesis, biological characterization, and SAR of highly potent compounds including 9 (IC(50) p38alpha = 0.006 microM; IC(50) CK1delta = 1.6 microM), 13 (IC(50) p38alpha = 2.52 microM; IC(50) CK1delta = 0.033 microM), 17 (IC(50) p38alpha = 0.019 microM; IC(50) CK1delta = 0.004 microM; IC(50) CK1epsilon = 0.073 microM), and 18 (CKP138) (IC(50) p38alpha = 0.041 microM; IC(50) CK1delta = 0.005 microM; IC(50) CK1epsilon = 0.447 microM) possessing differentiated specificity. Selected compounds were profiled over 76 kinases and evaluation of their cellular efficacy showed 18 (CKP138) to be a highly potent and dual-specific inhibitor of CK1delta and p38alpha.
D4476, a cell-permeant inhibitor of CK1, suppresses the site-specific phosphorylation and nuclear exclusion of FOXO1a.[Pubmed:14710188]
EMBO Rep. 2004 Jan;5(1):60-5.
The protein kinase CK1 phosphorylates serine residues that are located close to another phosphoserine in the consensus pSer-Xaa-Xaa-Ser. This specificity generates regions in its target proteins containing two or more neighbouring phosphoserine residues, termed here multisite phosphorylation domains (MPDs). In this paper, we demonstrate that D4476 is a potent and rather selective inhibitor of CK1 in vitro and in cells. In H4IIE hepatoma cells, D4476 specifically inhibits the phosphorylation of endogenous forkhead box transcription factor O1a (FOXO1a) on Ser322 and Ser325 within its MPD, without affecting the phosphorylation of other sites. Our results indicate that these residues are targeted by CK1 in vivo and that the CK1-mediated phosphorylation of the MPD is required for accelerated nuclear exclusion of FOXO1a in response to IGF-1 and insulin. D4476 is much more potent and specific than IC261 or CKI-7, and is therefore the most useful CK1 inhibitor currently available for identifying physiological substrates of CK1.