W-13 hydrochloride

CAS# 88519-57-7

W-13 hydrochloride

Catalog No. BCC6620----Order now to get a substantial discount!

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W-13 hydrochloride: 5mg $81 In Stock
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Chemical structure

W-13 hydrochloride

3D structure

Chemical Properties of W-13 hydrochloride

Cas No. 88519-57-7 SDF Download SDF
PubChem ID 16760706 Appearance Powder
Formula C14H18Cl2N2O2S M.Wt 349.27
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 100 mM in water and to 100 mM in DMSO
Chemical Name N-(4-aminobutyl)-5-chloronaphthalene-2-sulfonamide;hydrochloride
SMILES C1=CC2=C(C=CC(=C2)S(=O)(=O)NCCCCN)C(=C1)Cl.Cl
Standard InChIKey QKAALLVQBOLELJ-UHFFFAOYSA-N
Standard InChI InChI=1S/C14H17ClN2O2S.ClH/c15-14-5-3-4-11-10-12(6-7-13(11)14)20(18,19)17-9-2-1-8-16;/h3-7,10,17H,1-2,8-9,16H2;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.
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.
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.

Biological Activity of W-13 hydrochloride

DescriptionCalmodulin antagonist (inhibits calmodulin activated PDE activity with an IC50 of 68 μM). Inhibits growth of tamoxifen-resistant breast cancer cells.

W-13 hydrochloride Dilution Calculator

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W-13 hydrochloride Molarity Calculator

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Preparing Stock Solutions of W-13 hydrochloride

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.8631 mL 14.3156 mL 28.6311 mL 57.2623 mL 71.5779 mL
5 mM 0.5726 mL 2.8631 mL 5.7262 mL 11.4525 mL 14.3156 mL
10 mM 0.2863 mL 1.4316 mL 2.8631 mL 5.7262 mL 7.1578 mL
50 mM 0.0573 mL 0.2863 mL 0.5726 mL 1.1452 mL 1.4316 mL
100 mM 0.0286 mL 0.1432 mL 0.2863 mL 0.5726 mL 0.7158 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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References on W-13 hydrochloride

Calmodulin inhibitor W13 induces sustained activation of ERK2 and expression of p21(cip1).[Pubmed:9705360]

J Biol Chem. 1998 Aug 21;273(34):22145-50.

One of the major signaling pathways by which extracellular signals induce cell proliferation and differentiation involves the activation of extracellular signal-regulated kinases (ERKs). Because calmodulin is essential for quiescent cells to enter cell cycle, the role of calmodulin on ERK2 activation was studied in cultured fibroblasts. Serum, phorbol esters, or active Ras induced ERK2 activation in NIH 3T3 fibroblasts. This activation was not inhibited by calmodulin blockade. Surprisingly, inhibition of calmodulin prior to fetal bovine serum addition prolonged activation of ERK2. Furthermore, inactivation of calmodulin in serum-starved cells induced ERK2 phosphorylation that was dependent on MAP kinase kinase (MEK). Inactivation of calmodulin in serum-starved cells also induced activation of Ras, Raf, and MEK. On the contrary, tyrosine phosphorylation of tyrosine kinase receptors was not observed. These results indicate that calmodulin inhibits ERK2 activation pathway at the level of Ras. Calmodulin inhibition induced overexpression of p21(cip1) which was dependent on MEK activity. We propose that inhibition of Ras by calmodulin prevents the activation of ERK2 at low serum concentration. Thus, entering into the cell cycle after serum addition would imply the overcoming of the inhibitory effect of calmodulin and consequently ERK2 activation. Furthermore, down-regulation of Ras by calmodulin may be also important to determine the duration of ERK2 activation and to prevent a high p21(cip1) expression that would lead to an inhibition of cell proliferation.

Tamoxifen-resistant human breast cancer cell growth: inhibition by thioridazine, pimozide and the calmodulin antagonist, W-13.[Pubmed:1403784]

J Pharmacol Exp Ther. 1992 Oct;263(1):186-93.

Estrogen receptor (ER)-negative human breast cancer cell lines (MDA-MB-231 and MDA-MB-435) and ER-positive derivatives of the MCF-7 cell line selected for growth in the presence of antiestrogens (LY2 and RR) were used as in vitro models of tamoxifen-resistant human breast cancer in this study. The sensitivity of the tamoxifen-sensitive (MCF-7) and tamoxifen-resistant human breast cancer cell growth to two noncytotoxic neuroleptic drugs, pimozide and thioridazine, and the anticalmodulin agent, W-13, were compared. Inhibition of cell growth was measured as a decrease in cell number following a 72-h incubation with drug. Growth of the ER-negative cell lines MDA-MB-231 and MDA-MB-435 was inhibited by all three drugs. The average Ki values in these two lines were 6.3 and 3.8 microM for pimozide and 4.1 and 15 microM for thioridazine, respectively. Both ER-negative cell lines were more sensitive than MCF-7 cells to growth inhibition by W-13. MCF-7 cells selected for antiestrogen resistance were sensitive to growth inhibition by W-13 and thioridazine (LY2, average Ki = 10.4 microM; RR, average Ki = 5.2 microM). LY2 and RR cells were resistant to pimozide except when treated with estradiol (Ki = 4.6 and 7.9 microM, respectively). Pimozide, thioridazine and W-13 all exerted different effects on the distribution of human breast cancer cells within the cell cycle, suggesting that each drug may utilize a distinct pathway for inhibition of cell growth. We conclude that all three drugs are potential noncytotoxic alternatives to tamoxifen for the treatment of tamoxifen-resistant human breast cancer.

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