A-7 hydrochloride

CAS# 79127-24-5

A-7 hydrochloride

Catalog No. BCC6625----Order now to get a substantial discount!

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A-7 hydrochloride: 5mg $69 In Stock
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Chemical structure

A-7 hydrochloride

3D structure

Chemical Properties of A-7 hydrochloride

Cas No. 79127-24-5 SDF Download SDF
PubChem ID 44119113 Appearance Powder
Formula C20H30Cl2N2O2S M.Wt 433.44
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 50 mM in DMSO
Chemical Name N-(10-aminodecyl)-5-chloronaphthalene-1-sulfonamide;hydrochloride
SMILES C1=CC2=C(C=CC=C2Cl)C(=C1)S(=O)(=O)NCCCCCCCCCCN.Cl
Standard InChIKey XDJCAQBTSCRBHS-UHFFFAOYSA-N
Standard InChI InChI=1S/C20H29ClN2O2S.ClH/c21-19-13-9-12-18-17(19)11-10-14-20(18)26(24,25)23-16-8-6-4-2-1-3-5-7-15-22;/h9-14,23H,1-8,15-16,22H2;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 A-7 hydrochloride

DescriptionPotent calmodulin antagonist (inhibits calmodulin-activated PDE activity with an IC50 of 3 μM).

A-7 hydrochloride Dilution Calculator

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A-7 hydrochloride Molarity Calculator

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Preparing Stock Solutions of A-7 hydrochloride

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.3071 mL 11.5356 mL 23.0712 mL 46.1425 mL 57.6781 mL
5 mM 0.4614 mL 2.3071 mL 4.6142 mL 9.2285 mL 11.5356 mL
10 mM 0.2307 mL 1.1536 mL 2.3071 mL 4.6142 mL 5.7678 mL
50 mM 0.0461 mL 0.2307 mL 0.4614 mL 0.9228 mL 1.1536 mL
100 mM 0.0231 mL 0.1154 mL 0.2307 mL 0.4614 mL 0.5768 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 A-7 hydrochloride

Antitumor effect of NK012, a 7-ethyl-10-hydroxycamptothecin-incorporating polymeric micelle, on U87MG orthotopic glioblastoma in mice compared with irinotecan hydrochloride in combination with bevacizumab.[Pubmed:20068081]

Clin Cancer Res. 2010 Jan 15;16(2):521-9.

PURPOSE: To clarify the effect of bevacizumab on NK012 therapy in mice bearing U87MG glioblastoma orthotopic xenografts in comparison with the combination therapy of irinotecan hydrochloride (CPT-11) with bevacizumab. EXPERIMENTAL DESIGN: NK012 at 7-ethyl-10-hydroxycamptothecin (SN-38) equivalent dose of 30 mg/kg was administered intravenously three times every 4 days with or without bevacizumab. CPT-11 at 66.7 mg/kg was administered intravenously three times every 4 days or CPT-11 at 40 mg/kg/d over 5 consecutive days with or without bevacizumab. Bevacizumab was administered intraperitoneally six times every 4 days in each experiment. In vivo antitumor effects were evaluated by bioluminescence imaging, histopathologic evaluation, and immunohistochemistry. To evaluate interaction with bevacizumab, free SN-38 concentration in tumor tissues was examined by high-performance liquid chromatography. RESULTS: CPT-11 in combination with bevacizumab showed significantly more potent antitumor activity and longer survival than CPT-11 monotherapy (P < 0.05). However, there was no difference between NK012 monotherapy and NK012 in combination with bevacizumab. Concentration of free SN-38 released from NK012 in tumor tissue decreased in combination with bevacizumab (P = 0.027). NK012 monotherapy or NK012 with bevacizumab showed potent antitumor activity and longer survival than any dosing method of CPT-11 in combination with bevacizumab (P < 0.05). Orthotopic tumors treated with NK012 showed decreased tumor cellularity and lower Ki-67 index (P < 0.001) relative to those treated with CPT-11/bevacizumab. CONCLUSIONS: The present study using orthotopic glioblastoma model in mice may warrant further preclinical evaluation of NK012 before conducting the clinical trial of the drug, because the antitumor activity of NK012 monotherapy was superior to the combination therapy of CPT-11 with bevacizumab.

Direct interaction of calmodulin antagonists with Ca2+/calmodulin-dependent cyclic nucleotide phosphodiesterase.[Pubmed:6099352]

J Biochem. 1984 Dec;96(6):1721-6.

Trypsin-treated Ca2+/calmodulin-dependent phosphodiesterase (CA2+-PDE), which had lost its sensitivity to Ca2+-calmodulin, was inhibited by various calmodulin antagonists, trifluoperazine, chlorpromazine, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) and aminoalkyl chain analogues of W-7 (A-3, A-4, A-5, I-240, A-6, A-7). These inhibitory effects were less than those on calmodulin-activated Ca2+-PDE. The ability of these compounds to inhibit trypsin-treated Ca2+-PDE correlated well with the inhibitory effect on calmodulin-activated Ca2+-PDE. W-7 inhibited trypsin-treated Ca2+-PDE in a competitive fashion with respect to cyclic GMP and the Ki value was 300 microM. The inhibition of trypsin-treated Ca2+-PDE by W-7 (300 microM) or A-7 (100 microM) was overcome by the addition of excess calmodulin. Trypsin-treated Ca2+-PDE can bind to W-7-coupled cyanogen bromide-activated Sepharose 4B in the presence of 1 mM EGTA. These results suggest that Ca2+-PDE possesses a binding site for calmodulin antagonists and that the binding site for these antagonists on this enzyme may be structurally similar to the binding site on calmodulin itself.

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