Proglumide sodium saltCAS# 99247-33-3 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 99247-33-3 | SDF | Download SDF |
| PubChem ID | 23677833 | Appearance | Powder |
| Formula | C18H25N2NaO4 | M.Wt | 356.39 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | H2O : 100 mg/mL (280.59 mM; Need ultrasonic) | ||
| Chemical Name | sodium;4-benzamido-5-(dipropylamino)-5-oxopentanoate | ||
| SMILES | CCCN(CCC)C(=O)C(CCC(=O)[O-])NC(=O)C1=CC=CC=C1.[Na+] | ||
| Standard InChIKey | UFMWGCINVOIJSO-UHFFFAOYSA-M | ||
| Standard InChI | InChI=1S/C18H26N2O4.Na/c1-3-12-20(13-4-2)18(24)15(10-11-16(21)22)19-17(23)14-8-6-5-7-9-14;/h5-9,15H,3-4,10-13H2,1-2H3,(H,19,23)(H,21,22);/q;+1/p-1 | ||
| 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 | Non-selective cholecystokinin (CCK) antagonist. Inhibits CCK-stimulated amylase secretion and prevents CCK-induced 2-deoxyglucose uptake in mouse pancreatic acini. Blocks growth of HT29 colon carcinoma cells in response to gastrin 17 treatment. Orally active. |
Proglumide sodium salt Dilution Calculator
Proglumide sodium salt Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.8059 mL | 14.0296 mL | 28.0591 mL | 56.1183 mL | 70.1479 mL |
| 5 mM | 0.5612 mL | 2.8059 mL | 5.6118 mL | 11.2237 mL | 14.0296 mL |
| 10 mM | 0.2806 mL | 1.403 mL | 2.8059 mL | 5.6118 mL | 7.0148 mL |
| 50 mM | 0.0561 mL | 0.2806 mL | 0.5612 mL | 1.1224 mL | 1.403 mL |
| 100 mM | 0.0281 mL | 0.1403 mL | 0.2806 mL | 0.5612 mL | 0.7015 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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Effects of gastrin, proglumide, loxiglumide and L-365,260 on growth of human colon carcinoma cells.[Pubmed:8166452]
Anticancer Res. 1994 Jan-Feb;14(1A):215-20.
Gastrin-17 stimulated growth of the human colon carcinoma cell line HT29 but not of the human colon carcinoma cell lines T84, HCT116 and the mouse fibroblast cell line 3T3-L1. Correspondingly, specific gastrin binding sites were only found on HT29-cells. Proglumide, loxiglumide and L-365,260 inhibited gastrin-17 stimulated growth of HT29-cells at doses which did not influence cell growth when given without gastrin. At higher concentrations proglumide and loxiglumide reduced cell proliferation in all cell lines investigated. Gastrin-17 could not reverse these effects. This growth inhibition was therefore considered as not gastrin receptor mediated. The results demonstrate that only some human colon carcinoma cell lines are stimulated by gastrin. This stimulation can be inhibited by gastrin/CCK-antagonists.
In vitro and in vivo effect of proglumide on cholecystokinin-stimulated amylase release in mouse pancreatic acini.[Pubmed:6202584]
Gastroenterol Jpn. 1984 Feb;19(1):53-8.
The effect of proglumide on cholecystokinin (CCK)-stimulated amylase release was studied in vitro and in vivo in dispersed acini from mouse pancreas. In an in vitro study, proglumide at concentrations between 0.3-10 mM inhibited CCK-stimulated amylase release dose-dependently, while proglumide did not influence the basal amylase release at concentrations between 0-3 mM. Dose-response curves to CCK for amylase release shifted to the right with increase in proglumide concentration. This inhibition by proglumide was reversible. In addition, the effect of proglumide was selective for CCK and its related peptide, and this drug did not inhibit other secretagogues such as carbachol or gastrin releasing peptide in mouse acini. In contrast to its inhibitory effect in vitro, in vivo administration of proglumide (500 mg/kg/day, i.p., for 5 days) to mice did not cause the rightward shift of the dose-response curve to CCK for amylase release from dispersed acini.
Proglumide and benzotript: members of a different class of cholecystokinin receptor antagonists.[Pubmed:6171817]
Proc Natl Acad Sci U S A. 1981 Oct;78(10):6304-8.
In dispersed acini from guinea pig pancreas, proglumide (DL-4-benzamido-N, N-dipropylglutaramic acid) and benzotript (N-p-chlorobenzoyl-L-tryptophan) caused a rightward shift in the dose--response curve for cholecystokinin-stimulated amylase secretion but did not alter the maximal increase in amylase secretion caused by cholecystokinin. At relatively low concentrations, proglumide did not alter the stimulation of enzyme secretion caused by secretagogues whose effects are mediated by adenosine 3'5'-monophosphate (e.g., vasoactive intestinal peptide or secretin) and did not alter the stimulation of enzyme secretion caused by secretagogues that have a mode of action similar to that of cholecystokinin but act through different receptors (e.g., bombesin, physalaemin, eledoisin, and ionophore A23187). There was a close correlation between the ability of proglumide or benzotript to inhibit binding of 125I-labeled cholecystokinin to its receptors on pancreatic acini and the abilities of these compounds to inhibit the action of cholecystokinin on enzyme secretion and on calcium outflux. These results indicate that proglumide and benzotript are members of a different class of cholecystokinin receptor antagonists.
