4-benzamido-n,n-dipropyl-,sodiumsalt,dl-glutaramicaci
PROGLUMIDE, SODIUM SALT
CAS: 99247-33-3
Molecular Formula: C18H27N2NaO4
4-benzamido-n,n-dipropyl-,sodiumsalt,dl-glutaramicaci - Names and Identifiers
4-benzamido-n,n-dipropyl-,sodiumsalt,dl-glutaramicaci - Physico-chemical Properties
| Molecular Formula | C18H27N2NaO4 |
| Molar Mass | 358.41 |
| Solubility | H2O: soluble |
| Appearance | solid |
| Color | white |
| In vitro study | In an in vitro study, Proglumide at concentrations between 0.3-10 mM inhibits CCK-stimulated amylase release dose-dependently, while Proglumide does 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 is reversible. In addition, the effect of Proglumide is selective for CCK and its related peptide. The incubation of HT29 cells with Proglumide significantly reduces the [ 3 H]-thymidine incorporation to HT29 cells in a dose-dependent manner, with an IC 50 of 6.5 mM. Proglumide reduces in a dose-dependent manner the percentage of necrosis with a parallel increase of apoptosis up to 70%. |
4-benzamido-n,n-dipropyl-,sodiumsalt,dl-glutaramicaci - Risk and Safety
| WGK Germany | 3 |
4-benzamido-n,n-dipropyl-,sodiumsalt,dl-glutaramicaci - References
| biological activity | Proglumide sodium is a non-peptide and orally active cholecystokinin (CCK)-A/B receptor antagonist. Proglumide sodium selectively blocks the role of CCK in the central nervous system. Proglumide sodium has the ability to inhibit gastric secretion and protect gastric duodenal mucosa, and also has antiepileptic and antioxidant activities. |
| target | Cholecystokinin (CCK)-A/B receptors |
| Animal Model: | Adult male Sprague Dawley rats (200-250 g; 2 months old) are induced status epilepticus (SE) |
| Dosage: | 250 mg/kg, 500 mg/kg, and 750 mg/kg |
| Administration: | Intraperitoneal injection |
| Result: | Dose-dependently and significantly increased the latencies to seizure and SE. Significantly and dose-dependently attenuated Li-PC (SE) induced increase in thiobarbituric acid (TBARS) and catalase (CAT), attenuated Li-Pc induced decrease in SOD, and attenuated depletion of GSH and glutathione-S transferase (GST) in the hippocampus and striatum. |
Last Update：2024-04-09 20:13:35
