| Description | Proglumide hemicalcium is a antagonist of nonpeptide and orally active cholecystokinin (CCK)-A/B receptors, has antiepileptic and antioxidant activities. |
| In vitro | in vitro, 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[2]. |
| In vivo | Proglumide treatment is significantly effective in ameliorating the seizure activities, cognitive dysfunctions, and cerebral oxidative stress[1]. |
| molecular weight | 376.51 |
| Molecular formula | C18H28CaN2O4 |
| CAS | 85068-56-0 |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year |
| References | 1. Ahmad M, et al. The effects of quinacrine, proglumide, and pentoxifylline on seizure activity, cognitive deficit, and oxidative stress in rat lithium-pilocarpine model of status epilepticus. Oxid Med Cell Longev. 2014;2014:630509. 2. Iwamoto Y, et al. In vitro and in vivo effect of proglumide on cholecystokinin-stimulated amylase release in mouse pancreatic acini. Gastroenterol Jpn. 1984 Feb;19(1):53-8. 3. González-Puga C, et al. Selective CCK-A but not CCK-B receptor antagonists inhibit HT-29 cell proliferation: synergism with pharmacological levels of melatonin. J Pineal Res. 2005 Oct;39(3):243-50. 4. Bunney BS, et al. Further studies on the specificity of proglumide as a selective cholecystokinin antagonist in the central nervous system. Ann N Y Acad Sci. 1985;448:345-51. 5. Tariq M, et al. Gastric and duodenal antiulcer and cytoprotective effects of proglumide in rats. J Pharmacol Exp Ther. 1987 May;241(2):602-7. |