Proglumide sodium

CAS: 99247-33-3 F: C18H25N2NaO4 W: 356.39

Proglumide sodium is a nonpeptide and orally active cholecystokinin (CCK)-A/B receptors antagonist. Proglumide sodium se

Contact QiTai

This product is for research use only, not for human use. We do not sell to patients.

Bioactivity	Proglumide sodium is a nonpeptide and orally active cholecystokinin (CCK)-A/B receptors antagonist. Proglumide sodium selective blocks CCK’s effects in the central nervous system (CNS). Proglumide sodium has ability to inhibit gastric secretion and to protect the gastroduodenal mucosa. Proglumide sodium also has antiepileptic and antioxidant activities[1][2][3][4][5].
Target	Cholecystokinin (CCK)-A/B receptors
Invitro	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[2].The incubation of HT29 cells with Proglumide significantly reduces the [3H]-thymidine incorporation to HT29 cells in a dose-dependent manner, with an IC50 of 6.5 mM. Proglumide reduces in a dose-dependent manner the percentage of necrosis with a parallel increase of apoptosis up to 70%[3].
In Vivo	Proglumide (250-750 mg/kg; intraperitoneal injection; adult male Sprague Dawley rats) treatment is significantly effective in ameliorating the seizure activities, cognitive dysfunctions, and cerebral oxidative stress[1]. Animal Model:
Name	Proglumide sodium
CAS	99247-33-3
Formula	C18H25N2NaO4
Molar Mass	356.39
Appearance	Solid
Transport	Room temperature in continental US; may vary elsewhere.
Storage	4°C, stored under nitrogen *In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Reference	[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.