Disease relevance of Benzotript

• Caerulein-induced acute necrotizing pancreatitis in mice: protective effects of proglumide, benzotript, and secretin [1].
• These effects of G-Gly on the activity and expression of MMPs and the invasiveness of colon cancer cells were inhibited by treating the cells with a broad-spectrum metalloproteinase inhibitor (CGS27023A) and nonselective gastrin/CCK receptor antagonists (proglumide and benzotript) [2].
• In addition, benzotript inhibits the activities of multifunctional enzymes having similar structures, such as the peroxisomal enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase bifunctional protein and the Pseudomonas fragi fatty acid oxidation enzyme complex [3].

Psychiatry related information on Benzotript

• The behavioral effects of peripherally administered CCK, i.e. reduced food consumption and reduced exploratory behaviors in mice, were blocked effectively by pretreatment with proglumide (0.3-0.9 mmol/kg), and by benzotript (0.03 mmol/kg), but not by CCK30-33 (0.003 mmol/kg) [4].

High impact information on Benzotript

• YAMC cells bound 125I-glycine-extended gastrin17 (Kd, 0.36 nmol/L, 1810 sites/cell), but not 125I-amidated gastrin17, and binding was unaffected by gastrin receptor antagonists including benzotript [5].
• In addition, the protective effect of secretin was compared with that of the cholecystokinin-receptor antagonists proglumide and benzotript [1].
• Cross-linking is also inhibited by proglumide and benzotript, but no inhibition is seen with either the CCK-A receptor-selective antagonist L364,718 or the gastrin/CCK-B receptor-selective antagonist L365,260 [6].
• Proglumide and benzotript: members of a different class of cholecystokinin receptor antagonists [7].
• Proglumide (0.2 mg/kg, iv) and benzotript (0.2 mg/kg, iv), specific CCK receptor antagonists, blocked the icv CCK-8-induced increase in plasma PRL levels [8].

Biological context of Benzotript

• It is concluded that proglumide and benzotript bind independently to both the hydratase and dehydrogenase active sites of the GBP, while a single molecule of gastrin may bind simultaneously to both active sites [9].
• Benzotript, from another group of CCK antagonists had an IC50 of 52.5 (40.7-67.6) microM [10].
• CCK receptor antagonists benzotript and CR-1369 are able to block CCK 8 sulfated chemotaxis, thus suggesting the presence of CCK receptors on human monocytes [11].
• L-364,718 had no significant effect on food intake or exploratory activity when administered alone, over the dose range of 100 ng/kg-10 mg/kg i.p. This compound appears to be at least one hundred times more potent than proglumide or benzotript as an antagonist of the behavioral effects of peripherally administered cholecystokinin [12].

Anatomical context of Benzotript

• Evidence that proglumide and benzotript antagonize secretagogue stimulation of isolated gastric parietal cells [13].
• The relative potencies of C-terminal fragments of CCK-8(SO3H), benzotript and proglumide in inhibiting specific [3H]pentagastrin binding to CCK brain receptors reinforce the concept of different brain and pancreas CCK receptors [14].

Associations of Benzotript with other chemical compounds

• Proliferation of all YAMC clones was partially inhibited either by an antibody selective for glycine-extended gastrin or by preincubation with benzotript, and the inhibitory effects were additive [5].
• The cholecystokinin receptor antagonists benzotript and CR 1409 significantly decreased the bile flow and insulin and glucagon changes produced by exogenous CCK-8 [15].

Gene context of Benzotript

• Most active derivatives were 20-30 times more potent than the well-known gastrin antagonist derivatives proglumide and benzotript and had 20-200 times more binding affinity [16].

Analytical, diagnostic and therapeutic context of Benzotript

• Proglumide and benzotript were able to inhibit the shift to the right of the dose-response curve for morphine, i.e. they prevented the development of tolerance to morphine-induced analgesia [17].

References