Psychiatry related information on Parfezin

• Orphenadrine did not change motor activity, and profenamine had sedative properties [1].

High impact information on Parfezin

• The volume of the butyrylcholinesterase active site gorge is approximately 200 A3 larger than that of the acetylcholinesterase gorge, which allows the accommodation of ethopropazine in two different orientations as demonstrated by rigid-body refinement and molecular dynamics calculations [2].
• Volume calculations for the active site gorge showed that the poor inhibitory activity of ethopropazine toward acetylcholinesterase was due to the smaller dimension of the active site gorge which was unable to accommodate the bulky inhibitor molecule [2].
• In one group of controls ethopropazine was used to inhibit pseudocholinesterases and in another group BW 284C 51 was used to inhibit acetylcholinesterase (AChE) [3].
• For the analysis of the data in the presence of ethopropazine at two temperatures, we have enlarged the reaction scheme to allow primarily its competition with the substrate at the peripheral site, but the competition at the acylation site was not excluded [4].
• Cholinesterase inhibitors Ro 2-1250 and Ro 2-0638 inhibited both canine cholinesterases, while huperzine A preferentially inhibited canine AChE and ethopropazine inhibited canine BuChE [5].

Biological context of Parfezin

• Cell adhesion was affected by the BChE inhibitor, ethopropazine, and the AChE peripheral site inhibitor, BW284c51, but not by eserine which binds to the active site [6].
• Effects on gastric emptying and intestinal transit were seen after single and multiple oral doses of diphenhydramine and ethopropazine [7].
• However, neither the phenothiazines ethopropazine, methotrimeprazine, prochlorperazine and trifluoperazine nor the various commonly used heterocyclic antipsychotics tested, e.g., molindone, loxapine, clozapine, haloperidol, sulpiride and thiothixene inhibited plasma LEU degradation kinetics [8].
• Pharmacokinetics of ethopropazine in the rat after oral and intravenous administration [9].
• PURPOSE: To determine the in vitro plasma protein binding, and the in vivo brain, heart and plasma concentrations of ethopropazine (ET) enantiomers in the rat after iv doses [10].

Anatomical context of Parfezin

• Acetylcholinesterase (AChE) activity in amniotic fluid was assayed directly by a reaction rate method at 30 degrees C using acetylthiocholine iodide as substrate and ethopropazine as a safe 'pseudo' cholinesterase inhibitor [11].
• Mucosal delivery of cytotoxic therapeutic agents: response of rat nasal mucosa to microencapsulated ethopropazine HCl enantiomer [12].
• Specific AChE activity, assayed in the presence of 10(-4) M ethopropazine (a butyrylcholinesterase inhibitor), decreased 15-25% in striatum and cerebellum, increased 20-45% in hippocampus, but remained unchanged in cerebral cortex [13].
• For true ChE from bovine erythrocytes and pseudo ChE from horse serum BW 284C51 and ethopropazine therefore certainly have a potential as selective ChE inhibitors [14].

Associations of Parfezin with other chemical compounds

• Rivastigmine was equipotent to the specific acetylcholinesterase inhibitor BW284C51 and more potent than the butyrylcholinesterase inhibitors iso-OMPA and ethopropazine [15].
• Enantiomers of ethopropazine x HCl (10-(2-diethylaminopropyl)phenothiazine hydrochloride) were prepared by fractional crystallization of diastereomeric dibenzoyltartaric acid salts, and their optical purity (enantiomeric excess, ee) determined by HPLC on Chiralcel OJ column [16].
• Amitriptyline, ethopropazine and trihexyphenidyl increased the tolerated head movements but the increase was not statistically significant [17].

Gene context of Parfezin

• More than 97% of AChE activity was inhibited by 10 microM eserine or BW284C51, but only 53% of the activity was inhibited by ethopropazine at the same concentration [18].
• Ethopropazine totally depressed the pseudo ChE activity from horse serum at a concentration of 5 X 10(-5) M [14].
• An inhibition study with specific pseudo-chE inhibitor (ethopropazine), or with anti-human pseudo-chE sera, has produced evidence that this genetically variant chE is pseudo-chE [19].

Analytical, diagnostic and therapeutic context of Parfezin

• The pharmacokinetics of the anticholinergic drug ethopropazine (ET) have been studied in the rat after intravenous (i.v.) and oral administration [9].

References