High impact information on Aprofen

• The apparent affinities (Ki) of several antimuscarinic agents in pituitary cells were determined by their ability to reverse the carbachol inhibition of prolactin secretion: atropine 0.14 nM, scopolamine 0.26 nM, azaprophen 0.3 nM, aprophen 3.0 nM, pirenzepine 42 nM, benactyzine 80 nM and adiphenine 198 nM [1].
• The bimolecular rate constants, ki and kr, were not statistically perturbed when the reaction was monitored in the presence of aprophen with the fetal bovine serum acetylcholinesterase [2].
• Neither the inhibition (DFP) nor the regeneration (2-PAM) kinetics observed for the carboxylesterase was perturbed by the presence of aprophen [2].
• Comparative effects of aprophen, atropine and benactyzine on central and peripheral cholinoceptors and on acetylcholinesterase [3].
• The BuChE turnover number for aprophen was 2.0 X 10(-3) sec-1 [4].

Biological context of Aprofen

• It was interesting that although the biological effects of desethylaprophen were 100-fold lower than those of aprophen, it was equally able to compete for the binding sites of muscarinic receptors of the guinea pig ileum [5].
• The IC50 values for atropine, azaprophen and aprophen were 2.7 x 10(-6), 1.5 x 10(-6), and 3.2 x 10(-6) M, respectively [6].

Anatomical context of Aprofen

• Acetylcholinesterases from bovine erythrocyte and electric eel were not inhibited by aprophen nor was aprophen hydrolyzed by these enzymes [4].

Analytical, diagnostic and therapeutic context of Aprofen

• Determination of aprophen in biological samples by normal-phase high-performance liquid chromatography [7].

References