Cyclopentolate Hydrochloride

New psychoactive substances are constantly emerging, among which ketamine analogs with the core structure of 2‐amino‐2‐phenylcyclohexanone have attracted global attention due to their continued involvement in acute intoxications. The monitoring of these substances largely relies on the acquisition of metabolic data. However, the lack of in vitro human metabolism information for these emerging structural analogs presents significant challenges to drug control efforts. To address this challenge, we investigated the first‐phase metabolism patterns of four novel ketamine structural analogs of 2‐FXE [2‐(ethylamino)‐2‐(2‐fluorophenyl) cyclohexan‐1‐one], 2‐MDCK [2‐(methylamino)‐2‐(o‐tolyl) cyclohexan‐1‐one], 3‐DMXE [2‐(ethylamino)‐2‐(m‐tolyl) cyclohexan‐1‐one], and 2‐DMXE [2‐(ethylamino)‐2‐(o‐tolyl) cyclohexan‐1‐one] utilizing human liver microsomes for the first time. Metabolites were identified using ultra‐performance liquid chromatography coupled with high‐resolution tandem mass spectrometry. Our findings reveal that N‐dealkylation and hydroxylation are the primary metabolic reactions, alongside other notable reactions, including oxidation, reduction, and dehydration. Based on our extensive research, we propose N‐dealkylation and hydroxylation metabolites as appropriate analytical markers for monitoring the consumption of these substances.

Purpose: To evaluate the effects of topical cyclopentolate hydrochloride-induced cycloplegia on anterior segment biomechanics in emmetropic eyes using anterior segment-optical coherence tomography (AS-OCT). Methods: Twenty-five emmetropic eyes of 25 volunteers were included. All underwent central corneal thickness (CCT) and anterior chamber depth (ACD) measurements. Anterior scleral thickness (AST) was measured at the level of the scleral spur (SS)(AST-0), 1,000 μm posterior of the SS (AST-1), and 2,000 μm posterior of the SS (AST-2) in the nasal and temporal quadrants using AS-OCT. All measurements were repeated after cycloplegia. Results: The mean age was 30.6 ± 12.4 (8-45) years. The mean CCT did not significantly change after cycloplegia (P = 0.7). The mean ACD was significantly increased [3.3 ± 0.2 (2.7-3.9) to 3.7 ± 0.3 (3-4.2) μm; P = 0.001]. In the nasal quadrant, the mean AST-1 and AST-2 were 512.3 ± 34.4 (433-570) and 529.6 ± 34.2 (449-599); decreased to 478 ± 26.8 (423-530) and 486.2 ± 28.3 (422-544) μm, respectively, after cycloplegia (P = 0.00; P = 0.00). In the temporal quadrant, the mean AST-1 and AST-2 were 522.5 ± 24.7 (473-578) and 527.2 ± 39.9 (450-604); decreased to 481.1 ± 33.7 (421-550) and 484.6 ± 26.6 (433-528) μm, respectively (P = 0.00; P = 0.00). There was no significant difference in AST-0 after cycloplegia in both quadrants [from 697.5 ± 46 (605-785) to 709.5 ± 64.7 (565-785) for nasal and from 718.4 ± 40.1 (632-796) to 722.9 ± 60.6 (596-838) for temporal; P = 0.2; P = 0.3, respectively]. Conclusion: After cycloplegia, there was a significant thinning of ASTs posterior to SS and a slight increase in AST in the SS level. ACD deepened after cycloplegia, and there was no significant change in CCT. Cycloplegic agents temporarily inhibit ciliary muscle contraction and may affect anterior segment parameters and sclera. Inhibition of forward-inward movement of the ciliary body by cycloplegia affects ASTs and ACD by causing a change in the mechanical force of the ciliary muscle on the sclera.