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Handa, K.

Publications and source records attributed to Handa, K..

3 recordsLinked to original sources

Development of a novel in silico classification model to assess reactive metabolite formation in the cysteine trapping assay and investigation of important substructures

Predicting whether a compound can cause drug-induced liver injury (DILI) is difficult due to the complexity of its mechanism. The production of reactive metabolites is one of the major causes of DILI, particularly idiosyncratic DILI. The cysteine trapping assay is one of the methods to detect reactive metabolites which bind to microsomes covalently. However, it is cumbersome to use 35S isotope-labeled cysteine for this assay. Therefore, we constructed an in silico classification model for predicting a positive/negative outcome in the cysteine trapping assay to accelerate the drug discovery process. In this study, we collected 475 compounds (436 in-house compounds and 39 publicly available drugs). Using a Message Passing Neural Network (MPNN) and Random Forest (RF) with extended connectivity fingerprint (ECFP) 4, we built machine learning models to predict the covalent binding risk of compounds. The 5-fold cross-validation (CV) and hold-out test were evaluated in random- and time-split trials. Additionally, we investigated the substructures that contributed to positive results in the cysteine trapping assay through the framework of the MPNN model. In the random-split dataset, the AUC-ROC of MPNN and RF were 0.698 and 0.811 in the 5-fold CV, and 0.742 and 0.819 in the hold-out test, respectively. In the time-split dataset, AUC-ROC of MPNN and RF were 0.729 and 0.617 in the 5-fold CV, and 0.625 and 0.559 in the hold-out test, restrictively. This result suggests that the MPNN model has a higher predictivity than RF in the time-split dataset. Hence, we conclude that the in silico MPNN classification model for the cysteine trapping assay have better predictive power. Furthermore, most of the substructures that contributed positively to the cysteine trapping assay were consistent with previous reports such as propranolol, verapamil, and imipramine. This is a new machine learning model that can determine the outcome of the cysteine trapping assay, namely accurately predicting the covalent binding risk as the one of factors of idiosyncratic DILI. We believe that this can contribute to mitigating DILI risk for reactive metabolites at the early stages of drug discovery.

bioinformatics↗

Effects of age and sex on dendritic D2 autoreceptor inhibition in substantia nigra dopamine neurons

Substantia nigra pars compacta (SNc) dopamine neurons are required for voluntary movement and reward learning, and advanced age is associated with motor and cognitive decline. In the midbrain, D2-type autoreceptors located on dendrodendritic synapses between dopamine neurons control cell firing through G protein-activated potassium (GIRK) channels. We previously showed that aging disrupts dopamine neuron pacemaker firing in mice, but only in males. Here we show that D2-receptor inhibitory postsynaptic currents (D2-IPSCs) in aged male mice are moderately smaller compared to young males as well as females, regardless of age. Local application of dopamine revealed a reduction in the amplitude of the D2-receptor currents in old males compared to young, pointing to a postsynaptic mechanism that could not be explained by impairment of the GIRK channels or degeneration of the dendritic arbor. Kinetic analysis showed no differences in D2-IPSCs in old versus young mice or between sexes. Potentiation of D2-IPSCs by corticotropin releasing factor (CRF) is also conserved in aging, indicating preservation of plasticity mechanisms. These findings have implications for understanding dopamine transmission in aging in both sexes and could explain in part the increased susceptibility of males to SNc degeneration of dopamine neurons in neurodegenerative disorders such as Parkinsons disease (PD).

neuroscience↗

Facilitation of hERG channels by blockers: a mechanism predicted to reduce lethal cardiac arrhythmias

Fatal cardiac arrhythmias are caused by some, but not all, drugs that inhibit the cardiac rapid delayed-rectifier current (IKr) by blocking hERG channels. Here, we propose a novel mechanism that could make certain hERG blockers less proarrhythmic. Several drugs that block hERG channels, yet have favorable cardiac safety profiles, also evoke another effect; they increase the current amplitude upon low-voltage depolarization (facilitation). Voltage-clamp recordings of hERG block and facilitation by nifekalant, a Class III antiarrhythmic agent, constrained a model of human cardiac IKr. In human ventricular action potential simulations, nifekalant showed its therapeutic ability to suppress ectopic excitations, with or without facilitation. Without facilitation, excessive IKr block evoked early afterdepolarizations, which cause lethal arrhythmias. Facilitation prevented early afterdepolarizations at the same degree of block by increasing IKr during repolarization phase of action potentials. Thus, facilitation is proposed to reduce the arrhythmogenic risk of hERG blockers.\n\nAbbreviationsAP: action potential; APD: action potential duration; APD90: action potential duration measured at 90% repolarization; EAD: early afterdepolarization; hERG: human ether-ago-go-related gene; ICaL: L-type Ca2+ channel current; Inet: net ionic current; IK1: inward-rectifier potassium current; IKr: rapid component of the delayed-rectifier potassium current; INa: sodium current; ORd: OHara-Rudy dynamic

pharmacology and toxicology↗