Cohen Jennifer D, You Dahea, Sharma Ashok K, Takai Takafumi, Hara Hideto, Sales Vicencia T, Yukawa Tomoya, Cai Beibei
Drug Safety Research & Evaluation, Takeda Development Center Americas, Inc, San Diego, CA 92121-1964, United States.
Drug Safety Research & Evaluation, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa 251-8555, Japan.
Toxicol Sci. 2025 Feb 1;203(2):253-268. doi: 10.1093/toxsci/kfae148.
Seizure is among the most severe FDA black box warnings of neurotoxicity reported on drug labels. Gaining a better mechanistic understanding of off-targets causative of seizure will improve the identification of potential seizure risks preclinically. In the present study, we evaluated an in vitro panel of 9 investigational (Cav2.1, Cav3.2, GlyRA1, AMPA, HCN1, Kv1.1, Kv7.2/7.3, NaV1.1, Nav1.2) and 2 standard (GABA-A, NMDA) ion channel targets with strong correlative links to seizure, using automated electrophysiology. Each target was assessed with a library of 34 preclinical compounds and 10 approved drugs with known effects of convulsion in vivo and/or in patients. Cav2.1 had the highest frequency of positive hits, 20 compounds with an EC30 or IC30 ≤ 30 µM, and the highest importance score relative to the 11 targets. An additional 35 approved drugs, with categorized low to frequent seizure risk in patients, were evaluated in the Cav2.1 assay. The Cav2.1 assay predicted preclinical compounds to cause convulsion in nonclinical species with a sensitivity of 52% and specificity of 78%, and approved drugs to cause seizure in nonclinical species or in patients with a sensitivity of 48% or 54% and specificity of 71% or 78%, respectively. The integrated panel of 11 ion channel targets predicted preclinical compounds to cause convulsion in nonclinical species with a sensitivity of 68%, specificity of 56%, and accuracy of 65%. This study highlights the utility of expanding the in vitro panel of targets evaluated for seizurogenic activity, in order to reduce compound attrition early on in drug discovery.
癫痫发作是药物标签上报告的最严重的FDA黑框神经毒性警告之一。更好地从机制上理解导致癫痫发作的脱靶效应将有助于在临床前更好地识别潜在的癫痫发作风险。在本研究中,我们使用自动电生理学方法评估了一组体外离子通道靶点,其中包括9个研究性靶点(Cav2.1、Cav3.2、GlyRA1、AMPA、HCN1、Kv1.1、Kv7.2/7.3、NaV1.1、Nav1.2)和2个与癫痫发作有强关联的标准靶点(GABA-A、NMDA)。每个靶点用一个包含34种临床前化合物和10种已批准药物的文库进行评估,这些药物在体内和/或患者中具有已知的惊厥作用。Cav2.1的阳性命中频率最高,有20种化合物的EC30或IC30≤30µM,并且相对于11个靶点的重要性得分最高。另外35种在患者中癫痫发作风险分类为低到高的已批准药物在Cav2.1试验中进行了评估。Cav2.1试验预测临床前化合物在非临床物种中引起惊厥的敏感性为52%,特异性为78%,预测已批准药物在非临床物种或患者中引起癫痫发作的敏感性分别为48%或54%,特异性为71%或78%。11个离子通道靶点的综合面板预测临床前化合物在非临床物种中引起惊厥的敏感性为68%,特异性为56%,准确性为65%。本研究强调了扩大用于评估致痫活性的体外靶点面板的实用性,以便在药物发现的早期减少化合物的损耗。