Binkle-Ladisch Lars, Pironet Andy, Zaliani Andrea, Alcouffe Chantal, Mensching Daniel, Haferkamp Undine, Willing Anne, Woo Marcel S, Erdmann Alexandre, Jessen Timm, Hess Stephen D, Gribbon Philip, Pless Ole, Vennekens Rudi, Friese Manuel A
Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.
Laboratory of Ion Channel Research, Department of Cellular and Molecular Medicine, Katholieke Universiteit Leuven, Campus Gasthuisberg O/N1, Herestraat 49-Bus 802, 3000 Leuven, Belgium.
iScience. 2024 Nov 19;27(12):111425. doi: 10.1016/j.isci.2024.111425. eCollection 2024 Dec 20.
Neurodegeneration in central nervous system disorders is linked to dysregulated neuronal calcium. Direct inhibition of glutamate-induced neuronal calcium influx, particularly via N-methyl-D-aspartate receptors (NMDAR), has led to adverse effects and clinical trial failures. A more feasible approach is to modulate NMDAR activity or calcium signaling indirectly. In this respect, the calcium-activated non-selective cation channel transient receptor potential melastatin 4 (TRPM4) has been identified as a promising target. However, high affinity and specific antagonists are lacking. Here, we conducted high-throughput screening of a compound library to identify high affinity TRPM4 antagonists. This yielded five lead compound series with nanomolar half-maximal inhibitory concentration values. Through medicinal chemistry optimization of two series, we established detailed structure-activity relationships and inhibition of excitotoxicity in neurons. Moreover, we identified their potential binding site supported by electrophysiological measurements. These potent TRPM4 antagonists are promising drugs for treating neurodegenerative disorders and TRPM4-related pathologies, potentially overcoming previous therapeutic challenges.
中枢神经系统疾病中的神经退行性变与神经元钙调节异常有关。直接抑制谷氨酸诱导的神经元钙内流,尤其是通过N-甲基-D-天冬氨酸受体(NMDAR),已导致不良反应和临床试验失败。一种更可行的方法是间接调节NMDAR活性或钙信号传导。在这方面,钙激活的非选择性阳离子通道瞬时受体电位褪黑素4(TRPM4)已被确定为一个有前景的靶点。然而,目前缺乏高亲和力和特异性的拮抗剂。在此,我们对一个化合物文库进行了高通量筛选,以鉴定高亲和力的TRPM4拮抗剂。这产生了五个半数最大抑制浓度值为纳摩尔级的先导化合物系列。通过对两个系列进行药物化学优化,我们建立了详细的构效关系,并抑制了神经元中的兴奋性毒性。此外,我们通过电生理测量确定了它们潜在的结合位点。这些有效的TRPM4拮抗剂有望成为治疗神经退行性疾病和TRPM4相关病症的药物,有可能克服以往的治疗挑战。