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ACKR3 拮抗剂通过免疫调节和髓鞘修复作用增强脱髓鞘病变的修复。

ACKR3 Antagonism Enhances the Repair of Demyelinated Lesions Through Both Immunomodulatory and Remyelinating Effects.

机构信息

Idorsia Pharmaceuticals Ltd, Hegenheimermattweg 91, Allschwil 4123, Basel-Landschaft, Switzerland.

出版信息

Neurochem Res. 2024 Aug;49(8):2087-2104. doi: 10.1007/s11064-024-04173-1. Epub 2024 May 31.

Abstract

Addressing inflammation, demyelination, and associated neurodegeneration in inflammatory demyelinating diseases like multiple sclerosis (MS) remains challenging. ACT-1004-1239, a first-in-class and potent ACKR3 antagonist, currently undergoing clinical development, showed promise in preclinical MS models, reducing neuroinflammation and demyelination. However, its effectiveness in treating established disease and impact on remyelination after the occurrence of demyelinated lesions remain unexplored. This study assessed the therapeutic effect of ACT-1004-1239 in two demyelinating disease models. In the proteolipid protein (PLP)-induced experimental autoimmune encephalomyelitis (EAE) model, ACT-1004-1239 administered upon the detection of the first signs of paralysis, resulted in a dose-dependent reduction in EAE disease severity, concomitant with diminished immune cell infiltrates in the CNS and reduced demyelination. Notably, efficacy correlated with elevated plasma concentrations of CXCL11 and CXCL12, two pharmacodynamic biomarkers of ACKR3 antagonism. Combining ACT-1004-1239 with siponimod, an approved immunomodulatory treatment for MS, synergistically reduced EAE severity. In the cuprizone-induced demyelination model, ACT-1004-1239 administered after 5 weeks of cuprizone exposure, significantly accelerated remyelination, already quantifiable one week after cuprizone withdrawal. Additionally, ACT-1004-1239 penetrated the CNS, elevating brain CXCL12 concentrations. These results demonstrate that ACKR3 antagonism significantly reduces the severity of experimental demyelinating diseases, even when treatment is initiated therapeutically, after the occurrence of lesions. It confirms the dual mode of action of ACT-1004-1239, exhibiting both immunomodulatory effects by reducing neuroinflammation and promyelinating effects by accelerating myelin repair. The results further strengthen the rationale for evaluating ACT-1004-1239 in clinical trials for patients with demyelinating diseases.

摘要

在多发性硬化症(MS)等炎症性脱髓鞘疾病中,解决炎症、脱髓鞘和相关神经退行性变仍然具有挑战性。ACT-1004-1239 是一种首创的、有效的 ACKR3 拮抗剂,目前正在进行临床开发,在 MS 动物模型中表现出良好的效果,可减少神经炎症和脱髓鞘。然而,其在治疗已确诊疾病以及在脱髓鞘病变发生后对髓鞘再生的影响仍有待探索。本研究评估了 ACT-1004-1239 在两种脱髓鞘疾病模型中的治疗效果。在髓鞘少突胶质细胞糖蛋白(PLP)诱导的实验性自身免疫性脑脊髓炎(EAE)模型中,ACT-1004-1239 在出现瘫痪的第一个迹象时给药,可剂量依赖性地降低 EAE 疾病的严重程度,同时减少中枢神经系统中的免疫细胞浸润和脱髓鞘。值得注意的是,疗效与 CXCL11 和 CXCL12 两种 ACKR3 拮抗作用的药效学生物标志物的血浆浓度升高相关。ACT-1004-1239 与西尼莫德联合使用,西尼莫德是一种已批准用于多发性硬化症的免疫调节剂治疗药物,可协同降低 EAE 的严重程度。在铜诱导的脱髓鞘模型中,在铜暴露 5 周后给予 ACT-1004-1239,可显著加速髓鞘再生,在铜撤出后一周即可定量检测到。此外,ACT-1004-1239 穿透中枢神经系统,增加大脑 CXCL12 浓度。这些结果表明,ACKR3 拮抗作用可显著降低实验性脱髓鞘疾病的严重程度,甚至在发生病变后开始治疗时也是如此。这证实了 ACT-1004-1239 的双重作用模式,通过减少神经炎症发挥免疫调节作用,通过加速髓鞘修复发挥促髓鞘形成作用。结果进一步加强了在脱髓鞘疾病患者中评估 ACT-1004-1239 的临床试验的合理性。

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