Suppr超能文献

一项 I 期、随机、递增剂量研究,旨在评估 RIP1 抑制剂 GDC-8264 在健康志愿者中的安全性、药代动力学和活性。

A phase I, randomized, ascending-dose study to assess safety, pharmacokinetics, and activity of GDC-8264, a RIP1 inhibitor, in healthy volunteers.

机构信息

Genentech, Inc., South San Francisco, California, USA.

出版信息

Clin Transl Sci. 2023 Oct;16(10):1997-2009. doi: 10.1111/cts.13607. Epub 2023 Aug 24.

Abstract

Receptor-interacting protein 1 (RIP1) is a key regulator of multiple signaling pathways that mediate inflammatory responses and cell death. RIP1 kinase activity mediates apoptosis and necroptosis induced by tumor necrosis factor (TNF)-α, Toll-like receptors, and ischemic tissue damage. RIP1 has been implicated in several human pathologies and consequently, RIP1 inhibition may represent a therapeutic approach for diseases dependent on RIP1-mediated inflammation and cell death. GDC-8264 is a potent, selective, and reversible small molecule inhibitor of RIP1 kinase activity. This phase I, randomized, placebo-controlled, double-blinded trial examined safety, pharmacokinetics (PKs), and pharmacodynamics (PDs) of single- (5-225 mg) and multiple- (50 and 100 mg once daily, up to 14 days) ascending oral doses of GDC-8264 in healthy volunteers, and also tested the effect of food on the PKs of GDC-8264. All adverse events in GDC-8264-treated subjects in both stages were mild. GDC-8264 exhibited dose-proportional increases in systemic exposure; the mean terminal half-life ranged from 10-13 h, with limited accumulation on multiple dosing (accumulation ratio [AR] ~ 1.4); GDC-8264 had minimal renal excretion at all doses. A high-fat meal had no significant effect on the PKs of GDC-8264. In an ex vivo stimulation assay of whole blood, GDC-8264 rapidly and completely inhibited release of CCL4, a downstream marker of RIP1 pathway activation, indicating a potent pharmacological effect. Based on PK-PD modeling, the GDC-8264 half-maximal inhibitory concentration for the inhibition of CCL4 release was estimated to be 0.58 ng/mL. The favorable safety, PKs, and PDs of GDC-8264 support its further development for treatment of RIP1-driven diseases.

摘要

受体相互作用蛋白 1(RIP1)是调节多种信号通路的关键因子,这些信号通路介导炎症反应和细胞死亡。RIP1 激酶活性介导肿瘤坏死因子(TNF)-α、Toll 样受体和缺血性组织损伤诱导的细胞凋亡和坏死性凋亡。RIP1 参与了几种人类病理学,因此,RIP1 抑制可能代表了依赖于 RIP1 介导的炎症和细胞死亡的疾病的治疗方法。GDC-8264 是一种有效的、选择性的、可逆的 RIP1 激酶活性小分子抑制剂。这项 I 期、随机、安慰剂对照、双盲试验研究了健康志愿者单次(5-225mg)和多次(50 和 100mg 每日一次,最多 14 天)递增口服剂量的 GDC-8264 的安全性、药代动力学(PK)和药效学(PD),还测试了食物对 GDC-8264 PK 的影响。在两个阶段,GDC-8264 治疗的所有不良事件均为轻度。GDC-8264 表现出剂量比例增加的全身暴露;平均终末半衰期范围为 10-13 小时,多次给药时有限积累(积累比[AR]约为 1.4);GDC-8264 在所有剂量下均有最小的肾脏排泄。高脂肪餐对 GDC-8264 的 PK 没有显著影响。在全血的体外刺激试验中,GDC-8264 迅速且完全抑制 RIP1 通路激活的下游标志物 CCL4 的释放,表明具有强大的药理学作用。基于 PK-PD 建模,估计 GDC-8264 抑制 CCL4 释放的半最大抑制浓度为 0.58ng/mL。GDC-8264 的良好安全性、PK 和 PD 支持其进一步开发用于治疗 RIP1 驱动的疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d141/10582670/f1f5d6bdfb43/CTS-16-1997-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验