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DSP502结合了PD-L1和PVR的双重抑制,触发了抗癌免疫反应

Vinicio A Melo Gallegos¹, Shirley Greenwald², Ami Tamir³

¹Amsterdam UMC Location VUmc Amsterdam Netherlands.

Molecular cancer therapeutics

|January 24, 2026

概括

一种新的双免疫检查点抑制剂DSP502同时阻断TIGIT和PD-1通路. 这种方法增强了抗癌免疫力,并显示出治疗非小细胞肺癌 (NSCLC) 等癌症的前景.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
生物技术是生物技术.

背景情况:

使用PD-1阻断的免疫检查点抑制 (ICI) 对于许多癌症患者来说通常是无效的.
TIGIT (具有Ig和ITIM域的T细胞免疫受体) 是一个有前途的检查点目标,表达在耗尽的T和NK细胞上,其配体PVR在各种癌症中过度表达.
两种TIGIT和PVR都与患者预后不佳相关,突出显示了需要新的治疗策略的需要.

研究的目的:

开发和评估一种新的双作用免疫检查点抑制剂DSP502,针对TIGIT和PD-1通路.
评估DSP502阻止PVR/TIGIT和PD-L1/PD-1相互作用的能力,并重新激活抗癌免疫力.
在临床前癌症模型中研究DSP502的治疗潜力,包括非小细胞肺癌 (NSCLC).

主要方法:

DSP502是通过将TIGIT和PD-1的细胞外域融合到具有knob-in-hole突变的人类IgG1 Fc域来设计的.
在体外测试DSP502的有效性,使用来自NSCLC和结直肠癌患者的外周血液单核细胞 (PBMC) 和瘤透性淋巴细胞 (TIL).
在体内研究中,使用异种移植的卵巢和肺癌模型来评估DSP502的抗瘤作用.

主要成果:

DSP502治疗增强了NK细胞激活,并增强了PBMC和TIL对表达PD-L1和PVR的癌细胞的细胞毒性活性.
转录基因分析显示,TIGIT和PD-1在NSCLC中CD8+ T细胞的消耗上共同表达.
通过增强抗瘤免疫力,DSP502在体内抑制了瘤生长,并保留了协同刺激的配体DNAM-1.

结论:

DSP502通过同时阻断PVR/TIGIT和PD-L1/PD-1通路,表现出双重免疫检查点抑制活性.
工程蛋白可以招募FcR阳性效应细胞,进一步增强抗癌免疫力.
DSP502对各种癌症,特别是NSCLC具有显著的治疗潜力,需要进一步的临床研究.

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