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在非小细胞肺癌中ROR1 × CD3双特异抗体的抗瘤活性

Yi Wang¹, Yuxi Zhang¹, Haoyi Sun¹

¹School of Basic Medical Sciences, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, China.

International immunopharmacology

|July 27, 2023

概括

一种针对ROR1和CD3的新型双特异性抗体有效地消除非小细胞肺癌 (NSCLC) 细胞. 这种ROR1 x CD3双特异性抗体 (biAb) 在临床前模型中显示出强大的抗瘤活性,没有观察到副作用.

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:

针对CD3的双特异性抗体 (biAbs) 正在为免疫瘤学迅速发展.
在非小细胞肺癌 (NSCLC) 等固体瘤中biAbs的临床开发面临重大挑战.
向受体氨酸激酶类孤儿受体1 (ROR1) 是NSCLC治疗的潜在策略.

研究的目的:

在NSCLC中研究一种新的ROR1 × CD3双特异抗体 (biAb) 的瘤抑制潜力.
在ROR1阳性NSCLC模型中评估R11 × v9 biAb的疗效和安全性.

主要方法:

在scFv-Fc格式的ROR1 × CD3 biAb (R11 × v9) 的开发,ROR1与人类和小鼠目标结合.
评估R11 × v9 biAb与T细胞和ROR1+NSCLC细胞系的结合.
细胞毒性,细胞因子分泌和免疫细胞激活 (CD4 +,CD8 + T 细胞) 的体外评估.
在ROR1+NSCLC异种移植小鼠模型中的体内疗效和安全性研究.

主要成果:

R11 × v9 biAb 证明了对T细胞和ROR1+ NSCLC细胞的特定结合.
对各种ROR1+NSCLC细胞系观察到剂量依赖的细胞毒性.
这种biAb诱导的T细胞调解了促炎性细胞因子的分泌,并在CD8+T细胞中增强了细胞毒性分子 (granzyme B, perforin) 的产生.
R11 × v9 biAb促进T细胞透到瘤组织中.
在体内证实了显著的抗瘤活性,没有观察到任何不良影响.

结论:

R11 × v9 biAb有效地使T细胞参与消除ROR1+NSCLC细胞.
这种新型的biAb在NSCLC模型中显示出强大的临床前抗瘤疗效和有利的安全性.
在NSCLC治疗的临床前和临床研究中,R11 × v9 biAb值得进一步研究.

关键词:

双特异性抗体双特异性抗体在NSCLCLC中,我们可以看到.ROR1 是一个ROR1.在T细胞,T细胞.瘤免疫疗法免疫疗法

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