a Affimed GmbH, Research Department , Heidelberg , Germany.
MAbs. 2019 Jul;11(5):899-918. doi: 10.1080/19420862.2019.1616506. Epub 2019 Jun 7.
Redirection of immune cells to efficiently eliminate tumor cells holds great promise. Natural killer cells (NK), macrophages, or T cells are specifically engaged with target cells expressing markers after infection or neoplastic transformation, resulting in their activation and subsequent killing of those targets. Multiple strategies to redirect immunity have been developed in the past two decades, but they have technical hurdles or cause undesirable side-effects, as exemplified by the T cell-based chimeric antigen receptor approaches (CAR-T therapies) or bispecific T cell engager platforms. Our first-in-class bispecific antibody redirecting innate immune cells to tumors (AFM13, a CD30/CD16A-specific innate immune cell engager) has shown signs of clinical efficacy in CD30-positive lymphomas and the potential to be safely administered, indicating a wider therapeutic window compared to T cell engaging therapies. AFM13 is the most advanced candidate from our fit-for-purpose redirected optimized cell killing (ROCK®) antibody platform, which comprises a plethora of CD16A-binding innate immune cell engagers with unique properties. Here, we discuss aspects of this modular platform, including the advantages of innate immune cell engagement over classical monoclonal antibodies and other engager concepts. We also present details on its potential to engineer a fit-for-purpose innate immune cell engager format that can be equipped with unique CD16A domains, modules that influence pharmacokinetic properties and molecular architectures that influence the activation of immune effectors, as well as tumor targeting. The ROCK® platform is aimed at the activation of innate immunity for the effective lysis of tumor cells and holds the promise of overcoming limitations of other approaches that redirect immune cells by widening the therapeutic window.
将免疫细胞重新定向以有效消除肿瘤细胞具有巨大的潜力。自然杀伤细胞 (NK)、巨噬细胞或 T 细胞在感染或肿瘤转化后与表达标志物的靶细胞特异性结合,导致其激活,并随后杀死这些靶细胞。在过去的二十年中,已经开发出多种重新定向免疫的策略,但它们存在技术障碍或引起不良的副作用,例如基于 T 细胞的嵌合抗原受体方法(CAR-T 疗法)或双特异性 T 细胞衔接器平台。我们的首创双特异性抗体将先天免疫细胞重新定向到肿瘤(AFM13,一种 CD30/CD16A 特异性先天免疫细胞衔接器)在 CD30 阳性淋巴瘤中显示出临床疗效的迹象,并且具有安全给药的潜力,表明与 T 细胞结合疗法相比,有更宽的治疗窗口。AFM13 是我们适用于定向优化细胞杀伤 (ROCK®) 抗体平台的最先进候选药物,该平台包含大量具有独特特性的 CD16A 结合先天免疫细胞衔接器。在这里,我们讨论了这个模块化平台的各个方面,包括先天免疫细胞结合相对于经典单克隆抗体和其他衔接器概念的优势。我们还介绍了其潜力,可以设计出适用于特定目的的先天免疫细胞衔接器形式,可以配备独特的 CD16A 结构域、影响药代动力学特性的模块以及影响免疫效应物激活和肿瘤靶向的分子结构。ROCK®平台旨在激活先天免疫以有效裂解肿瘤细胞,并有望克服通过拓宽治疗窗口重新定向免疫细胞的其他方法的局限性。