Lešnik Samo, Hodošček Milan, Podobnik Barbara, Konc Janez
National Institute of Chemistry, Hajdrihova 19, SI-1000 Ljubljana, Slovenia.
Biologics Technical Development Mengeš, Technical Research & Development Novartis, Lek Pharmaceuticals d.d., Kolodvorska 27, SI-1234 Mengeš, Slovenia.
J Chem Inf Model. 2020 Nov 23;60(11):5475-5486. doi: 10.1021/acs.jcim.9b01198. Epub 2020 May 19.
Reduction of the affinity of the fragment crystallizable (Fc) region with immune receptors by substitution of one or a few amino acids, known as Fc-silencing, is an established approach to reduce the immune effector functions of monoclonal antibody therapeutics. This approach to Fc-silencing, however, is problematic as it can lead to instability and immunogenicity of the developed antibodies. We evaluated loop grafting as a novel approach to Fc-silencing in which the Fc loops responsible for immune receptor binding were replaced by loops of up to 20 amino acids from similar local environments in other human and mouse antibodies. Molecular dynamics simulations of the designed variants of an Fc region in a complex with the immune receptor FcγIIIa confirmed that loop grafting potentially leads to a significant reduction in the binding of the antibody variants to the receptor, while retaining their stability. In comparison, standard variants with less than eight substituted amino acids showed possible instability and a lower degree of Fc-silencing due to the occurrence of compensatory interactions. The presented approach to Fc-silencing is general and could be used to modulate undesirable side effects of other antibody therapeutics without affecting their stability or increasing their immunogenicity.
通过替换一个或几个氨基酸来降低可结晶片段(Fc)区域与免疫受体的亲和力,即所谓的Fc沉默,是一种已确立的降低单克隆抗体治疗药物免疫效应功能的方法。然而,这种Fc沉默方法存在问题,因为它可能导致所开发抗体的不稳定性和免疫原性。我们评估了环移植作为一种新的Fc沉默方法,其中负责免疫受体结合的Fc环被来自其他人和小鼠抗体相似局部环境的多达20个氨基酸的环所取代。与免疫受体FcγIIIa形成复合物的Fc区域设计变体的分子动力学模拟证实,环移植可能导致抗体变体与受体的结合显著减少,同时保持其稳定性。相比之下,由于发生补偿性相互作用,取代氨基酸少于八个的标准变体显示出可能的不稳定性和较低程度的Fc沉默。所提出的Fc沉默方法具有通用性,可用于调节其他抗体治疗药物的不良副作用,而不影响其稳定性或增加其免疫原性。