Gupta Paridhi, Srivastava Ashish, Ryman Josiah T, Swanson Michael D, Kozhich Alexander, Jawa Vibha, Meibohm Bernd
Department of Pharmaceutical Sciences, University of Tennessee Health Science Center, Memphis, Tennessee, U.S.A.
Quantitative Pharmacology and Pharmacometrics, Merck & Co., Inc., Rahway, New Jersey, U.S.A.
AAPS J. 2025 May 16;27(4):94. doi: 10.1208/s12248-025-01083-0.
Administration of human therapeutic proteins such as monoclonal antibodies (mAb) to animals during preclinical drug development often leads to the development of anti-drug antibodies (ADA). ADA may reduce the systemic exposure of the mAb by enhancing its immune-complex mediated clearance. Thus, ADA may hinder the preclinical pharmacokinetic and toxicology assessments of mAbs. To mitigate this effect, we explored the ability of short-term administration of immunosuppressants to induce prolonged immune tolerance towards a human mAb, erenumab, in rats. In two studies, we investigated dosing regimens using the immunosuppressants methotrexate and tacrolimus/sirolimus combination, and compared them to non-immunosuppressed control groups. Each study comprised three phases: induction (weeks 1-4), washout (weeks 5-8), and rechallenge (weeks 9-12). Animals received mAb during the induction and rechallenge phase, while immunosuppression was limited to the induction and washout phase. Blood samples were collected at predefined time-points for erenumab and ADA quantification. The tacrolimus/sirolimus regimen, but not the tested methotrexate regimens, completely prevented ADA formation in all treated animals relative to the control groups. The tacrolimus/sirolimus treated animals not only remained ADA-negative with initial immunosuppression during the induction phase but remained ADA-negative even after erenumab rechallenge suggesting the induction of immune-tolerance beyond the immunosuppressive treatment period. Correspondingly, erenumab systemic exposures were maintained throughout the study period in all animals in the tacrolimus/sirolimus group and were similar to the erenumab exposures in ADA-negative animals of the control group. In contrast, ADA-positive animals in the control group exhibited a 60-80% reduction in erenumab exposures.
在临床前药物研发过程中,向动物体内施用单克隆抗体(mAb)等人类治疗性蛋白质,往往会导致抗药物抗体(ADA)的产生。ADA可能会通过增强其免疫复合物介导的清除作用,降低mAb的全身暴露量。因此,ADA可能会妨碍mAb的临床前药代动力学和毒理学评估。为减轻这种影响,我们探究了短期施用免疫抑制剂诱导大鼠对人源mAb依瑞奈尤单抗产生长期免疫耐受的能力。在两项研究中,我们研究了使用免疫抑制剂甲氨蝶呤和他克莫司/西罗莫司组合的给药方案,并将其与未进行免疫抑制的对照组进行比较。每项研究包括三个阶段:诱导期(第1 - 4周)、洗脱期(第5 - 8周)和再激发期(第9 - 12周)。动物在诱导期和再激发期接受mAb,而免疫抑制仅限于诱导期和洗脱期。在预定时间点采集血样,用于依瑞奈尤单抗和ADA定量分析。与对照组相比,他克莫司/西罗莫司给药方案(而非所测试的甲氨蝶呤给药方案)在所有接受治疗的动物中完全阻止了ADA的形成。接受他克莫司/西罗莫司治疗的动物不仅在诱导期初始免疫抑制期间保持ADA阴性,甚至在依瑞奈尤单抗再激发后仍保持ADA阴性,这表明在免疫抑制治疗期之后诱导出了免疫耐受。相应地,他克莫司/西罗莫司组所有动物在整个研究期间依瑞奈尤单抗的全身暴露量均得以维持,且与对照组ADA阴性动物中依瑞奈尤单抗的暴露量相似。相比之下,对照组中ADA阳性的动物依瑞奈尤单抗暴露量降低了60 - 80%。