Demin Oleg, Ou Ying, Kolesova Galina, Shchelokov Dmitry, Stepanov Alexander, Musatova Veronika, Sahasranaman Sri, Zhao Yating, Liu Xiangyu, Tang Zhiyu, Hanley William D
InSysBio CY, Limassol, Cyprus.
Clinical Pharmacology, BeiGene USA Inc., San Mateo, California, USA.
CPT Pharmacometrics Syst Pharmacol. 2025 Apr;14(4):706-717. doi: 10.1002/psp4.13307. Epub 2025 Feb 12.
The effectiveness of Bruton tyrosine kinase (BTK) inhibitors is influenced by the level of BTK occupancy in target tissues. In randomized phase 3 studies, progression-free survival (PFS) with zanubrutinib was superior to ibrutinib, whereas acalabrutinib was noninferior to ibrutinib in previously treated chronic lymphocytic leukemia. To establish a link between numerical differences in BTK occupancy and differentiated efficacy profiles among three covalent BTK inhibitors, quantitative systems pharmacology (QSP) modeling was employed. The model was developed to describe available clinical BTK occupancy data in patients with B-cell malignancies. Simulations of BTK occupancy were conducted for various clinical scenarios (e.g., dose interruption) and for bone marrow (BM), for which routine measurements are difficult. This model describes pharmacokinetics of BTK inhibitors; intracellular concentration of BTK inhibitors in peripheral blood mononuclear cells (PBMCs), BM, and lymph nodes (LNs); binding of BTK inhibitors with BTK; and BTK turnover rate. The model was validated using available clinical BTK occupancy data. Consistent with observed clinical data, the model predicted that zanubrutinib 160 mg twice daily resulted in higher median trough BTK occupancy in PBMCs, LNs, and BM compared with ibrutinib and acalabrutinib. Although the BTK occupancy differences at trough were relatively small between the BTK inhibitors, the differences were more pronounced after dose interruption. The current work underscores the importance of maintaining high BTK occupancy at steady-state trough and during treatment interruption to ensure maximal efficacy and provides an example of combining in vitro and clinical data to model receptor occupancy in tissues where measurements are challenging.
布鲁顿酪氨酸激酶(BTK)抑制剂的疗效受靶组织中BTK占有率水平的影响。在随机3期研究中,泽布替尼的无进展生存期(PFS)优于伊布替尼,而在既往治疗的慢性淋巴细胞白血病中,阿卡拉布替尼不劣于伊布替尼。为了建立三种共价BTK抑制剂在BTK占有率数值差异与不同疗效之间的联系,采用了定量系统药理学(QSP)建模。该模型用于描述B细胞恶性肿瘤患者中现有的临床BTK占有率数据。针对各种临床情况(如剂量中断)以及骨髓(BM)进行了BTK占有率模拟,而骨髓的常规测量较为困难。该模型描述了BTK抑制剂的药代动力学;外周血单核细胞(PBMC)、骨髓和淋巴结(LN)中BTK抑制剂的细胞内浓度;BTK抑制剂与BTK的结合;以及BTK周转率。该模型使用现有的临床BTK占有率数据进行了验证。与观察到的临床数据一致,该模型预测,与伊布替尼和阿卡拉布替尼相比,每日两次服用160mg泽布替尼可使PBMC、LN和BM中的中位谷值BTK占有率更高。尽管在谷值时BTK抑制剂之间的占有率差异相对较小,但在剂量中断后差异更为明显。当前的研究强调了在稳态谷值和治疗中断期间维持高BTK占有率以确保最大疗效的重要性,并提供了一个将体外和临床数据相结合以模拟在测量具有挑战性的组织中受体占有率的示例。