TY - JOUR
T1 - A mechanistic quantitative systems pharmacology framework enriched by multiscale data enables model-informed translational development of mesenchymal stem cell therapy in lupus nephritis
AU - Zhang, Sujie
AU - Zhang, Qixiang
AU - Wang, Dandan
AU - Li, Zichun
AU - Xiao, Xia
AU - Rao, Qi
AU - Yang, Siyuan
AU - Qu, Yuchen
AU - Xu, Yiyang
AU - Wei, Ning
AU - Wang, Jing
AU - Gao, Yuan
AU - Sun, Lingyun
AU - Wang, Guangji
AU - Zhou, Fang
AU - Zhao, Chen
N1 - Publisher Copyright:
© 2026 The Authors. Published by Elsevier B.V. on behalf of Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. This is an open access article under the CC BY license. http://creativecommons.org/licenses/by/4.0/
PY - 2026
Y1 - 2026
N2 - Lupus nephritis (LN) is a complex autoimmune disease and mesenchymal stem cells (MSCs), given their unique immune-modulatory potential, have emerged as a promising route for treating LN. Understanding the multiscale dynamic LN–MSC interactions and selecting the optimal clinical design for MSCs is critical to enhance their therapeutic potential and achieve meaningful benefit-risk differentiation in patients. To guide MSC clinical development, we constructed the first mechanistic quantitative systems pharmacology model of LN pathophysiology that integrated multimodal preclinical–clinical data, with detailed illustration of standard-of-care immunosuppressant pharmacology and physiologically-based biodistribution and therapeutic mechanisms of MSCs. We created model-based virtual LN patients that well captured clinical interpatient heterogeneity and were validated by numerous sets of clinical efficacy readouts, including first-hand results from our investigator-initiated trial testing MSCs in LN patients. We used this computational framework and identified that a spaced two-infusion MSC dosing strategy would yield optimal clinical response in LN patients, which directly informed the phase 2 design of a novel MSC therapy. Modeling analyses further identified that CXCL10 in combination with proteinuria are potential predictive biomarkers that could boost clinical renal response to MSCs. These results demonstrated the exceptional importance of our QSP framework in driving MSC clinical development for LN patients.
AB - Lupus nephritis (LN) is a complex autoimmune disease and mesenchymal stem cells (MSCs), given their unique immune-modulatory potential, have emerged as a promising route for treating LN. Understanding the multiscale dynamic LN–MSC interactions and selecting the optimal clinical design for MSCs is critical to enhance their therapeutic potential and achieve meaningful benefit-risk differentiation in patients. To guide MSC clinical development, we constructed the first mechanistic quantitative systems pharmacology model of LN pathophysiology that integrated multimodal preclinical–clinical data, with detailed illustration of standard-of-care immunosuppressant pharmacology and physiologically-based biodistribution and therapeutic mechanisms of MSCs. We created model-based virtual LN patients that well captured clinical interpatient heterogeneity and were validated by numerous sets of clinical efficacy readouts, including first-hand results from our investigator-initiated trial testing MSCs in LN patients. We used this computational framework and identified that a spaced two-infusion MSC dosing strategy would yield optimal clinical response in LN patients, which directly informed the phase 2 design of a novel MSC therapy. Modeling analyses further identified that CXCL10 in combination with proteinuria are potential predictive biomarkers that could boost clinical renal response to MSCs. These results demonstrated the exceptional importance of our QSP framework in driving MSC clinical development for LN patients.
KW - Clinical translation
KW - Clinical trial simulation
KW - Lupus nephritis
KW - Mesenchymal stem cell
KW - Model-informed drug development
KW - Patient stratification
KW - Quantitative systems pharmacology
KW - Virtual patients
UR - https://www.scopus.com/pages/publications/105049124891
U2 - 10.1016/j.apsb.2026.08.018
DO - 10.1016/j.apsb.2026.08.018
M3 - 文章
AN - SCOPUS:105049124891
SN - 2211-3835
JO - Acta Pharmaceutica Sinica B
JF - Acta Pharmaceutica Sinica B
ER -