The placenta serves as a critical interface for maternal-fetal substance exchange, including the active transport of immunoglobulin G (IgG), which is essential for neonatal immune protection. While mechanisms of IgG transfer are well-studied, the impact of therapeutic monoclonal antibodies (mAbs) on placental IgG dynamics during pregnancy remains unclear. This study aimed to predict maternal and fetal drug concentrations of ustekinumab (UST), an IgG1 monoclonal antibody used for treating inflammatory bowel disease (IBD), using a physiologically based pharmacokinetic (PBPK) model. The study utilized an established PBPK framework, incorporating pregnancy-specific physiological changes to construct and validate an endogenous IgG placental transfer model using clinical data. This model was subsequently extended to simulate maternal-fetal drug transfer in IBD pregnancies treated with UST. This model was extended to simulate maternal-fetal drug transfer in IBD pregnancies treated with UST, incorporating gestational age-specific parameters and the neonatal Fc receptor (FcRn) - mediated IgG transport. Competitive dynamics between endogenous IgG and UST were evaluated. Key findings included accurate predictions of endogenous IgG and UST plasma concentrations in both maternal and neonatal compartments. Results indicated that UST had minimal impact on endogenous IgG transfer kinetics, though scenarios such as mid-pregnancy UST discontinuation significantly reduced fetal UST exposure and potentially slowed IgG placental transfer due to decreased maternal IgG levels. The use of UST during pregnancy does not significantly affect the dynamics of endogenous IgG maternal-fetal transfer. This model provides a robust tool for assessing the safety and dosing strategies of monoclonal antibodies during pregnancy.