This integrated framework demonstrates tumour-specific retention and distribution in therapeutic interventions, implying enhanced effectiveness in treatment.
LTD-C310 (C31H43BN7O10) is presented as an integrated physiologically based pharmacokinetic/pharmacodynamic (PBPK/PD) framework describing a multi-functional therapeutic conjugate designed for selective tumour accumulation. The model consists of 32 coupled ordinary differential equations describing dissolution, enterocyte uptake with TPGS-mediated efflux inhibition, portal and lymphatic absorption pathways, perfusion-limited organ distribution, hepatic metabolism, enterohepatic recycling, and tumour-specific retention mechanisms. Additional components include pH-dependent tumour partitioning, intracellular ion-trap retention, ROS-mediated elimination suppression, and tumour spatial heterogeneity. Pharmacodynamic behaviour follows an extended Simeoni tumour growth inhibition model with optional boron neutron capture therapy (BNCT) and adaptive resistance dynamics. The framework is derived axiomatically from physical and biochemical principles, with stability, global mass balance, and structural identifiability explicitly demonstrated.
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Lance Thomas Davidson (2026) studied this question.
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