May 30, 2026 to June 3, 2026
Henry Cheng International Conference Centre
Asia/Hong_Kong timezone

Interspecies Metabolism of the Oral CSF1R Inhibitor C019199 and Kinase Inhibitory Profile of Its Major Circulating Metabolite

Not scheduled
20m
Henry Cheng International Conference Centre

Henry Cheng International Conference Centre

DMPK (Drug Metabolism and Pharmacokinetics) of New Molecules

Speaker

Ziyi Zhou ((1) School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, China (2)Drug Clinical Trial Institution, The First Affiliated Hospital of Xiamen University, Xiamen, China)

Description

Abstract:

Background: C019199 is a novel oral inhibitor of CSF1R currently in clinical trials. This study aimed to characterize its interspecies metabolic profiles and to evaluate the kinase inhibitory activity of its major circulating metabolite, M7 (also known as Y019009-L).

Methods: C019199 was incubated with human, monkey, dog, rat and mouse liver microsomes. Metabolites were profiled by ultra-performance liquid chromatography-ultraviolet/quadrupole time-of-flight mass spectrometry (UPLC-UV/Q-TOF MS). The half-maximal inhibitory concentration (IC50) of the major metabolite M7 against CSF1R, KIT, platelet-derived growth factor receptor alpha (PDGFR-alpha) and kinase insert domain receptor (KDR) was measured by homogeneous time-resolved fluorescence (HTRF) kinase assay and compared with the parent drug.

Results: Eight metabolites were identified. The mono-oxidized metabolite M7 was the predominant species detected across all five test species. M7 inhibited CSF1R with an IC50 of 6.09 nM, threefold more potent than C019199 (18.13 nM). It also showed strong activity against PDGFR-alpha (19.44 nM) and moderate activity against KIT (51.04 nM). Notably, M7 was markedly weaker against KDR (1087 nM) than the parent (86.17 nM), indicating an improved selectivity profile.

Conclusions: M7 is the major circulating metabolite of C019199, demonstrating superior CSF1R potency and favorable kinase selectivity, which may contribute significantly to the pharmacological activity of the oral CSF1R inhibitor.

Acknowledgments:

Supported by the Science and Technology Plan Guiding Project of Xiamen (3502Z20244ZD1042).

Author

Ziyi Zhou ((1) School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, China (2)Drug Clinical Trial Institution, The First Affiliated Hospital of Xiamen University, Xiamen, China)

Co-authors

Mrs Mengxin Huang ((1) School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, China (2)Drug Clinical Trial Institution, The First Affiliated Hospital of Xiamen University, Xiamen, China) Wenrui Zhang ((1) School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, China (2)Drug Clinical Trial Institution, The First Affiliated Hospital of Xiamen University, Xiamen, China) Xi Luo ((2)Drug Clinical Trial Institution, The First Affiliated Hospital of Xiamen University, Xiamen, China) Xiaoqing Wen (Drug Clinical Trial Institution, The First Affiliated Hospital of Xiamen University, Xiamen, China) Yueyuan Huang ((2)Drug Clinical Trial Institution, The First Affiliated Hospital of Xiamen University, Xiamen, China)

Presentation materials