TY - JOUR
T1 - Integrated Strategic Design and In Situ Click Chemistry Approach to Rapid Discovery of Novel Potent Covalent TEAD Inhibitors
AU - Miao, Yuhui
AU - Xu, Dounan
AU - Yang, Xu
AU - Sun, Hanrui
AU - Luo, Yipan
AU - Liang, Xiaochen
AU - Hu, Shuang
AU - Lin, Xiao
AU - Gao, Jing
AU - Luo, Xiaolin
AU - Pan, Yi
AU - Xiong, Huan
AU - Luo, Cheng
AU - Chen, Shijie
N1 - Publisher Copyright:
© 2026 American Chemical Society
PY - 2026/5/14
Y1 - 2026/5/14
N2 - Transcriptional enhanced associated domain (TEAD) proteins, activated by YAP/TAZ, are oncogenic drivers. While parallel synthesis has advanced lead discovery, most libraries are assembled randomly or in a scaffold-centric manner, which results in low efficiency for inhibitor discovery. In this study, we leveraged a strategy integrating structure-based design with CuAAC-enabled parallel synthesis to build a covalent, hydrophobic-fragment library. Combined with in situ screening, this approach rapidly identified hits at 8.33%, among which LC-TEAD01 emerged as a selective inhibitor showing a 17-fold preference for NF2-deficient NCI-H226 cells. Biochemical and structural studies confirmed covalent engagement of the conserved cysteine and occupancy of the hydrophobic channel, disrupting YAP–TEAD interaction and suppressing TEAD-dependent transcription. In vivo, LC-TEAD01 inhibited tumor growth in NF2-deficient xenografts. Collectively, this work integrates structure-based design with CuAAC-enabled parallel synthesis and in situ screening, enabling rapid discovery of TEAD inhibitors and offering a generalizable route for targets with structurally defined pockets.
AB - Transcriptional enhanced associated domain (TEAD) proteins, activated by YAP/TAZ, are oncogenic drivers. While parallel synthesis has advanced lead discovery, most libraries are assembled randomly or in a scaffold-centric manner, which results in low efficiency for inhibitor discovery. In this study, we leveraged a strategy integrating structure-based design with CuAAC-enabled parallel synthesis to build a covalent, hydrophobic-fragment library. Combined with in situ screening, this approach rapidly identified hits at 8.33%, among which LC-TEAD01 emerged as a selective inhibitor showing a 17-fold preference for NF2-deficient NCI-H226 cells. Biochemical and structural studies confirmed covalent engagement of the conserved cysteine and occupancy of the hydrophobic channel, disrupting YAP–TEAD interaction and suppressing TEAD-dependent transcription. In vivo, LC-TEAD01 inhibited tumor growth in NF2-deficient xenografts. Collectively, this work integrates structure-based design with CuAAC-enabled parallel synthesis and in situ screening, enabling rapid discovery of TEAD inhibitors and offering a generalizable route for targets with structurally defined pockets.
UR - https://www.scopus.com/pages/publications/105038783816
U2 - 10.1021/acs.jmedchem.6c00104
DO - 10.1021/acs.jmedchem.6c00104
M3 - 文章
C2 - 42085464
AN - SCOPUS:105038783816
SN - 0022-2623
VL - 69
SP - 10905
EP - 10923
JO - Journal of Medicinal Chemistry
JF - Journal of Medicinal Chemistry
IS - 9
ER -