tead auto-palmitoylation

VT107 is a potent pan-TEAD autopalmitoylation inhibitor. VT-107 can be used in cancer therapy research.[1]

VT103 is an orally active and selective inhibitor of TEAD1 protein palmitoylation and is an analog of VT101. VT103 has potential antitumor activity by inhibiting YAP TAZ-TEAD-promoted gene transcriptionment, blocking TEAD auto-palmitoylation, and blocking the interaction between YAP TAZ and TEAD.VT103 can be used in the study of HER2-positive breast cancer, prostate cancer, and triple-negative breast cancer.

TEAD-IN-1 (Compound 2) is an effective inhibitor of TEAD auto-palmitoylation with an IC50 of 603 nM. It enhances the interaction between TEAD and VGLL4, while diminishing the interaction between YAP and TEAD. TEAD-IN-1 is applicable for cancer research.

MSC-4106, an orally active and potent YAP TAZ-TEAD inhibitor, disrupts TEAD1 and TEAD3 auto-palmitoylation and demonstrates significant efficacy in the NCI-H226 tumor xenograft model [1].

DC-TEADin02 is an inhibitor of TEAD auto palmitoylation (IC50 = 197 nM). DC-TEADin02 can be in studies about development, regeneration, and tissue homeostasis.

VT101 is a TEAD Auto-palmitoylation inhibitor that Selectively Inhibit Proliferation and Tumor Growth of NF2-deficient Mesothelioma. VT101 inhibited the firefly luciferase reporter dose-dependently and had no 204 effect on the Renilla luciferase reporter.

VT-102 is a TEAD Auto-palmitoylation inhibitor that Selectively Inhibit Proliferation and Tumor Growth of NF2-deficient Mesothelioma. VT102 inhibited the firefly luciferase reporter dose-dependently and had no 204 effect on the Renilla luciferase reporter.

TM2 TEAD inhibitor, a robust and reversible inhibitor of the TEA domain transcription factor, presents dual inhibitory concentrations (IC50) of 38 nM for TEAD4 auto-palmitoylation and 156 nM for TEAD2 palmitoylation. It effectively blocks the TEAD-YAP association and their transcriptional activities, leading to significant antiproliferative effects in YAP-dependent cancer cell lines, both as a standalone agent and in combination with a MEK inhibitor. Additionally, it impedes YAP-dependent liver organoid growth ex vivo.

MGH-CP1 is a potent and selective inhibitor of TEAD palmitoylation, demonstrating dose-dependent and potent inhibition of TEAD2 4 auto-palmitoylation in vitro with IC50 values of 710 nM and 672 nM, respectively.