tead

YAP-TEAD-IN-3 is an inhibitor of YAP/TAZ-TEAD interactions with an IC50 of 9 nM for Avi-human TEAD (4217-434). YAP-TEAD-IN-3 inhibits YAP reporter gene expression (IC50 = 0.048 μM) and NCI-H2052 cell proliferation (IC50 = 0.048 μM).

TM2 TEAD inhibitor is an effective and reversible inhibitor of TEA domain transcription factors, exhibiting IC₅₀ values of 38 nM and 156 nM for TEAD4 auto-palmitoylation and TEAD2 palmitoylation, respectively. TM2 TEAD inhibitor blocks TEAD-YAP binding and suppresses its transcriptional activity, exhibiting significant antiproliferative effects in YAP-dependent cancer cells. It demonstrates potent efficacy both as a monotherapy and in combination with MEK inhibitors. Furthermore, TM2 TEAD inhibitor strongly inhibits YAP-dependent liver organoid growth in vitro, supporting its potential application as an anticancer therapeutic strategy.

YAP-TEAD-IN-1 is a competitive inhibitor of YAP–TEAD interaction (IC50: 25 nM) and exhibits higher binding affinity to TEAD1 (Kd: 15 nM) compared to YAP (50-171) (Kd: 40 nM).

YAP-TEAD-IN-1 TFA, a competitive inhibitor of the YAP–TEAD interaction (IC50: 25 nM), exhibits higher binding affinity to TEAD1 (Kd: 15 nM) compared to YAP (50-171) (Kd: 40 nM).

YAP-TEAD-IN-1 acetate is an effective and competitive inhibitor of YAP–TEAD interaction with an IC50 of 25 nM.

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

MYF-01-37 (1-[3-Methyl-3-[3-(trifluoromethyl)anilino]pyrrolidin-1-yl]prop-2-en-1-one) is a novel covalent TEAD inhibitor.

VT-105 is a potent and selective TEAD autopalmitoylation inhibitor that hinders proliferation and tumor growth in NF2-deficient mesotheliomas.

GNE-7883 is an inhibitor targeting TEAD transcription factor, inhibits cell proliferation and suppresses YAP/TAZ activation, and can be used to study YAP/TAZ-dependent tumors.

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.

K-975 is a highly selective, orally active TEAD inhibitor, effectively inhibiting protein-protein interactions between TEAD and YAP1/TAZ.

VT104 is a potent and orally active YAP/TAZ inhibitor for cancer research. VT104 blocks palmitoylation of endogenous TEAD1 and TEAD3 proteins.

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.

Super-TDU, an inhibitory peptide, targets YAP-TEADs interaction.

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].

YAP/TAZ inhibitor-2 is a potent, orally active TEAD-YAP/TAZ inhibitor with an EC50 value of 3 nM, demonstrating anti-proliferative and antitumor activity [1].

MYF-03-69 (TEAD-IN-3) is a covalent and irreversible pan-TEAD inhibitor with IC₅₀ values of 385/143/558/173 nM for TEAD1/TEAD2/TEAD3/TEAD4, respectively. MYF-03-69 inhibits TEAD transcriptional activity (IC₅₀ = 56 nM), upregulates the pro-apoptotic gene BMF, and suppresses mesothelioma cancer cells with defective Hippo signaling, making it suitable for malignant pleural mesothelioma (MPM).

TT-10 (TAZ-K), an activator of YES-associated protein (YAP)-transcriptional enhancer factor domain (TEAD) activity, has potential application in heart disease research, specifically for conditions characterized by loss of cardiomyocytes.

IK-930 is an orally active TEAD inhibitor (EC50 < 0.1 µM) with potent potency.

pan-TEAD-IN-1 (Compound 3) is an orally active pan-inhibitor of TEAD, disrupting its interaction with coactivators YAP/TAZ by targeting the palmitoylation site of TEAD. This inhibition leads to the downregulation of oncogene transcription, such as Ctgf and Cyr61, within the Hippo signaling pathway. Demonstrating outstanding efficacy, pan-TEAD-IN-1 has an IC50 of 0.36 nM for luciferase and 1.52 nM for H226 cells, along with favorable pharmacokinetic properties (AUC0–∞= 228.7 μg/mL·min, T1/2= 183.9 min). The compound significantly inhibits tumor growth in xenograft models of TEAD-dependent cancers, indicating its potential for research in these cancer types.

YAP/TEAD-IN-1 (compound 4) is a potent inhibitor of YAP and TEAD, exhibiting antioxidant properties. It demonstrates antiproliferative effects on tumor cells while showing minimal cytotoxic activity towards normal human cells.

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.

TEAD-IN-19 (Compound 1l) is a transcriptional inhibitor of TEAD, showing inhibition rates of 38.5%, 36.2%, 57.8%, and 71.3% for TEAD1, TEAD2, TEAD3, and TEAD4, respectively, at 10 μM. It exhibits strong antiproliferative and antimigratory effects on prostate cancer cell lines and significantly reduces the expression of TEAD-regulated downstream genes. TEAD-IN-19 holds potential for research in the field of cancer therapeutics.