yap/taz

YAP TAZ inhibitor-1 is a YAP TAZ inhibitor (IC50 <0.100 μΜ) for the study of abnormal immune function and cancer.

YAP TAZ Inhibitor-4 (Compound 45) acts as an inhibitor of YAP TAZ, exhibiting inhibitory activity on TEAD transcriptional activation by preventing the interaction between YAP or TAZ and TEAD.

YAP TAZ-TEAD-IN-2 (Compound 51) is a YAP TAZ-TEAD inhibitor that disrupts the interaction between YAP TAZ and TEAD. It inhibits the transcriptional activity of TEAD with an IC50 of 1.2 nM. Additionally, YAP TAZ-TEAD-IN-2 suppresses the expression of target genes (Cyr61, CTGF, AXL, and Survivin) and the proliferation of breast cancer cells.

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].

Compound 24, also known as YAP TAZ inhibitor-3, effectively inhibits YAP TAZ. It displays significant inhibitory activity against firefly luciferase, demonstrating an IC 50 value of less than 0.1 μM [1].

GA-017 is a potent, selective inhibitor of LATS1 and LATS2 (large tumor suppressor kinase 1 2), exhibiting IC50 values of 4.10 and 3.92 nM, respectively. This compound simultaneously acts as an activator of cell proliferation by promoting YAP TAZ activation and their nuclear translocation. Additionally, GA-017 enhances cell growth in 3D culture conditions and augments the ex vivo formation of mouse intestinal organoids [1].

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

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).

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.

EN171, a covalent ligand, selectively binds to C38 and C96 on 14-3-3, intensifying 14-3-3's interactions with ERα, YAP, and TAZ. This action impairs both estrogen receptor and Hippo pathway transcriptional activities. Beyond serving as a molecular glue to augment native protein interactions, EN171 also functions as a covalent recruiter for 14-3-3 in heterobifunctional molecules. This facilitates the sequestration of nuclear neo-substrates, such as BRD4 and BLC6, into the cytosol.

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.

MY-1576 is a FAK inhibitor with an IC50 of 8 nM. It activates the Hippo pathway, thereby inhibiting YAP TAZ regulation. Additionally, MY-1576 effectively suppresses tumor growth in the KYSE30 xenograft mouse model, demonstrates good safety, and efficiently downregulates FAK autophosphorylation and YAP TAZ levels in vivo.

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].

Ki16425 (Debio 0719) is a competitive, potent, and reversible antagonist to LPA1, LPA2, and LPA3, with Ki values of 0.34 μM, 6.5 μM, and 0.93 μM, respectively.

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.

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.

SWTX-143, a novel covalent inhibitor, specifically and irreversibly binds to the palmitoylation pocket of all four TEAD isoforms, inhibiting the transcriptional activity of the YAP TAZ-TEAD complex and demonstrating antitumor activity [1].

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