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-TEAD-IN-3 is an inhibitor of YAP/TAZ-TEAD interactions with an IC50 of 1.8 nM. It can be utilized as a TEAD1 ligand for constructing PROTACs, such as PROTAC TEAD degrader-2.

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].

YAP/TAZ inhibitor-3 (Compound 24) is a YAP/TAZ inhibitor applicable for relevant research within the life sciences field.

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.

IAG933 (YAP-TEAD-IN-3) belongs to small molecule inhibitors and is a TEAD-targeted YAP/TAZ-TEAD protein-protein interaction inhibitor (IC50 = 9 nM) with oral activity and selective inhibitory capability against all four TEAD isoforms. IAG933 is used in antitumor and pro-apoptosis research.

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.

TEAD1/3/4-IN-1 (compound 1) is an inhibitor of TEAD1/3/4 that suppresses YAP/TAZ-TEAD interactions. It exhibits antitumour activity against NF2-deficient NCI-H226 cells and may be employed in studies of cancer and diseases mediated by Hippo pathway abnormalities.

Acid Ceramidase-IN-3 is an inhibitor of acid ceramidase (aCDase). It shows a pIC50 of 8.5 in enzymatic assays and a pIC50 of 6.8 in A375 melanoma cell assays for aCDase enzyme activity inhibition. Acid Ceramidase-IN-3 promotes hepatic stellate cell (HSC) inactivation, measured by dose-dependent reduction of COL1A1 and ACTA2 levels. Additionally, it inhibits aCDase activity in HSCs, facilitating their inactivation and inhibiting YAP/TAZ nuclear localization. The compound enhances the expression of dynein/kinesin-related proteins (NDE1, NDEL1, KIF3B, KIF15) while reducing the expression of proteins related to various signaling pathways (SARM1, RGAP1, PDGF-D, PDGFR-B). Acid Ceramidase-IN-3 is valuable for fibrosis disease research.

PROTACTEAD degrader-2 (Compound 31) is a potent TEAD1 PROTAC degrader with a DC50 of 0.6 nM. It inhibits the YAP/TAZ-TEAD interaction with an IC50 of 1.8 nM and shows significant selective inhibitory activity against YAP-dependent cancer cells, effectively suppressing YAP-mediated transcriptional activity. This compound is applicable in mesothelioma and glioma 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].

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.

alpha-Ionone acts as an agonist for the olfactory receptor OR10A6. It induces apoptosis by activating OR10A6 and increasing the phosphorylation level of the LATS-YAP-TAZ signaling axis in the Hippo pathway, thereby inhibiting tumorigenesis and tumor progression in both in vitro and in vivo experiments.

MACTIDE-V is an orally active and selective peptide-drug conjugate targeting CD206. This compound delivers Verteporfin to CD206+ tumor-associated macrophages (TAM), thereby inhibiting the YAP/TAZ signaling pathway. It facilitates YAP exclusion from the nucleus, induces TAM polarization toward an anti-tumor phenotype, enhances phagocytosis and antigen presentation, and promotes T cell infiltration and NK cell activity. MACTIDE-V suppresses primary tumor growth and lung metastasis in triple-negative breast cancer (TNBC) mouse models.