YAP Inhibitor

M3686 (Compound 29) is a potent, selective TEAD1 inhibitor with an IC₅₀ value of 51 nM. M3686 also shows weaker binding activity on TEAD3. M3686 potently inhibits cell viability against YAP-dependent NCI-H226 cell line with an IC₅₀ value of 0.06 uM. M3686 shows strong anti-tumor effects in the NCI-H226 xenograft model.

AICAR-¹³C₂,¹⁵N (Acadesine-¹³C₂,¹⁵N; AICA Riboside-¹³C₂,¹⁵N) is the ¹³C and ¹⁵N labeled AICAR (HY-13417). AICAR (Acadesine) is an adenosine analog and a AMPK activator. AICAR regulates the glucose and lipid metabolism, and inhibits proinflammatory cytokines and iNOS production. AICAR is also an autophagy, YAP and mitophagy inhibitor.

TEAD-IN-20 is a TEAD inhibitor. The IC₅₀ values of TEAD-IN-20 in TEAD4 FRET and TEAD4 MCF7-Tead cell lines are 0.021 and 0.044 μM, respectively. TEAD-IN-20 can be used in cancer research.

TEAD-IN-21 is a potent and orally active pan-TEAD inhibitor with an IC₅₀ of 3 nM. TEAD-IN-21 effectively inhibited the proliferation of Huh-7 cells. TEAD-IN-21 selectively downregulates TEAD-dependent downstream genes. TEAD-IN-21 achieves tumor regression in a liver cancer-derived tumor xenograft mice model. TEAD-IN-21 can be used in the research of hepatocellular carcinoma (HCC).

AZ'4331 is an orally active pan-TEAD family inhibitor, with an IC₅₀ of 0.381 μM against TEAD1, 0.020 μM against TEAD2, 0.014 μM against TEAD3, and 0.031 μM against TEAD4. AZ'4331 slows cell cycle progression. AZ'4331 exerts effects in cancer xenograft models with dysregulated Hippo pathway. AZ'4331 can be used to study cancers with altered Hippo pathways, including mesothelioma, head and neck squamous cell carcinoma, and EGFR-mutant non-small cell lung cancer.

LC-TEAD01 is a potent covalent transcription enhancer-associated domain (TEAD) inhibitor with an IC₅₀ of 116 nM and a K_i of 0.132 μM. LC-TEAD01 disrupts the TEAD-YAP interaction and inhibits TEAD-dependent transcriptional activity. LC-TEAD01 suppresses the proliferation of NF2-deficient cancer cells. LC-TEAD01 inhibits tumor growth in NF2-deficient xenograft models. LC-TEAD01 can be used in studies related to NF2-deficient malignant pleural mesothelioma.

OPN-9643 is a covalent inhibitor targeting the central palmitate binding pocket of TEADs with an IC₅₀ of 15 nM, preventing autopalmitoylation and reducing TEAD-driven luciferase activity and canonical TEAD targets, CTGF and CYR61. OPN-9643 can be used for the research of cancer, such as melanoma.

VS3 is a YAP-TEAD interaction inhibitor. VS3 directly disrupts the interaction between YAP-TEAD by binding to TEAD4 Interface 3 (K_d = 6 μM) on the surface. VS3 exhibits anti-proliferative activity against HT29, HCT116, and A2780. VS3 can be used for research on colorectal adenocarcinoma and ovarian cancer.

EA-C15 is a potent and selective TEAD inhibitor with an IC₅₀ of 0.34 μM. EA-C15 covalently binds to the TEAD palmitoylation site, blocks palmitoylation and transcriptional activity, and inhibits YAP-dependent cancer cell proliferation and YAP-TEAD target gene (CTGF and CYR61) transcription. EA-C15 can be used for cancer research.

MSC-1254 is a reversible, selective and covalent TEAD1 inhibitor. MSC-1254 can be used for the study of cancer.

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

USP10-IN-4 is a potent ubiquitin-specific protease 10 (USP10) inhibitor with an IC₅₀ of 10.87 μM and a K_d of 365 nM. USP10-IN-4 effectively inhibits USP10-mediated proteasomal degradation of downstream proteins YAP and p53, leading to the subsequent downregulation of CDK4 in the p53 signaling pathway. USP10-IN-4 promotes apoptosis in HCC cells and inhibits the onset and progression of liver cancer. USP10-IN-4 can used for the study of hepatocellular carcinoma (HCC).

VT102 is a TEAD1 inhibitor with a human IC₅₀ of 391 nM. VT102 inhibits auto-palmitoylation, attenuates YAP/TEAD1 interaction, reduces expression of TEAD target genes, and inhibits YAP-mediated luciferase reporter activity. VT102 exerts weak cell growth inhibitory activity in cancer cells. VT102 can be used for the research of cancer.

TEAD-IN-13 (64) is an orally active TEAD inhibitor, with an IC₅₀ of <100 nM and a half-life of 3.2 h in mouse.

TEAD-IN-23 (Compound 22) is an efficient pan-TEAD inhibitor with an IC₅₀ of 10 nM. TEAD-IN-23 exhibits potent anti-proliferative activity in both NCI-H226 and MSTO-211H. TEAD-IN-23 causes complete tumor regression in the MSTO-211H xenograft tumor model. TEAD-IN-23 can be used for the study of mesothelioma and hepatocellular carcinoma.

TEAD-IN-12 (58B) is an orally active TEAD inhibitor, with an IC₅₀ of <100 nM and a half-life of 3.6 h in mouse.

Verteporfin (Standard) is the analytical standard of Verteporfin. This product is intended for research and analytical applications. Verteporfin (CL 318952) is a photosensitizer for photodynamic therapy to eliminate the abnormal blood vessels in the eye associated with conditions such as age-related macular degeneration. Verteporfin is a YAP inhibitor which disrupts YAP-TEAD interactions. Verteporfin induces cell apoptosis. Verteporfinis an autophagy inhibitor that blocks autophagy at an early stage by inhibiting autophagosome formation.

YL-602 is an orally active Hippo pathway activator. YL-602 activates the Hippo pathway via MST1/2, with downstream pathway activation. YL-602 inhibits YAP and CTGF expression in cells irrespective of cell density and serum presence. YL-602 induces tumor cell apoptosis and inhibits colony formation. YL-602 suppresses tumor growth in mice. YL-602 can be used for the research of cancer, such as breast cancer.

CX-Se13 is an orally active pulmonary fibrosis inhibitor with anti-inflammatory and antioxidant activities. CX-Se13 regulates the Keap1/Nrf2/HO-1/NQO1, YAP/TAZ-TEAD, NF-κB p65 and TGF-β/Smads signaling pathways. CX-Se13 activates the cellular antioxidant defense system, restores redox balance, alleviates inflammatory responses, reduces collagen deposition, decreases pro-inflammatory cytokine levels and inhibits pathological progression. CX-Se13 can be used in studies related to pulmonary fibrosis.

TEAD-IN-14 (75a) is an orally active TEAD inhibitor, with an IC₅₀ of <100 nM and a half-life of 2.3 h in mouse.