mesothelioma

Suberoyl bis-hydroxamic acid (SBHA) is a Histone deacetylase (HDAC) inhibitor. HDAC is required for transcriptional modulation, cell cycle regulation and development. It is an enzyme that deacetylates lysine residues on the N-terminal of the core histones.

ODQ is an effective and selective soluble guanylyl cyclase (sGC) inhibitor.

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

Dihydro-5-azacytidine FA (DHAC) is a pyrimidine analog that has antitumor activity, inhibits cell growth, inhibits DNA methylation, and may be used in the study of malignant mesothelioma.

Pemetrexed disodium (LY-231514) is a parenterally administered folate antagonist and antineoplastic agent, used in the treatment of non-small cell lung cancer and malignant mesothelioma. Pemetrexed disodium therapy has been associated with moderate rates of serum enzyme elevations during therapy, but has not been convincingly linked to instances of acute, clinically apparent liver injury.

Pemetrexed disodium heptahydrate (LY231514) is an antifolate that inhibits thymidylate synthase (TS), dihydrofolate reductase (DHFR), and glycinyl-adenosine 5'-monophosphate (GARMT) with K_i values of 1.3 nM, 7.2 nM, and 65 nM respectively. This inhibits the formation of precursor purine and pyrimidine nucleotides and cancer cell proliferation, making it suitable for research into pleural mesothelioma and non-small cell lung cancer (NSCLC).

(E)-KPT330 is a CRM1-selective inhibitor of nuclear export. It inhibits protein trafficking from the nucleus and induces cell cycle arrest and apoptosis in mesothelioma cells.

NR6 is an innovative and potent ALDH1A3 inhibitor with high selectivity. It effectively suppresses the growth of mesothelioma multicellular spheroids and the recruitment of neutrophils.

1,2-Dipalmitoleoyl-sn-glycero-3-phosphoethanolamine (16:1 PE) is a phosphatidylethanolamine that can enhance the activities of PP2A and PTP1B in malignant pleural mesothelioma cells. Additionally, 1,2-Dipalmitoleoyl-sn-glycero-3-phosphoethanolamine induces apoptosis in NCI-H28 malignant pleural mesothelioma cells.

TrkA-IN-9 (VMD-928) is an orally active and selective inhibitor of tropomyosin receptor kinase A (TrkA). It disrupts downstream signaling pathways activated by nerve growth factor (NGF) binding to TrkA, thereby inhibiting cell proliferation and invasion, and promoting cancer cell death. TrkA-IN-9 shows potential for research in various cancers, including prostate cancer, thymic carcinoma, mesothelioma, head and neck squamous cell carcinoma, lung cancer, ovarian cancer, and hepatocellular carcinoma.

Ifebemtinib (tosylate) (BI-853520 (tosylate); IN-10018 (tosylate)) is a highly selective PTK2 kinase inhibitor with anti-tumor properties. It inhibits FAK autophosphorylation in prostate cancer cells and suppresses spheroid formation and in situ tumor growth in vivo. Ifebemtinib (tosylate) is applicable in cancer research, including studies on solid tumors, breast cancer, and malignant pleural mesothelioma.

YAP/TEAD-IN-2 (Compound T-1) is an inhibitor of YAP/TEAD. This compound suppresses luciferase activity driven by YAP/TEAD in 293T cells and exhibits strong antiproliferative effects on human pleural mesothelioma NCI-H226 cells. YAP/TEAD-IN-2 is applicable for studying diseases associated with disruptions in the Hippo pathway, particularly cancer.

TEAD-IN-23 (Compound 22) is a potent pan-TEAD inhibitor with an IC50 of 10 nM. It exhibits strong antiproliferative activity against NCI-H226 and MSTO-211H cell lines. In the MSTO-211H xenograft tumor model, TEAD-IN-23 causes complete tumor regression. This compound is suitable for research on mesothelioma and hepatocellular carcinoma.

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.

TEAD ligand-Linker Conjugate 3 (A536) is an IAP-recruiting bifunctional degrader (IPD) in the ALP2 series, specifically targeting TEAD1, with a degradation DC50 of 110 nM for human TEAD1 and a maximum degradation efficiency (Dmax) of 51%. This compound binds effectively to cIAP1 and induces its degradation (IC50=122 nM), while also possessing good cell permeability. It is composed of ALP2 target protein ligand and PROTA Clinker, making it suitable for PROTAC synthesis. A536 demonstrates dose-dependent inhibition of cell proliferation in Hippo pathway-dependent human malignant mesothelioma cells and downregulates the transcriptional expression of the TEAD1 downstream target gene CTGF. Additionally, A536 is useful for studying mechanisms in malignancies with abnormal Hippo pathway activation, particularly in NF2-mutant mesothelioma.

PROTAC TEAD1/IAP degrader-3 is a TEAD1/IAP PROTAC degrader that facilitates the formation of a ternary complex by recruiting cIAP1 and XIAP E3 ligase, leading to the proteasomal degradation of TEAD1. It also triggers the autoubiquitination and proteasomal degradation of cIAP1. This compound can inhibit cell proliferation and regulate the Hippo pathway activity by downregulating CTGF gene expression in a TEAD-dependent manner. PROTAC TEAD1/IAP degrader-3 is applicable in mesothelioma research.

IAP ligand 9 is a SMAC mimetic and binds to the IAP (inhibitor of apoptosis protein) BIR domains, selectively targeting cIAP1-BIR3 and XIAP-BIR3, while showing minimal affinity for XIAP-BIR2, with SPR pKD values of 7.0, 8.0, and 5.0, respectively. As an IAP ligand module, it can be conjugated via linkers with degraders targeting the TEAD1 P site to form IAP-recruiting proteolysis-targeting chimeras (PROTACs/IPDs). This IPD recruits the IAPE3 ubiquitin ligase to form the TEAD1-IPD-IAP ternary complex, mediating ubiquitination and proteasome-dependent degradation of TEAD1 and inducing autodegradation of cIAP1. IAP ligand 9 and related degraders are useful in the study of solid tumors such as malignant pleural mesothelioma associated with abnormal activation of the Hippo pathway.

PROTAC TEAD/IAP degrader-1 is a TEAD/IAP PROTAC degrader that facilitates the recruitment of cIAP1 to form a ternary complex, inducing ubiquitination and proteasomal degradation of TEAD1 and TEAD4. This compound suppresses the transcriptional activity of TEAD, decreases the expression level of CTGF, and inhibits cell proliferation. It is applicable in mesothelioma research.

KG-FP-003 is a highly effective, selective, and durable TEAD PROTAC degrader featuring degradation concentrations of TEAD1DC50= 6 ± 4 nM, TEAD2DC50= 68 ± 15 nM, TEAD3DC50= 12 ± 5 nM, and TEAD4DC50= 7 ± 5 nM. It facilitates the ubiquitination and degradation of TEAD and exhibits anticancer activity against mesothelioma and ovarian cancer.

PROTAC TEAD1/IAP degrader-1 (Compound A232) is a selective PROTAC-based degrader targeting TEAD1 and cIAP1, with DC50 values of 14 nM and 270 nM, respectively. This compound facilitates the ubiquitination and degradation of TEAD1 and cIAP1, and it reduces the expression of the TEAD-dependent gene CTGF. Additionally, PROTAC TEAD1/IAP degrader-1 exhibits anticancer activity against mesothelioma.

IAP ligand 6 (A250) is an IAP ligand with a binding affinity (Ka) of 0.1 μM to the human XIAPBIR3 domain. It can bind to the XIAPBIR3 domain and serves as an alkynyl pyridine scaffold for developing TEAD degraders that recruit IAP. IAP ligand 6 is applicable in mesothelioma-related research.

PROTAC TEAD1/IAP degrader-2 is an IAP-recruiting TEAD1 PROTAC degrader with a DC50 of 170 nM for TEAD1 in NCI-H2052 cells. It exhibits moderate antiproliferative activity in mesothelioma cells that depend on the Hippo pathway. PROTAC TEAD1/IAP degrader-2 also inhibits CTGF expression, though less effectively than the TEAD inhibitor VT-107, and is applicable for mesothelioma research.

Pemetrexed tromethamine is a chemotherapy drug used for pleural mesothelioma and non-small cell lung cancer.

JY-1-106 is a BH3 α-helix mimetic, inducing apoptosis in a subset of cancer cells (lung cancer, colon cancer and mesothelioma) by disrupting Bcl-xL and Mcl-1 protein-protein interactions with Bak.