CSC

Thioridazine hydrochloride (Mellaril) , an antipsychotic drug, is used in the therapy of psychosis and schizophrenia and shows serotonin antagonism or D4 selectivity.

Cyclosporin C (Cs-C) is a fungal metabolite against filamentous phytopathogenic fungi. Cyclosporin C has antifungal, antiviral, and immunosuppressant properties.

CSC-6 is an inhibitor of NLRP3. It significantly reduces the secretion of IL-1β in PMATHP-1 cells, with an IC50 of 2.3 μM. CSC-6 specifically binds to NLRP3 and prevents its activation by obstructing ASC oligomerization during the NLRP3 assembly process. It effectively alleviates symptoms of sepsis and gout mediated by excessive NLRP3 activation in mouse models.

8-CSC is a dual agent endowed with good hMAO-B inhibitory activity (Ki: 235 nM in baboon liver mitochondria) and A2A affinity (Ki: 36 nM in rat brain striatal membranes receptor).

EGFR/CSC-IN-1 is a dual inhibitor of the epidermal growth factor receptor (EGFR [IC50 10.52 nM]) and cancer stem cells (CSC), potentially applicable in triple-negative breast cancer research.

GBM CSCs-IN-1 (Compound (−)-20), a rocaglate derivative, potently inhibits glioblastoma stem cells (GBM CSCs) and exhibits an EC50 of 45 nM by targeting the RNA helicase DDX3. Additionally, it induces apoptosis in these cells.

MTOB (α-keto-γ-Methylthiobutyric acid) is a substrate for c-terminal binding protein (CtBP) that interferes with the carcinogenic activity of CtBP in cell culture and mice. It also actively regulates TCF-4 signaling, leading to cancer stem cell (CSC) growth and self-renewal.

MC-1-F2 is a direct FOXC2 inhibitor with anticancer activity, inhibits cancer stem cell (CSC) characteristics, and reduces the invasive ability of castration-resistant prostate cancer (CRPC) cell lines. MC-1-F2 can be used to study prostate cancer.

CWP232228, a potent and selective Wnt / β-catenin signaling inhibitor, antagonizes the binding of β-catenin to T-cell factor (TCF) in the nucleus. CWP232228 inhibits the formation and metastasis of tumors by inhibiting the growth of breast cancer and live

GTCpFE, a compound synthesized from Dimethyl fumarate (DMF) and Aspirin (ASA), inhibits IKKα β in the NF-κB pathway, exhibiting anti-inflammatory activity by preventing p65 from entering the nucleus. It selectively inhibits cancer stem cell (CSC) activity by reducing the growth of mammospheres and the expression of the CD44+CD24- immune phenotype. Furthermore, GTCpFE targets breast cancer stem cells, crucial in aggressive cancer phenotypes that depend on NFκB and PGE2.

Ovalitenone suppresses EMT by inhibiting the AKT mTOR signaling pathway and shows potential in inhibiting the CSC phenotype.

In platinum-resistant A2780cis human ovarian cancer cells, thioxodihydroquinazolinone-19 is an inducer of apoptotic cell death. It acts by exhibiting a strong inhibitory effect in ovarian CSC-LCs in combination with cisplatin.

OTS514 (OTS514 Hydrochloride) is a potent TOPK inhibitor. OTS514 exhibits a growth-suppressive effect on small cell lung cancer. OTS514 effectively suppressed the growth of SCLC cell lines (IC50: 0.4 ~ 42.6 nM). Treatment with OTS514 suppressed forkhead box protein M1 (FOXM1) activity. OTS514 treatment reduced CD90-positive SCLC cells and showed a higher cytotoxic effect against lung sphere-derived CSC-like SCLC cells.

Sulconazole is an imidazole compound with effective antifungal effect. Sulconazole vs. NF- κ B/IL-8 signal pathway has blocking effect and inhibiting effect on the formation of cancer stem cells (CSC). Sulconazole has inhibitory effect on tumor growth, which can be used in breast cancer research.

673-A is an aldehyde dehydrogenase (ALDH1A) inhibitor that depletes CD133+ cancer stem cells (CSC) in ovarian cancer cell lines. 673-A triggers necroptosis in ovarian CSCs and induces expression of mitochondrial uncoupling proteins (UCP). 673-A also overcomes chemotherapy resistance in vivo.

cRIPGBM chloride is an apoptosis-promoting derivative present in GBM cancer stem cells with antitumor activity. It induces caspase-1 dependent cell apoptosis by interacting with receptor-interacting protein kinase 2 (RIPK2) and acting as a molecular switch. cRIPGBM chloride reduces the formation of pro-survival RIPK2/TAK1 complexes and increases the formation of pro-apoptotic RIPK2/caspase 1 complexes, which can be used to study brain tumors.