tumoral cell

Cyclo(-RGDfK) is a potent and selective inhibitor of integrin αvβ3 with IC50 of 0.94 nM. Cyclo specifically targets tumor microvasculature and cancer cells by binding to αvβ3 integrin on the cell surface.

Cyclo(-RGDfK) is a selective αvβ3 integrin inhibitor(IC50 : 0.94 nM).

CV-4-26 (Compound 22) acts as a covalent inhibitor of TEAD. By inhibiting YAP/TEAD-driven transcription, it diminishes the expression of CTGF and CYR61. Furthermore, CV-4-26 impedes colony formation in Huh7 and HepG2 cells, inducing cell cycle arrest and apoptosis (apoptosis). This compound demonstrates anti-tumoral activity against hepatocellular carcinoma (HCC) and hepatoblastoma (HB).

BI-1347 is a potent, selective inhibitor of CDK8/cyclinC (IC50: 1 nM). It shows tumor growth inhibition in an in vivo xenograft model.

FB49 is a selective Bcl-2-associated athanogene 3 (BAG3) inhibitor with a Ki of 45 μM. It inhibits the proliferation of human tumoral cells without affecting the viability of human peripheral mononuclear cells. Additionally, FB49 arrests the cell cycle at the G1 phase and induces apoptosis and autophagy in treated medulloblastoma HD-MB03 cells [1].

Keap1-Nrf2-IN-21 (compound 4d) acts as an inhibitor of glucose metabolism with anti-tumoral properties. It targets the glycolytic pathway by affecting the Keap1-Nrf2 signaling pathway, which in turn suppresses glycolytic activity in cancer cells and inhibits tumor growth. Additionally, Keap1-Nrf2-IN-21 exhibits cytotoxic effects on the HEC1A cell line with an IC50 value of 2.60 μM.

(Rac)-Hydnocarpin is a natural flavonolignan derived from the flowers of Pueraria lobata that demonstrates strong cytotoxic effects against multiple ovarian cancer cell lines while maintaining minimal toxicity toward normal ovarian surface epithelial cells. (Rac)-Hydnocarpin triggers intrinsic apoptotic signaling through activation of caspase-9 and caspase-3 with limited involvement of caspase-8, driven by reactive oxygen species generation as a dominant mediator of apoptosis. (Rac)-Hydnocarpin additionally reprograms tumor-associated immune cells by reducing M2 macrophage markers and pro-tumoral mediators including matrix metalloproteinase-2/9, C–C motif chemokine ligand 5, transforming growth factor-β, and vascular endothelial growth factor, while enhancing macrophage phagocytosis, reinforcing its role as a multifunctional anticancer agent.