Viriditoxin

Viriditoxin (10-100 µM; 1 h) promotes the polymerization of purified porcine brain tubulin in vitro^[1].
Viriditoxin (0-100 µM; 24 h) converts soluble tubulin into polymerized particulate fractions in SK-OV-3 cells in a concentration-dependent manner, enhances tubulin polymerization and stabilizes microtubules in SK-OV-3 cells, leading to the formation of dense pericytoplasmic microtubule structures and disorganized perinuclear microtubule bundles^[1].
Viriditoxin (0.048-30 µM; 24 h) inhibits the viability of SK-OV-3 cells with an IC₅₀ of 14.3 µM, and induces characteristic cytotoxic morphological changes^[1].
Viriditoxin (0-40 µM; 24 h) induces concentration-dependent G2/M phase arrest, concentration-dependent apoptosis, and inhibits migration and colony formation in SK-OV-3 cells^[1].
Viriditoxin (0.05-20 μM; 24-48 h) inhibits the proliferation of LNCaP, DU145 and PC3 cells, with the strongest inhibitory activity against LNCaP cells (48 h IC₅₀ = 0.63 μM)^[2].
Viriditoxin (0.1-1 μM; 48 h) induces G₂/M phase arrest in LNCaP cells, increases the proportion of cells in the sub-G₁ phase, and is accompanied by altered expression of key cell cycle regulatory proteins. It also mildly induces apoptosis, triggers autophagic cell death, and induces mitotic catastrophe^[2].
Viriditoxin (0.0002-200 μg/mL; 15 min) potently inhibits the polymerization of fluorescein-labeled *E. coli* FtsZ^T65C protein, with a mean IC₅₀ value of 8.2 μg/mL^[3].
Viriditoxin (200 μg/mL; 120 min) inhibits the GTPase activity of wild-type and luciferase-labeled *Escherichia coli* FtsZ protein, with an average IC₅₀ of 7.0 μg/mL^[3].
Viriditoxin (12.5-100 μg/mL; 75 min) induces filament formation in permeabilized, SulA-deficient E. coli MB5431 cells, indicating that it inhibits bacterial cell division^[3].
Viriditoxin (2-32 μg/mL; 20-24 h) exhibits broad-spectrum antibacterial activity against Gram-positive pathogens (including drug-resistant strains), inhibits permeabilized E. coli MB5431 at a concentration of 25 μg/mL, and shows no cytotoxicity against Candida albicans or HeLa cells at concentrations >64 μg/mL and >66.7 μg/mL, respectively^[3].
Viriditoxin (0.01-100 μM; 5 min-72 h) potently induces cytotoxicity in human leukemia and lymphoma cell lines, with IC₅₀ values ranging from 0.04 μM (72 h, Ramos) to 1.66 μM (24 h, K562), and even a short exposure of only 5 minutes causes irreversible cell death in Ramos cells^[5].
Viriditoxin (0.01-30 μM; 8-24 h) potently induces caspase-dependent apoptosis in Ramos and Jurkat cells with a rapid kinetic process: it activates caspase-3, cleaves PARP, and increases the number of apoptotic nuclei in a dose-dependent manner at 3-5 h^[5].
Viriditoxin (0.01-30 μM; 8-24 h) activates the mitochondrial apoptotic pathway independently of Bcl-2 overexpression and the presence of Bax/Bak, but its induction of apoptosis in leukemia/lymphoma cells requires the involvement of caspase-9^[5].
Viriditoxin (0.01-100 μM; 5 min-24 h) impairs the structure and function of mitochondria in leukemia/lymphoma cells, triggering rapid collapse of membrane potential, cytochrome c release, OPA1 cleavage, mitochondrial fragmentation, and ROS production, with its cytotoxicity partially mediated by ROS^[5].
Viriditoxin (0.01-10 μM; 15 min-24 h) impairs mitochondrial respiratory function in leukemia cells by inhibiting the activity of ETC complex I and reducing the expression of key ETC subunits, thereby leading to decreases in ATP levels and oxygen consumption^[5].
Viriditoxin (0.16-0.21 mg/mL) potently inhibits the growth of Gram-positive fish pathogens Streptococcus iniae, Streptococcus parauberis, as well as the human pathogen Staphylococcus aureus, with MIC values ranging from 0.16 to 0.21 mg/mL, but shows no activity against the Gram-negative fish pathogen Vibrio ichthyoenteri strains^[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.