Striatisporolide A

Striatisporolide A (0-400 µM; 24 h) exhibits mild antibacterial activity against Escherichia coli ATCC 8739. After 24 h of incubation, the maximum growth inhibition rates reach 32.74% at 200 µM and 31.24% at 400 µM^[1].
Striatisporolide A (200-400 µM; 20 h) produces small inhibition zones against Escherichia coli ATCC 8739 in the disk diffusion assay (7.03 mm at 200 µM and 7.08 mm at 400 µM)^[1].
Striatisporolide A (200-400 µM; 0-24 h) disrupts the cell wall of Escherichia coli ATCC 8739 and increases extracellular AKP activity^[1].
Striatisporolide A (200-400 µM; 0-2 h) rapidly disrupts the cell membrane of Escherichia coli ATCC 8739 and induces ATP leakage, which reaches a peak at 0.5 h: the ATP level is 0.83 µM in the 200 µM treatment group and 0.96 µM in the 400 µM treatment group^[1].
Striatisporolide A (200-400 µM; 24-32 h) alters protein expression in Escherichia coli ATCC 8739: after incubation at 200 or 400 µM for 24 or 32 h, it increases the level of the 35 kDa protein in aqueous suspensions and decreases the level of the 10 kDa protein in lysates^[1].
Striatisporolide A (200-400 µM; 20 h) induces morphological changes in Escherichia coli ATCC 8739. After incubation at 200 or 400 µM for 20 h, the strain exhibits rough cell surfaces, irregular sizes and shortened lengths^[1].
Striatisporolide A (200-400 µM; 24 h) disrupts the ultrastructure of Escherichia coli ATCC 8739 and induces abnormal cell morphology after 24 h of incubation at concentrations of 200 or 400 µM^[1].
Striatisporolide A (0-150 μM; 48 h) promotes the proliferation of human umbilical vein endothelial cells (HUVECs), with the peak effect observed at 100 μM, which increases cell viability to 128.72%^[2].
Striatisporolide A (0-150 μM; 48 h pre-incubation prior to 40 min H₂O₂ exposure) exerts cytoprotective activity against H₂O₂-induced oxidative damage in human umbilical vein endothelial cells (HUVECs), and pre-incubation at a concentration of 50 μM increases the cell survival rate to 56.94%^[2].
Striatisporolide A (100 μM; 48 h) inhibits apoptosis of HUVECs under basal conditions and after H₂O₂-induced oxidative stress, reducing the apoptosis rate to 2.17% and 3.1%, respectively, at the concentration of 100 μM^[2].
Striatisporolide A (50-150 μM; pre-incubated for 48 h prior to 40 min of H₂O₂ exposure) inhibits excessive intracellular ROS production induced by H₂O₂ in HUVECs, reducing the fluorescence intensity to 9.47 at a concentration of 100 μM^[2].

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