CI-930

CI-930 (0.10-100.00 μM; 10 min) significantly inhibits soluble PDE activity in human coronary artery smooth muscle cells (HCASMCs), reaching a maximum inhibition rate of approximately 43% at concentrations of 10-100 μM^[3].
PDE3, the PDE isoform inhibited by CI-930 (10 μM), is expressed in both soluble and particulate fractions of quiescent HCASMCs, accounting for 42%-44% of total PDE activity^[3].
CI-930 (10 μM) inhibits PDE3, a PDE that is expressed in both the soluble and particulate fractions of proliferative HCASMCs, accounting for 44%-45% of total PDE activity^[3].
CI-930 (10-20 μM; 24-30 h) inhibits the proliferation of human coronary artery smooth muscle cells (HCASMCs): at a concentration of 10 μM, the proportion of S-phase cells decreases significantly by 33%; at a concentration of 20 μM, the proportion of S-phase cells also decreases significantly^[3].
CI-930 (20 μM; 15-25 h) alone does not induce a statistically significant increase in cAMP levels in HCASMCs^[3].
CI-930 (10 μM; 6 h) does not affect the steady-state level of IL-2 mRNA in human Jurkat leukemia T cells activated by PHA/PMA^[4].
CI-930 (1 nM-10 μM; 72 h) inhibits Concanavalin A (Con A, HY-P2149, 2.5 μg/mL)-induced proliferation of mouse splenocytes with an IC₅₀ of 4.4 μM, and results from MTT-based cell viability assays demonstrate that the inhibitory effect on cells is not caused by cell death^[4].

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