RNP-11

RNP-11 (0.5-256 μg/mL; 18-24 h) potently inhibits the growth of Gram-positive bacteria, including MRSA, VRSA and VRE isolates, with MIC values of 2-8 μg/mL. It exhibits limited activity against Gram-negative bacteria, but this activity can be enhanced by outer membrane permeabilization. Moreover, it retains most of its antibacterial efficacy in the presence of human serum^[1].
RNP-11 (2-20 μg/mL; 24 h) acts as a bacteriostatic agent against S. aureus ATCC 29213 at a concentration of 1× MIC, and functions as a bactericidal agent at concentrations of 5× and 10× MIC. At higher concentrations, it reduces the bacterial load by approximately 6.0 log₁₀ CFU/mL within 24 h^[1].
RNP-11 (2-10 μg/mL; 2 h PI uptake, 30 min SEM/TEM) induces concentration-dependent membrane depolarization, permeabilization and structural damage in S. aureus ATCC 29213, confirming its membrane-disrupting activity^[1].
RNP-11 (administered at a concentration of 25 μg/mL for 4 hours following 10 minutes of LPS pretreatment) inhibits the production of proinflammatory cytokines (IL-6, TNF-α, IL-1β) induced by LPS (HY-D1056) in human THP-1 monocytes, exhibiting anti-inflammatory activity^[1].
RNP-11 (125-250 μg/mL; 1-24 h) exhibits extremely weak hemolytic effects on human red blood cells, and shows no significant cytotoxicity against HEK-293T cells at the highest concentration of 125 μg/mL; compared with its toxicity to Vero cells, its selectivity index against S. aureus ATCC 29213 reaches as high as 40^[1].
RNP-11 (0.01-100 μM; 15 min) exerts selective inhibitory effects on COX-2, which are stronger than its inhibitory effects on COX-1; its IC₅₀ against COX-2 is 42.85 μg/mL, with a selectivity index of 2.79^[1].

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