In vitro activity: Rifampin inhibits IκBα degradation and mitogen-activated protein kinase (MAPK) phosphorylation. Rifampin is found to bind to human MD-2 in a Rifampin and MD-2 concentration-dependent manner. Rifampin inhibits NF-κB activation induced by LPS (20 ng/ml) in a dose-dependent manner, with an IC50 of 44.1 μM in Blue hTLR4 293 cells (A) and immunocompetent microgial BV-2 cell. Rifampin (50 μM) suppresses NF-κB activation at varying LPS doses, and the maximum NF-κB level induced by LPS in the presence of Rifampin (50 μM) is much lower than that in the absence of Rifampin. Rifampin inhibits NO production induced by LPS (200 ng/ml) in a dose-dependent manner in BV-2 cells, with an IC50 of 21.2 μM. Rifampin suppresses LPS induced TNF-α and IL-1β production in both microglia BV-2 and RAW 264.7 macrophage cells. Rifampin-inhibiting innate immune signaling is independent of the pregnane X receptor NR1I2. Rifampin combined with polyester vascular prostheses (PVP) functionalised with cyclodextrin (PVP-CD) results in significant bacterial adhesion reduction and growth inhibition against Gram-positive bacteria. Rifampin (50 μg/mL) significantly reduces the CFU counts of stationary-phase cultures and reduces the CFU counts of the log-phase culture to zero. Rifampin is particularly suitable since it is bactericidal and starts killing M. tuberculosis within an hour of exposure.