methicillin-resistant Staphylococcus aureus (MRSA) in hospitals have become a serious clinical problem. A glycopeptide antibiotic, vancomycin, has been used for the treatment of infections due to MRSA. Enterococci, which have some a part of the normal faecal flora of humans and animals have generally emerged as important nosocomial pathogens. Acquired resistance to vancomycin and teicoplanin in enterococci is due to the replacement of the cell wall component DAla–D-Ala replaced by the depsipeptide D-Ala–D-lactate. This substitution leads to the formation of modified peptidoglycan precursors, for which glycopeptides exhibit 1000-fold lower binding affinities. In most clinical isolates of enterococci, resistance is due to acquisition for plasmids that are often transferable to other gram-positive bacteria by conjugation. Recently, MRSA strain which has vanA gene with high resistance to vancomycin (minimum inhibitory concentration (MIC) 128 mg/ml), has been reported in clinical isolates. Therefore, a new anti-MRSA antibiotic, which differs from vancomycin in its mode of action, is clinically of interest. In the course of our screening system for new anti-MRSA and anti-vancomycin resistant Enterococci (VRE) antibiotics from some phenolic compounds, we investigated the antibacterial activity of propofol (2,6-diisopropylphenol), tocopherol, eugenol, butylated hydroxyanisole (BHA), and several of their dimer compounds. Dipropofol, which is an oxidative compound of propofol, showed inhibitory activity against gram-positive bacteria. The present study deals with antibacterial activities of propofol, dipropofol and related phenols.