Table 1.

Non-antibiotic agents with antimicrobial activity, their antimicrobial spectrum and approved or potential mechanisms of action.

Non Antibiotic Agent	Antimicrobial Spectrum	Suggested Mechanisms of Action	References
NSAIDs
Acetysalicylic acid/salicylic acid	Staphylococcus aureus, Ps. aeruginosa, Campylobacter pylori, Helicobacter pylori, Epidermophyton floccosum, Microsporum spp., Trichophyton spp. Hepatitis C virus, influenza virus	Modulation of the expression of many genes, reduction of polysacharide capsule production, in S. aureus reduction of hemolysin production, in Ps. aeruginosa reduction of elastase, hemolysin, protease pyocyanin production, in H. pylori reduction in hemolysin production	[4]
Ibuprofen, diclofenac, fulbiprofen	Escherichia coli, Staphylococcus aureus, Microsporum spp., and Trichophyton spp., E. faecalis	Inhibition of DNA synthesis. In E. coli: inhibition of the DNA polymerase III β subunit	[6]
Local anaesthtetics:
Lidocaine, bupivacaine	Escherichia coli, Ps. aeruginosa, Staphylococcus aureus, Candida albicans, Coagulase(-) Staphylococcus, MRSA, Klebsiella, Enterobacter, E. coli, E. Faecalis and Proteus species	Disruption of bacterial cell membrane, inhibition of cell wall synthesis, dysfunction of cellular respiration, alteration in DNA synthesis, lysis of protoplasts, alteration in permeability and leakage of intracellular components, ultrastructural changes, inhibition of membrane-bound enzymatic activities	[8,9]
Opioids
Tramandol, meperidine	Escherichia coli, S. aureus S. epidermidis, Ps. aeruginosa S. pneumoniae, S. pyogenes, MRSA	No data exist on possible mechanism	[11,13]
Antipsychotics:
Phenothiazines(chlorpromazine, thioridazine, fluphenazin)	Gram(+)cocci, Mycobacteria, Shigella spp., E. coli, Salmonella spp., Acinetobacter baumanii, Klebsiella pneumonia, Plasmodium falciparum, herpes simplex, HBV, measles influenza, SV40, HIV, human herpes virus, JC virus	Adherence reduction in the pathogens in the endothelial cells, efflux pumps inhibition. Inhibition of: the binding of virus to host cell membrane receptors, the calcium-dependent endocytosis of viruses and the viral DNA replicatiοn	[20,21]
Antidepressants:
Sertraline, fluoxetine, paroxetine	Staphylococcus spp, Enterococcus, Citrobacter spp, Ps. aeruginosa, Klebsiella pneumoniae and Morganella morganii, Haemophilus influenza, Moraxella catarrhalis, Campylobacter jejuni, Acinetobacter, Bacteroides fragilis, Clostridium perfringens and Clostridium difficile	Inhibition of efflux pumps, antiplasmid activity targeting the replicating plasmid DNA and the DNA gyrase enzyme.	[25,26]
Amitriptyline hydrochloride	Aspergillus and Fusarim, Aspergillus spp, Candida parapsilosis, Plasmodium falciparum, Leishmania spp, Staphylococcus spp., Bacillus spp., Vibrio Cholerae, Micrococcus spp., Lactobacilus sporogenes, Citrobacter spp., Shigella, Salmonella, V. parahaemolyticus, E. coli, K. pneumonia, Pseudomonas spp
Antiplatelets
ticagrelor	MRSE, MSSA, MRSA, glycopeptide intermediate Staphylococcus aureus (GISA); Enterococcus faecalis; vancomycin-resistant E. faecalis (VRE); Streptococcus agalactiae	No data exist on possible mechanism of action	[32,33]
Antihistamines
Azelastine	Staphylococcus aureus, S. epidermidis, Enterococcus faecium, Escherichia coli, Klebsiella spp	Alteration of membrane permeability Absorption of the antihistamines onto the bacterial cell surface, expanding the hydrophobicity which, in turn, would increase the surface activity, so antimicrobial response could be due to surface action and due toincreased hydrophobic character Inhibition of efflux pumps,	[35,39,40]
Ceritizine	Bacillus sp., Vibrio cholera, S. aureus, Escherichia coli and Shigella sp, S. aureus and S. typhi
Terfenadine	MRSA, vancomycin intermediate (VISA), vancomycin-resistant S. aureus, Enterococcus faecium, Enterococcus faecalis, and M. tuberculosis
Mepyramine	Escherichia coli , K. pneumoniae
Statins:
Atorvastatin, simvastatin, rosuvastatin	MSSA, MRSA, Εnterococci VSE, Enterococcus VRE, Acinetobacter baumannii, Staphylococcus epidermidis, Enterobacter aerogenes, Escherichia coli, Proteus mirabilis, Enterobacter cloacae	Inhibition of HMG-CoA reductase Cytotoxicity, cells growth suppression, apoptosis promotion	[45,46]