Table 2.
Drug A & its mechanism of action | Drug B & its mechanism of action | Reported effects | Possible mechanism of action |
---|---|---|---|
Cycloserine (inhibits bacterial cell-wall synthesis) | Epigallocatechin gallate (interruption of bacterial cell wall integrity) | Destruction of bacteria cell wall due to the synergistic antibacterial action | The presence of both the component together complements each other. Epigallocatechin disrupts the integrity of bacterial cell wall and cycloserine act as an inhibitor for cell wall synthesis, which hampers the restoration of the cell wall |
Ampicillin (interrupt bacterial cell-wall synthesis by blocking PBP2A (peptidoglycan transpeptidase) | Daptomycin (break down of bacterial cell membrane structure) |
Strong synergistic antibacterial action | Membrane disruption due to daptomycin, perhaps supported by the presence of ampicillin |
Artemisinin (disrupts parasite mitochondrial function, modulates host immune function) | Curcumin (generates ROs and produce cytotoxicity for malaria parasites) | Synergic/additiveantimalarial activities | They act at different sites in a non-interfering manner |
Ampicillin (inhibit bacterial cell-wall synthesis by blocking PBP2A | Imipenem inhibits bacterial cell-wall synthesis by blocking PBP1A, 1B | Synergic/additiveantibacterial effect | Both act at the same active site. Due to the presence of both at relatively high MICs (minimum inhibitory concentration), may make it responsible for the better antibacterial effect |