One potential strategy for inhibitor design for PDF would be to target the PDF binding site on the ribosome. Due to the differences in prokaryotic and eukaryotic ribosome, it could be postulated that an inhibitor binding here would only interact with the ribosomes in bacteria.
A pseudosubstrate could also be used, binding to the orthosteric (active) site of the enzyme to prevent fMet from binding. This competitive inhibition strategy would be effective if high doses could be administered without severe adverse reactions in the patient (ie- high specificity is necessary to prevent off-target effects).
Non-hydrolysable molecules are also a possible inhibitor mimicking an intermediate, binding to the orthosteric site to prevent any further reactions.
Biological drugs could also be used, such as antisense oligonucleotides (ASOs). Due to the high cost of these drugs, it would be unlikely they could be used in routine infections, such as an ear infection. They would likely be reserved for life-threatening infections, where the causative agent is quantitatively and definitively identified. ASOs have been demonstrated to be effective antivirals, helping resolve Ebolavirus infections in in vivo studies.