Targocil functions as a bacteriostatic inhibitor of wall teichoic acid (WTA) biosynthesis which can inhibit the growth of methicillin-susceptible S. aureus (MSSA) and methicillin-resistant S. aureus (MRSA) with MIC₉₀s of 2 μg/ mL for both MRSA and MSSA. IC50 & Target: MIC90: 2 μg/mL (MSSA), 2 μg/mL (MRSA)^[1] In Vitro: MICs of Targocil against S. aureus strains Newman, MW2, MG2375, and MG2389 are 1 μg/mL for all strains. Targocil shows excellent activity against S. aureus isolates from suspected cases of bacterial keratitis, including both MSSA and MRSA isolates, with MICs that range from 1 to 2 μg/ mL. Targocil, a derivative of 1835F03, exhibits better activity against all keratitis isolates than the original lead compound, 1835F03. Bovine serum exhibits a detectable but moderate inhibitory effect on the in vitro antimicrobial activities of both 1835F03 and Targocil, increasing the MICs of both by 4- to 8-fold. Compare to the vehicle alone, Targocil at 5 μg/mL exhibits little toxicity for HCECs, even after 24 h of exposure. However, 40 μg/mL Targocil shows toxicity at all time points tested. Targocil at levels equal to 10×MIC in vitro readily inhibits growth of Newman and MG2375 in the presence of HCECs^[1]