W(Dab)L

W(Dab)L (15-20 μM) inhibits planktonic MRSA growth with an MIC of 15 μM in salt-free conditions and 20 μM in the presence of physiological salts, displaying partial salt tolerance^[1].
W(Dab)L (15 μM; up to 90 min) rapidly eliminates planktonic MRSA at its 15 μM MIC, achieving complete bacterial kill within 90 min^[1].
W(Dab)L (15 μM) inhibits 95% of S. aureus (MRSA) biofilm growth at its MBIC of 15 μM^[1].
W(Dab)L (30 μM) eradicates ~80% of 2-day mature S. aureus MRSA biofilms at its MBEC of 30 μM^[1].
W(Dab)L (15-50 μM; 4 h) shows minimal hemolysis (<25%) of human RBCs at 50 μM and no hemolysis at its 15 μM MIC^[1].
W(Dab)L (2.5-160 μM) is noncytotoxic to HeLa, HEK 293, and HDF cells at biologically active concentrations, with high cell survival observed even at concentrations up to 160 μM^[1].
W(Dab)L (Sub-MIC concentrations; 30 days, 96 bacterial generations) does not induce resistance development in MRSA over 96 bacterial generations when exposed to sub-MIC concentrations^[1].
W(Dab)L (15 μM; 6 h) remains stable after 6 h of incubation with a trypsin-chymotrypsin-proteinase K cocktail and retains full antimicrobial activity against MRSA with an MIC of 15 μM^[1].
W(Dab)L (15 μM; 6 h) remains stable after 6 h of incubation in human serum and retains full antimicrobial activity against MRSA with an MIC of 15 μM^[1].
W(Dab)L selectively interacts with bacterial membrane mimic SDS micelles (showing an 18 nm tryptophan fluorescence blue shift) and does not interact with mammalian membrane mimic DPC micelles^[1].
W(Dab)L disrupts the S. aureus (MRSA) inner membrane, increasing PI fluorescence by 50% relative to Triton X-100 control, confirming membrane permeabilization^[1].
W(Dab)L (15-30 μM) causes membrane deformation, blistering, and lysis of planktonic MRSA cells at 1× MIC (15 μM) and 2× MIC (30 μM), as observed via FESEM and TEM^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.