AAP-SO2

AAP-SO2 (10 µM; 10 min) directly binds to purified Mtb RNA polymerase core complex, with a higher binding efficiency than MMV688845^[1].
AAP-SO₂ (10 µM; 10 min) significantly increases the transcription termination efficiency of purified wild-type (WT) and βS450L mutant Mtb RNA polymerase (RNAP) holoenzymes, with a stronger effect on the βS450L mutant^[1].
AAP-SO2 (0.01-10 µM; 5 min) potently inhibits the transcriptional activity of purified wild-type Mtb RNA polymerase holoenzyme, with an IC₅₀ of 0.0251 µM^[1].
AAP-SO2 (serial concentrations; 7 days) inhibits the growth of actively replicating wild-type Mtb strains, and the Mtb^βS450L mutant strain is approximately 1.8-fold more sensitive than the wild-type strain^[1].
AAP-SO2 (69 nM; grown to stationary phase) reduces the emergence rate of Rifampicin (HY-B0272) tolerance in wild-type H37Rv Mtb and alters the mutation spectrum to decrease the proportion of βS450L mutations^[1].
AAP-SO2 (7 days) alone eliminates non-replicating Mtb HN878 from rabbit caseous necrosis in vitro, with a casMBC₉₀ of 7.89 µM; it also exerts a synergistic effect with Rifampicin at equimolar concentrations of 0.5 µM and 2 µM^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.