AAP-SO2 

AAP-SO2 is a Bactericide and Mycobacterium tuberculosis RNA polymerase (Mtb RNAP) inhibitor, with an IC₅₀ of 0.025 μM against Mtb RNAP. AAP-SO2 allosterically slows the nucleotide addition rate during transcriptional elongation and enhances transcription termination efficiency. AAP-SO2 exhibits increased activity against β^S450L-type Mtb, possesses activity against non-replicating Mtb, and shows whole-cell activity against Mtb and related mycobacterial species. AAP-SO2 reduces the overall emergence rate of Rifampicin (HY-B0272) tolerance in Mtb, alters the mutation spectrum, and decreases the proportion of β^S450L-type Rifampicin-resistant mutants. AAP-SO2 acts synergistically with Rifampicin to kill non-replicating Mtb in a rabbit caseous necrosis model. AAP-SO2 can be used for the research of tuberculosis^[1].

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.

495.57

C₂₆H₂₆FN₃O₄S

3033990-94-9

FC1=CC=CC=C1C(N[C@H](CC2=CC=CC=C2)C(NC3=CC=CC=C3N4CCS(CC4)(=O)=O)=O)=O

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• [1]. Bosch B, et al. Transcription co-inhibition alters drug resistance evolution and enhances Mycobacterium tuberculosis clearance from granulomas. Nature microbiology. 2026 Jan;11(1):180-194.