DprE1-IN-1 

DprE1-IN-1 is a potent, orally active DprE1 inhibitor with favorable hepatocyte stability, low cytotoxicity and low hERG channel inhibition. DprE1-IN-1 displays potent activity against both agent-susceptible and clinically isolated drug-resistant Tuberculosis strains with MICs10 CFU reduction in macrophages.

MICs: <0.1 μg/mL (Tuberculosis strains)^[1]

DprE1-IN-1 (compound 17b) (64 to 0.26 μg/mL; 48 hours) has high safety with low cytotoxicity towards HepG2, J774A.1 macrophage cells (IC₅₀>60 μg/mL) and Vero (IC₅₀=58.18 μg/mL) alongside potent efficacy and good druggability^[1].
DprE1-IN-1 can reduce 1.19 and 1.29 log₁₀ CFU M. tuberculosis in J774A.1 macrophages at 5 μg/mL and 10 μg/mL, respectively, for 3 days treatment^[1].
DprE1-IN-1 (compound 17b) (1 μM; 0-120 minutes) has high stability in human and mice hepatocytes (remaining of 42% and 49.7%, respectively; t_1/2 of 24.0 and 29.7 min, respectively)^[1].

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

DprE1-IN-1 (100 mg/kg; oral gavage; 5 days per week from day 10 until day 30) can reduce the bacterial burden in the lungs by 0.54 log₁₀ CFU after three weeks of treatment in M. tuberculosis H37Rv infected mice^[1].

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

451.52

C₁₉H₂₁N₃O₆S₂

920459-41-2

O=C(OCC)NC(C1=C(NC(C2=CC=C(S(=O)(N3CCCC3)=O)C=C2)=O)SC=C1)=O

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Qin R, et al. Identification of thiophene-benzenesulfonamide derivatives for the treatment of multidrug-resistant tuberculosis. Eur J Med Chem. 2022;231:114145.  [Content Brief]