| Bioactivity | Quabodepistat (OPC-167832) is a potent and orally active dprE1 inhibitor with an IC50 of 0.258 μM. Quabodepistat has antituberculosis activity and can be used for the research of tuberculosis caused by Mycobacterium tuberculosis[1]. | ||||||||||||
| Invitro | Quabodepistat (OPC-167832) exhibits very low MICs against laboratory strains of M. tuberculosis H37Rv (MIC: 0.0005 μg/ml) and Kurono (MIC: 0.0005 μg/ml) and strains with monoresistance to rifampin (RIF), isoniazid (INH), ethambutol (EMB), streptomycin (STR), and pyrazinamide (PZA) (MIC: 0.00024-0.001 μg/ml). However, Quabodepistat has minimal or no activity against standard strains of nonmycobacterial aerobic and anaerobic bacteria[1].The IC90 values of Quabodepistat against intracellular M. tuberculosis strains H37Rv and Kurono are 0.0048 and 0.0027 μg/ml, respectively. Quabodepistat shows bactericidal activity against intracellular M. tuberculosis at a low concentration, and the bactericidal activity is saturated at concentrations of 0.004 μg/ml or higher[1]. | ||||||||||||
| In Vivo | Quabodepistat (OPC-167832) (oral administration; 0.625-10 mg/kg) exhibits a good pharmacokinetic characteristic. The plasma reaches peak at 0.5 h to 1.0 h (tmax) and is eliminated with a half-life (t1/2) of 1.3 h to 2.1 h Quabodepistat distribution in the lungs is approximately 2 times higher than that in plasma, and the Cmax and AUCt of Quabodepistat in plasma and the lungs shows dose dependency[1].Quabodepistat (oral administration; 0.625-10 mg/kg; 4 weeks) significantly reduces lung CFU compared to the vehicle group. The dose-dependent decrease of lung CFU is observed from 0.625 mg/kg to 2.5 mg/kg. In a M. tuberculosis Kurono-infected ICR female mice model. Quabodepistat combines with DMD, BDQ, or LVX via oral gavage exhibits significantly higher efficacies than each single agent alone[1].[1].Quabodepistat (oral gavage; 2.5 mg/kg; combination with DCMB; 12 weeks) demonstrates the most potent efficacy when compares with DC, DCB. The lung CFU count after 6 weeks of treatment is below the detection limit, and at the end of just 8 weeks of treatment, the bacteria in the lungs of all the evaluated mice had already been eradicate[1]. Animal Model: | ||||||||||||
| Name | Quabodepistat | ||||||||||||
| CAS | 1883747-71-4 | ||||||||||||
| Formula | C21H20ClF3N2O4 | ||||||||||||
| Molar Mass | 456.84 | ||||||||||||
| Appearance | Solid | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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| Reference | [1]. Norimitsu Hariguchi, et al. OPC-167832, a Novel Carbostyril Derivative with Potent Antituberculosis Activity as a DprE1 Inhibitor.Antimicrob Agents Chemother. 2020 May 21;64(6):e02020-19. |
Quabodepistat
CAS: 1883747-71-4 F: C21H20ClF3N2O4 W: 456.84
Quabodepistat (OPC-167832) is a potent and orally active dprE1 inhibitor with an IC50 of 0.258 μM. Quabodepistat has a
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