Delamanid has been studied extensively and approved for the treatment of pulmonary multidrug-resistant tuberculosis; however, its potential in the treatment of extrapulmonary tuberculosis remains unknown. We previously reported that in rats, delamanid was broadly distributed to various tissues in addition to the lungs. In this study, we simulated human plasma concentration–time courses (pharmacokinetic profile) of delamanid, which has a unique property of metabolism by albumin, using two different approaches (steady-state concentration of plasma-mean residence time [C
ss
-MRT] and physiologically based pharmacokinetic [PBPK] modeling). In C
ss
-MRT, allometric scaling predicted the distribution volume at steady state based on data from mice, rats, and dogs. Total clearance was predicted by
in vitro
–
in vivo
extrapolation using a scaled albumin amount. A simulated human pharmacokinetic profile using a combination of human predicted C
ss
and MRT was almost identical to the observed profile after single oral administration, which suggests that the pharmacokinetic profile of delamanid could be predicted by allometric scaling from these animals and metabolic capacity
in vitro
. The PBPK model was constructed on the assumption that delamanid was metabolized by albumin in circulating plasma and tissues; to which, the simulated pharmacokinetic profile was consistent. Moreover, the PBPK modeling approach demonstrated that the simulated concentrations of delamanid at steady state in the lung, brain, liver, and heart were higher than the
in vivo
effective concentration for
Mycobacterium tuberculosis
. These results indicate that delamanid may achieve similar concentrations in various organs to that of the lung and may have the potential to treat extrapulmonary tuberculosis.