Displays specific TAFC esterase activity but does not hydrolyze fusarinine C, which has the same core structure as TAFC (PubMed:17586718). Hydrolysis optimizes but is not essential for TAFC-mediated iron uptake (PubMed:17586718).Both extra- and intracellular siderophores have been shown to be crucial for the virulence (PubMed:17586718). Subsequent to chelation of iron and uptake, FsC and TAFC are hydrolyzed and the iron is transferred to the metabolism or to the intracellular siderophore ferricrocin (FC) for transport and storage of iron (PubMed:17586718). Hydrolyzes both TAFC and DF-TAFC with equal efficiencies, suggesting that its function might not be restricted to the release of iron from the siderophore but might also include the degradation of the iron-free chelator to protect cells (PubMed:17586718). Optimum pH is 6.0-7.0. Optimum temperature is 25 to 37 degrees Celsius. Expression is induced during iron deprivation (PubMed:17586718). Eliminates TAFC esterase activity and causes increased intracellular accumulation of TAFC and TAFC hydrolysis products (PubMed:17586718). Reduces the intracellular transfer rate of iron from TAFC to DF-FC and delays iron sensing (PubMed:17586718). Causes a decreased radial growth rate under iron-depleted but not iron-replete conditions (PubMed:17586718). Belongs to the esterase D family.