TAML activators enable unprecedented, rapid, ultradilute oxidation catalysis where substrate inhibitions might seem improbable. Nevertheless, while TAML/H2O2 rapidly degrades the drug propranolol, a micropollutant (MP) of broad concern, propranolol is shown to inhibit its own destruction under concentration conditions amenable to kinetics studies ([propranolol] = 50 mu M). Substrate inhibition manifests as a decrease in the second-order rate constant k(I) for H2O2 oxidation of the resting Fe-III-TAML (RC) to the activated catalyst (AC), while the second-order rate constant k(II) for attack of AC on propranolol is unaffected. This kinetics signature has been utilized to develop a general approach for quantifying substrate inhibitions. Fragile adducts [propranolol, TAML] have been isolated and subjected to ESI-MS, florescence, UV-vis, FTIR, H-1 NMR, and IC examination and DFT calculations. Propranolol binds to Fe-III-TAMLs via combinations of noncovalent hydrophobic, coordinative, hydrogen bonding, and Coulombic interactions. Across four studied TAMLs under like conditions, propranolol reduced k(I) 4-32-fold (pH 7, 25 degrees C) indicating that substrate inhibition is controllable by TAML design. However, based on the measured k(I) and calculated equilibrium constant K for propranolol-TAML binding, it is possible to project the impact on k(I) of reducing [propranolol] from 50 mu M to the ultradilute regime typical of MP contaminated waters (<= 2 ppb, <= 7 nM for propranolol) where inhibition nearly vanishes. Projecting from 50 mu M to higher concentrations, propranolol completely inhibits its own oxidation before reaching mM concentrations. This study is consistent with prior experimental findings that substrate inhibition does not impede TAML/H2O2 destruction of propranolol in London wastewater while giving a substrate inhibition assessment tool for use in the new field of ultradilute oxidation catalysis.