Initially, we studied the kinetics of the signal amplification system by tracking the UV-vis absorbance changes of TPPTS. Amplification experiments were performed at optimized conditions with 9.0 mM phosphonium ion 1 (1.0 eq.) and 1.5 eq. of disulfide 3. We used thiolsignal 4 as model trigger for the system (Figure ). When adding SH-trigger to the mixture, the release of TPPTS was monitored at λ = 300 nm upon conversion of 1 and the subsequent different ratios of SH-trigger (0.10, 0.15 and 0.25 eq.) (Figure ). Additionally, we used the kinetic model to describe the reaction and quantified the fit between model and experimental data by determining the coefficients of determination R 2 . From the kinetic experiments, we found that TPPTS concentration increased with increasing SH-signal. As expected, the release of TPPTS (k4 = 0.0020 M -1 s -1 ) is approximately three times as fast as the oxidation of TPPTS in the presence of 3 (k4 = 0.00071 M -1 s -1 ) based on their rate determining step rate constants. As seen from Figure , once the trigger is applied, the initiation speed and the maximum concentration of TPPTS from 0 to 5 hours differ notably (0 -5 h), while TPPTS depletion (5 -35 h) propagates at approximately the same rate. Using the kinetic model, we were able to predict the signal amplification cascade for concentrations of 10, 15 and 25% SH-trigger with R 2 -values of 0.91, 0.92 and 0.93, respectively. Although the model is in good agreement with experimental data, it underestimates the amplitudes of released TPPTS in all three cases. An explanation for the discrepancy could be the influence of electrostatic interactions between 1, TPPTS and OTPPTS, that lead to lower reactivities during consumption, which have not been considered in our model. Importantly, however, these results confirmed that the amplification cascade detects and translates the amount of trigger, causing signal-dependent amplitude curves of released TPPTS and time-dependent consumption of 1.