Additional file 1: Table S1 summarizes the plasma and brain interstitial pharmacokinetic data for each patient, accounting for in vitro fractional recovery . We opted to only assess plasma and brain dialysate samples for temozolomide because the active temozolomide metabolite, MTIC, was associated with poor acid stabilization and recovery . Comparing plasma concentrations of temozolomide alone vs. temozolomide with regadenoson, neither the Cmax nor AUCs were impacted by regadenoson (Fig. 2, Additional file 2: Fig S1). Peak temozolomide plasma concentrations with temozolomide alone or combined with regadenoson were: 3.5 ± 1.6 µg/ml vs. 4.8 ± 1.2 µg/ml, respectively. Non-contrast enhancing brain concentrations for temozolomide alone or combined with regadenoson were: 0.55 ± 0.26 µg/ml vs. 0.57 ± 0.32 µg/ml, respectively. The non-contrast enhancing brain:plasma AUC ratio was 19.1 ± 10.7% when temozolomide was administered alone and 18.0 ± 7.8% when combined with regadenonson Three patients (patients 2, 3 and 5) demonstrated a rise in non-contrast enhancing mean brain AUC with regadenoson by approximately 53%. But this increase can be mostly attributed to patient 2 who demonstrated a significant rise in temozolomide brain AUC concentration with regadenoson; doubling AUC from 0.6 to 1.2 µg/ml h. Overall, evaluation of non-enhancing brain interstitium mean concentrations for all 5 patients demonstrated no significant difference in Cmax or AUCs between treatment groups, but individual variations existed.Fig. 2Mean temozolomide concentrations. Plasma temozolomide systemic concentrations unchanged with regadenoson treatment (a). Non-contrast enhancing brain interstitium (BI) temozolomide concentration over time failed to increase with regadenoson (b). Contrast enhancing BI temozolomide concentration demonstrated a slight increase in temozolomide concentration over time (c). Error bars represent standard error of mean values