Immunological endpoints
Peanut SPT wheal size decreased significantly from baseline to end-of-treatment (P=0.006) and remained significantly decreased at both 8-weeks post-treatment (P=0.002) and 3-years post-treatment (P=0.001). Similarly, there was significant reduction from baseline in peanut sIgE at end-of-treatment (P=0.0007) that was sustained at 3-years post-treatment (P=0.002). Levels of peanut sIgG4 were significantly increased from baseline at end-of-treatment (P=0.0007) and at 8-weeks post-treatment (P=0.001) (Table 2).
At 3-years post-treatment, participants with persistent SU had lower peanut SPT wheal size (unadjusted P=0.06, age- and sex- adjusted P=0.05) and lower peanut sIgE level (unadjusted P=0.06, age- and sex- adjusted P=0.04) than subjects without persistent SU (Table 3). Corresponding reductions in sIgE and increases in sIgG4 against peanut component (Ara h1, h2, h3) were observed at end-of-treatment and 8-weeks post-treatment (Table S3 in supporting information). There were no significant changes from baseline in Ara h8 and Ara h9 sIgE and sIgG4 levels.
Safety
TEAEs are summarized in Table 4. 17/20 (85%) participants reported a total of 176 treatment-related AE, representing 8.8 AE per participant. No SAEs were reported. Table 5 presents treatment-related AEs reported by at least 10% of the study population. The most frequently reported treatment-related AEs were abdominal pain (49 events) and hypersensitivity (64 events). The majority of treatment-related AEs were mild (93%, 164/176 events). Hypersensitivity was the most frequently reported treatment-related AE of at least moderate intensity (10 events), followed by wheezing and abdominal pain (1 event each). The number of treatment-related AEs by treatment phase were: rush 3 (2%), buildup 110 (63%) and maintenance 63 (35%) (Table S4 and S5 in supporting information).