brodalumab was 43% (3/7), whereas 39% (5/13) of those with 2 prior biologic treatments and 58% (7/12) of those with 3 prior biologic treatments achieved PASI 90 with brodalumab. Moreover, two-thirds of those treated with 6 previous biologics (67% [2/3]) achieved PASI 90 with brodalumab.24 Patients switching from secukinumab to brodalumab were more likely to achieve PASI 100 (57% [8/14]) compared with those switching from ixekizumab (31% [4/13]). Secondary nonresponders (ie, those with loss of IL-17A–antagonist treatment response after achieving PASI 75 at weeks 12 to 16) also had a greater rate of PASI 100 compared with primary nonresponders (ie, those who did not achieve PASI 75 at weeks 12 to 16), with differences observed when stratified by prior biologic treatment. Whereas 62% (13/21) and 44% (10/23) of secondary nonresponders to secukinumab and ixekizumab, respectively, achieved PASI 100 with brodalumab, 25% (3/12) and 13% (1/8) of primary nonresponders achieved PASI 100 with brodalumab. This study provides real-world evidence that a meaningful proportion of patients may experience substantial or even complete clearance of psoriatic lesions when switching to brodalumab after failure with other IL-17 biologics.
Brodalumab Has Long-term Effectiveness After Failure of TNFα Inhibitors
The TNFα inhibitor adalimumab is a commonly prescribed biologic for the treatment of several autoimmune disorders, including plaque psoriasis.29 Treatment history of adalimumab was analyzed in post hoc analyses of phase 3 brodalumab trials. Among 3712 patients in the AMAGINE-2/-3 trials, 386 (10%) received prior adalimumab; of these, 199 (52%) did not respond to adalimumab treatment. At 120 weeks of continuous brodalumab treatment, 88%, 73%, and 52% of adalimumab nonresponders achieved PASI 75, PASI 90, and PASI 100, respectively. Notably, treatment success was similar in patients whose disease responded to prior adalimumab treatment (74%, 67%, and 44% for PASI 75, PASI 90, and PASI 100, respectively).2,30,31 Furthermore, in adalimumab nonresponders, brodalumab was associated with greater skin clearance compared with ustekinumab at week 52; whereas 41% of adalimumab nonresponders treated with brodalumab achieved PASI 100, complete skin clearance was seen in only 8% of adalimumab nonresponders treated with ustekinumab.32
Brodalumab Produces Treatment Response in Patients Previously Treated With IL-12/IL-23 Inhibitors
Ustekinumab modulates inflammation by binding to a subunit common to IL-12 and IL-23 and is approved for the treatment of moderate-to-severe psoriasis in patients who are candidates for systemic therapy.33,34 In the AMAGINE-2/-3 trials, ustekinumab was utilized as a head-to-head comparator of brodalumab. Initially, patients were randomized to brodalumab (1 of 2 regimens), ustekinumab, or placebo for a 12-week induction period. At week 12, patients receiving brodalumab were rerandomized to 1 of 4 brodalumab regimens, those receiving placebo switched to brodalumab, and those receiving ustekinumab remained on ustekinumab through week 52. However, patients receiving ustekinumab were “rescued” with brodalumab at week 16 if they had inadequate treatment response (defined as a static
Brodalumab Has Long-term Effectiveness After Failure of TNFα Inhibitors
The TNFα inhibitor adalimumab is a commonly prescribed biologic for the treatment of several autoimmune disorders, including plaque psoriasis.29 Treatment history of adalimumab was analyzed in post hoc analyses of phase 3 brodalumab trials. Among 3712 patients in the AMAGINE-2/-3 trials, 386 (10%) received prior adalimumab; of these, 199 (52%) did not respond to adalimumab treatment. At 120 weeks of continuous brodalumab treatment, 88%, 73%, and 52% of adalimumab nonresponders achieved PASI 75, PASI 90, and PASI 100, respectively. Notably, treatment success was similar in patients whose disease responded to prior adalimumab treatment (74%, 67%, and 44% for PASI 75, PASI 90, and PASI 100, respectively).2,30,31 Furthermore, in adalimumab nonresponders, brodalumab was associated with greater skin clearance compared with ustekinumab at week 52; whereas 41% of adalimumab nonresponders treated with brodalumab achieved PASI 100, complete skin clearance was seen in only 8% of adalimumab nonresponders treated with ustekinumab.32
Brodalumab Produces Treatment Response in Patients Previously Treated With IL-12/IL-23 Inhibitors
Ustekinumab modulates inflammation by binding to a subunit common to IL-12 and IL-23 and is approved for the treatment of moderate-to-severe psoriasis in patients who are candidates for systemic therapy.33,34 In the AMAGINE-2/-3 trials, ustekinumab was utilized as a head-to-head comparator of brodalumab. Initially, patients were randomized to brodalumab (1 of 2 regimens), ustekinumab, or placebo for a 12-week induction period. At week 12, patients receiving brodalumab were rerandomized to 1 of 4 brodalumab regimens, those receiving placebo switched to brodalumab, and those receiving ustekinumab remained on ustekinumab through week 52. However, patients receiving ustekinumab were “rescued” with brodalumab at week 16 if they had inadequate treatment response (defined as a static
