Patient Functioning and Disability among Patients with Migraine: Evaluation of Galcanezumab in a Long-Term, Open-Label Study (4002)

Objective: Evaluate changes from baseline in migraine-specific patient-reported outcomes (PRO) measures of functioning and disability among patients treated with galcanezumab (GMB). Background: Galcanezumab is a humanized monoclonal antibody that binds to calcitonin gene-related peptide which is approved for the prevention of migraine. Design/Methods: CGAJ was a randomized, open-label study on episodic or chronic migraine (12-month open-label treatment phase). Patients aged 18–65 years were randomized 1:1 to subcutaneous GMB 120mg (with a loading dose of 240mg) or GMB 240mg given once monthly for 12 months. PRO measures included Migraine-Specific Quality of Life Questionnaire v2.1 (MSQ; scale: 0–100) and Migraine Disability Assessment (MIDAS; scale: 0–270). Results: 135 patients were randomized to each GMB dose group. 82.6% of patients were females (average age 42 years) with a predominant diagnosis of episodic migraine (78.8%). Mean (SD) baseline MSQ total scores: 53.85 (20.34) [GMB 120mg] and 53.69 (18.79) [GMB 240mg]. Overall least squares (LS) mean change±SE from baseline across the entire 12-month treatment phase in MSQ total scores: 28.27±1.16 (GMB 120mg) and 30.25±1.13 (GMB 240mg). Greatest improvement was observed in the RF-R domain, 31.55±1.20 (GMB 120mg) and 33.40±1.16 (GMB 240mg). For MIDAS, mean (SD) baseline total scores were 45.77 (42.06) [GMB 120mg] and 53.96 (61.24) [GMB 240mg], overall LS mean change ±SE from baseline across the entire 12-month treatment phase in total scores were −33.58±2.11 (GMB 120mg) and −32.67±2.04 (GMB 240mg). Within-group mean improvement from baseline on MSQ, MIDAS total scores, and all individual item/domain scores were statistically significant for both GMB groups at all time-points during the treatment phase (p Conclusions: Galcanezumab-treated patients had improved functioning and reduced disability with clinically meaningful and statistically significant changes from baseline overall across the entire treatment phase. Disclosure: Dr. McAllister has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Amgen Inc., Teva Neuroscience, Alder, Promius, Electrocore, and Allergen, Inc. Dr. McAllister has received personal compensation in an editorial capacity for Practical Neurology. Dr. McAllister has received research support from Alder, Amgen Inc., Teva Neuroscience, Sunovion, San-bio, Biohaven, Allergan, Inc., Novartis, ATI, Roche Diagnostics Corporation, Esai Inc., and Biogen Idec.Dr. Ford has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Eli Lilly and Company (Dr. Ford is an employee). Dr. Ford holds stock and/or stock options in Eli Lilly and Company. Dr. Ford has received research support from Eli Lilly and Company. Dr. Stauffer has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Employee of Eli Lilly and Company. Dr. Stauffer holds stock and/or stock options in Minor stockholder of Eli Lilly and Company which sponsored research in which Dr. Stauffer was involved as an investigator. Dr. Stauffer holds stock and/or stock options in Eli Lilly and Company as minor stockholder. Dr. Sexson has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Eli Lilly and Company. Dr. Ayer has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Eli Lilly & Company. Dr. Ayer has received research support from Eli Lilly & Company. Dr. Wang has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Eli Lilly and Company.