BackgroundFor patients with psoriatic arthritis (PsA), delays in diagnosis and treatment can lead to permanent radiographic damage, even early in the course of disease.1 In the phase 3 FUTURE 5 study (NCT02404350), treatment with secukinumab (SEC) was shown to inhibit progression of structural damage through Week 104 in patients with PsA.2 However, the effect of disease duration on inhibition of radiographic progression by SEC has not been characterized.ObjectivesThis post hoc analysis explored relationships between time since diagnosis (TSD) of ≤1 year vs >1 year and radiographic progression among patients with PsA receiving SEC over 2 years in FUTURE 5.MethodsPatient data from FUTURE 5 were stratified by TSD ≤1 year vs >1 year and analyzed by treatment arm. Through Week 24, patients received SEC 300 or 150 mg with subcutaneous loading dose (LD), SEC 150 mg without LD, or placebo (PBO) (period 1). After Week 24, patients receiving PBO were switched to SEC 300 or 150 mg (period 2), and a protocol amendment allowed those with suboptimal clinical response to SEC 150 mg to escalate to SEC 300 mg after Week 52 per investigator judgment.2 The proportion of patients with no radiographic progression, defined as change from baseline in van der Heijde total modified Sharp score ≤0.0, was analyzed at Weeks 24, 52, and 104. Mean total Sharp score was evaluated at baseline, and mean change from baseline was determined at Weeks 24, 52, and 104.ResultsOf 996 patients with PsA included here, 217 (21.8%) had a TSD ≤1 year and 779 (78.2%) had a TSD >1 year. At baseline, patients with TSD >1 year had greater radiographic damage than patients with TSD ≤1 year as determined by mean total Sharp score (Table 1). As early as Week 24, patients receiving SEC had less radiographic progression than those receiving PBO, regardless of TSD. From Week 24 to Week 104, radiographic progression remained low among all patients receiving SEC, with a trend of least progression among patients randomized to SEC 300 mg at baseline. Regardless of treatment, patients with TSD >1 year had numerically greater radiographic progression than those patients with TSD ≤1 year. Overall, the proportion of patients receiving SEC who did not have any radiographic progression was higher than that of placebo at Week 24 irrespective of TSD, with a trend towards a higher number of non-progressors among those treated with SEC 300 mg (Figure). Patients randomized to SEC 300 mg were the least likely to experience radiographic progression through 52 weeks.Table 1.Baseline Total Sharp Score and Change From Baseline at Weeks 24, 52, and 104 by TSDTotal Sharp scoreTSD ≤1 yearTSD >1 yearPeriod 1SEC 300 mg n = 54SEC 150 mg n = 46SEC 150 mg NL n = 43PBO n = 74SEC 300 mg n = 168SEC 150 mg n = 174SEC 150 mg NL n = 179PBO n = 258Baseline, mean (SD)8.02 (20.77)8.82 (12.06)12.74 (33.67)8.84 (20.42)14.37 (24.17)14.67 (28.01)15.56 (37.52)17.34 (41.21)Week 24 change from baseline, mean (SD)0.05 (0.72)−0.08 (1.40)−0.61 (5.25)0.76 (2.05)0.09 (1.37)0.23 (1.24)0.03 (2.05)0.42 (1.56)Period 2SEC 300 mg* n = 54SEC 150 mg†n = 46SEC 150 mg NL†n = 43PBO ‒ 300 mg n = 40PBO ‒ 150 mg†n = 30SEC 300 mg* n = 168SEC 150 mg†n = 174SEC 150 mg NL†n = 179PBO ‒ 300 mg n = 113PBO ‒ 150 mg†n = 123Week 52 change from baseline, mean (SD)0.05 (0.48)−0.03 (1.22)0.35 (2.25)0.22 (0.70)0.18 (0.75)−0.07 (1.16)0.26 (1.96)0.26 (1.05)0.16 (0.94)0.40 (2.00)Week 104 change from baseline, mean (SD)0.06 (0.63)0.11 (0.99)0.20 (2.71)0.11 (0.68)−0.07 (0.50)0.11 (2.00)0.62 (2.94)0.46 (2.08)0.12 (0.90)0.81 (2.66)NL, no loading dose; PBO, placebo; SEC, secukinumab; TSD, time since diagnosis.* One outlier in the 300-mg dose group was excluded.† Includes patients who received dose escalation to SEC 300 mg after Week 52.ConclusionSEC resulted in low rates of radiographic progression through 2 years of treatment among patients in FUTURE 5, regardless of time since PsA diagnosis.References[1]Haroon M, et al. Ann Rheum Dis. 2015;74:1045-50.[2]Mease P, et al. RMD Open. 2021;7:e001600.AcknowledgementsThis study was funded by Novartis Pharmaceuticals Corporation. Medical writing support was provided by Richard Karpowicz, PhD, CMPP, of Health Interactions, Inc, and was funded by Novartis Pharmaceuticals Corporation. This abstract was developed in accordance with Good Publication Practice (GPP3) guidelines. Authors had full control of the content and made the final decision on all aspects of this publication.Disclosure of InterestsChristopher T. Ritchlin Consultant of: AbbVie, Amgen, Eli Lilly, Janssen, Pfizer, Novartis, Gilead, and UCB, Ana-Maria Orbai Consultant of: Bristol Myers Squibb, Janssen, Lilly, Novartis, Pfizer, and UCB, Grant/research support from: to Johns Hopkins University from AbbVie, Amgen, Celgene, Horizon, Janssen, Lilly, and Novartis, Bhumik Parikh Employee of: Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA, Corine Gaillez Employee of: Novartis Pharma AG, Basel, Switzerland, Xiangyi Meng Employee of: Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA, Philip J Mease Speakers bureau: AbbVie, Amgen, Janssen, Eli Lilly, Novartis, Pfizer, and UCB, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Galapagos, Gilead, GlaxoSmithKline, Janssen, Eli Lilly, Novartis, Pfizer, Sun Pharma, and UCB, Grant/research support from: AbbVie, Amgen, Bristol Myers Squibb, Celgene, Gilead, Janssen, Eli Lilly, Novartis, Pfizer, Sun Pharma, and UCB