Trial of Upadacitinib or Abatacept in Rheumatoid Arthritis.


Journal

The New England journal of medicine
ISSN: 1533-4406
Titre abrégé: N Engl J Med
Pays: United States
ID NLM: 0255562

Informations de publication

Date de publication:
15 10 2020
Historique:
entrez: 14 10 2020
pubmed: 15 10 2020
medline: 28 10 2020
Statut: ppublish

Résumé

Upadacitinib is an oral selective Janus kinase inhibitor to treat rheumatoid arthritis. The efficacy and safety of upadacitinib as compared with abatacept, a T-cell costimulation modulator, in patients with rheumatoid arthritis refractory to biologic disease-modifying antirheumatic drugs (DMARDs) are unclear. In this 24-week, phase 3, double-blind, controlled trial, we randomly assigned patients in a 1:1 ratio to receive oral upadacitinib (15 mg once daily) or intravenous abatacept, each in combination with stable synthetic DMARDs. The primary end point was the change from baseline in the composite Disease Activity Score for 28 joints based on the C-reactive protein level (DAS28-CRP; range, 0 to 9.4, with higher scores indicating more disease activity) at week 12, assessed for noninferiority. Key secondary end points at week 12 were the superiority of upadacitinib over abatacept in the change from baseline in the DAS28-CRP and the percentage of patients having clinical remission according to a DAS28-CRP of less than 2.6. A total of 303 patients received upadacitinib, and 309 patients received abatacept. From baseline DAS28-CRP values of 5.70 in the upadacitinib group and 5.88 in the abatacept group, the mean change at week 12 was -2.52 and -2.00, respectively (difference, -0.52 points; 95% confidence interval [CI], -0.69 to -0.35; P<0.001 for noninferiority; P<0.001 for superiority). The percentage of patients having remission was 30.0% with upadacitinib and 13.3% with abatacept (difference, 16.8 percentage points; 95% CI, 10.4 to 23.2; P<0.001 for superiority). During the treatment period, one death, one nonfatal stroke, and two venous thromboembolic events occurred in the upadacitinib group, and more patients in the upadacitinib group than in the abatacept group had elevated hepatic aminotransferase levels. In patients with rheumatoid arthritis refractory to biologic DMARDs, upadacitinib was superior to abatacept in the change from baseline in the DAS28-CRP and the achievement of remission at week 12 but was associated with more serious adverse events. Longer and larger trials are required in order to determine the effect and safety of upadacitinib in patients with rheumatoid arthritis. (Funded by AbbVie; SELECT-CHOICE Clinicaltrials.gov number, NCT03086343.).

Sections du résumé

BACKGROUND
Upadacitinib is an oral selective Janus kinase inhibitor to treat rheumatoid arthritis. The efficacy and safety of upadacitinib as compared with abatacept, a T-cell costimulation modulator, in patients with rheumatoid arthritis refractory to biologic disease-modifying antirheumatic drugs (DMARDs) are unclear.
METHODS
In this 24-week, phase 3, double-blind, controlled trial, we randomly assigned patients in a 1:1 ratio to receive oral upadacitinib (15 mg once daily) or intravenous abatacept, each in combination with stable synthetic DMARDs. The primary end point was the change from baseline in the composite Disease Activity Score for 28 joints based on the C-reactive protein level (DAS28-CRP; range, 0 to 9.4, with higher scores indicating more disease activity) at week 12, assessed for noninferiority. Key secondary end points at week 12 were the superiority of upadacitinib over abatacept in the change from baseline in the DAS28-CRP and the percentage of patients having clinical remission according to a DAS28-CRP of less than 2.6.
RESULTS
A total of 303 patients received upadacitinib, and 309 patients received abatacept. From baseline DAS28-CRP values of 5.70 in the upadacitinib group and 5.88 in the abatacept group, the mean change at week 12 was -2.52 and -2.00, respectively (difference, -0.52 points; 95% confidence interval [CI], -0.69 to -0.35; P<0.001 for noninferiority; P<0.001 for superiority). The percentage of patients having remission was 30.0% with upadacitinib and 13.3% with abatacept (difference, 16.8 percentage points; 95% CI, 10.4 to 23.2; P<0.001 for superiority). During the treatment period, one death, one nonfatal stroke, and two venous thromboembolic events occurred in the upadacitinib group, and more patients in the upadacitinib group than in the abatacept group had elevated hepatic aminotransferase levels.
CONCLUSIONS
In patients with rheumatoid arthritis refractory to biologic DMARDs, upadacitinib was superior to abatacept in the change from baseline in the DAS28-CRP and the achievement of remission at week 12 but was associated with more serious adverse events. Longer and larger trials are required in order to determine the effect and safety of upadacitinib in patients with rheumatoid arthritis. (Funded by AbbVie; SELECT-CHOICE Clinicaltrials.gov number, NCT03086343.).

Identifiants

pubmed: 33053283
doi: 10.1056/NEJMoa2008250
doi:

Substances chimiques

Antirheumatic Agents 0
Heterocyclic Compounds, 3-Ring 0
Inducible T-Cell Co-Stimulator Protein 0
Janus Kinase Inhibitors 0
upadacitinib 4RA0KN46E0
Abatacept 7D0YB67S97
C-Reactive Protein 9007-41-4

Banques de données

ClinicalTrials.gov
['NCT03086343']

Types de publication

Clinical Trial, Phase III Comparative Study Journal Article Multicenter Study Randomized Controlled Trial Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1511-1521

Commentaires et corrections

Type : CommentIn
Type : CommentIn
Type : CommentIn

Informations de copyright

Copyright © 2020 Massachusetts Medical Society.

Auteurs

Andrea Rubbert-Roth (A)

From the Division of Rheumatology, Cantonal Clinic St. Gallen, St. Gallen, Switzerland (A.R.-R.); AbbVie, North Chicago, IL (J.E., A.L.P., N.K., Y.Z., N.M.); Centre Hospitalier de l'Université de Montréal, Montreal (B.H.); Queen Elizabeth Hospital and University of Adelaide, Adelaide, SA, Australia (M.R.); and Universidade Federal do Rio Grande do Sul, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil (R.M.X.).

Jeffrey Enejosa (J)

From the Division of Rheumatology, Cantonal Clinic St. Gallen, St. Gallen, Switzerland (A.R.-R.); AbbVie, North Chicago, IL (J.E., A.L.P., N.K., Y.Z., N.M.); Centre Hospitalier de l'Université de Montréal, Montreal (B.H.); Queen Elizabeth Hospital and University of Adelaide, Adelaide, SA, Australia (M.R.); and Universidade Federal do Rio Grande do Sul, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil (R.M.X.).

Aileen L Pangan (AL)

From the Division of Rheumatology, Cantonal Clinic St. Gallen, St. Gallen, Switzerland (A.R.-R.); AbbVie, North Chicago, IL (J.E., A.L.P., N.K., Y.Z., N.M.); Centre Hospitalier de l'Université de Montréal, Montreal (B.H.); Queen Elizabeth Hospital and University of Adelaide, Adelaide, SA, Australia (M.R.); and Universidade Federal do Rio Grande do Sul, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil (R.M.X.).

Boulos Haraoui (B)

From the Division of Rheumatology, Cantonal Clinic St. Gallen, St. Gallen, Switzerland (A.R.-R.); AbbVie, North Chicago, IL (J.E., A.L.P., N.K., Y.Z., N.M.); Centre Hospitalier de l'Université de Montréal, Montreal (B.H.); Queen Elizabeth Hospital and University of Adelaide, Adelaide, SA, Australia (M.R.); and Universidade Federal do Rio Grande do Sul, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil (R.M.X.).

Maureen Rischmueller (M)

From the Division of Rheumatology, Cantonal Clinic St. Gallen, St. Gallen, Switzerland (A.R.-R.); AbbVie, North Chicago, IL (J.E., A.L.P., N.K., Y.Z., N.M.); Centre Hospitalier de l'Université de Montréal, Montreal (B.H.); Queen Elizabeth Hospital and University of Adelaide, Adelaide, SA, Australia (M.R.); and Universidade Federal do Rio Grande do Sul, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil (R.M.X.).

Nasser Khan (N)

From the Division of Rheumatology, Cantonal Clinic St. Gallen, St. Gallen, Switzerland (A.R.-R.); AbbVie, North Chicago, IL (J.E., A.L.P., N.K., Y.Z., N.M.); Centre Hospitalier de l'Université de Montréal, Montreal (B.H.); Queen Elizabeth Hospital and University of Adelaide, Adelaide, SA, Australia (M.R.); and Universidade Federal do Rio Grande do Sul, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil (R.M.X.).

Ying Zhang (Y)

From the Division of Rheumatology, Cantonal Clinic St. Gallen, St. Gallen, Switzerland (A.R.-R.); AbbVie, North Chicago, IL (J.E., A.L.P., N.K., Y.Z., N.M.); Centre Hospitalier de l'Université de Montréal, Montreal (B.H.); Queen Elizabeth Hospital and University of Adelaide, Adelaide, SA, Australia (M.R.); and Universidade Federal do Rio Grande do Sul, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil (R.M.X.).

Naomi Martin (N)

From the Division of Rheumatology, Cantonal Clinic St. Gallen, St. Gallen, Switzerland (A.R.-R.); AbbVie, North Chicago, IL (J.E., A.L.P., N.K., Y.Z., N.M.); Centre Hospitalier de l'Université de Montréal, Montreal (B.H.); Queen Elizabeth Hospital and University of Adelaide, Adelaide, SA, Australia (M.R.); and Universidade Federal do Rio Grande do Sul, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil (R.M.X.).

Ricardo M Xavier (RM)

From the Division of Rheumatology, Cantonal Clinic St. Gallen, St. Gallen, Switzerland (A.R.-R.); AbbVie, North Chicago, IL (J.E., A.L.P., N.K., Y.Z., N.M.); Centre Hospitalier de l'Université de Montréal, Montreal (B.H.); Queen Elizabeth Hospital and University of Adelaide, Adelaide, SA, Australia (M.R.); and Universidade Federal do Rio Grande do Sul, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil (R.M.X.).

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