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Diabetes

A real-world analysis of glycemic control among patients with type 2 diabetes treated with canagliflozin versus dapagliflozin

, , , , &
Pages 1143-1152 | Received 22 Feb 2018, Accepted 26 Mar 2018, Published online: 20 Apr 2018
 

Abstract

Objective: This US retrospective cohort study compared the real-world effectiveness of canagliflozin 300 mg versus dapagliflozin 10 mg on HbA1c reduction in patients with type 2 diabetes mellitus (T2DM).

Methods: Patients initiated on canagliflozin 300 mg or dapagliflozin 10 mg were identified from de-identified claims data in the Optum Clinformatics database (1 January 2014–30 September 2016). Propensity score matching was used to create balanced cohorts. The primary outcome was the proportion of patients with HbA1c <8.0% (HEDIS target); secondary outcomes included the proportion of patients with HbA1c <7.0% (ADA target) and >9.0% (HEDIS poor control), absolute change in HbA1c, and treatment patterns.

Results: At 6 months post-index (intent-to-treat population), a significantly higher proportion of patients in the canagliflozin 300 mg versus dapagliflozin 10 mg cohort achieved HbA1c <8.0% (70.8% vs. 59.1%; OR [95% CI]: 1.60 [1.26, 2.04]; p = .0001) and HbA1c <7.0% (36.7% vs. 25.1%; OR [95% CI]: 1.75 [1.34, 2.27]; p < .0001). A similar proportion of patients had HbA1c >9.0%. Mean HbA1c reduction was −1.17% with canagliflozin 300 mg and −0.91% with dapagliflozin 10 mg (difference of −0.26%; p = .0049). HbA1c results from a sensitivity analysis in the on-treatment population were consistent with the primary analysis. Patients in the canagliflozin 300 mg versus dapagliflozin 10 mg cohort were less likely to discontinue treatment (OR [95% CI]: 0.75 [0.57, 0.99]; p = .0400) or switch medication (OR [95% CI]: 0.72 [0.54, 0.96]; p = .0229).

Conclusions: In this real-world study, patients with T2DM initiated on canagliflozin 300 mg had better HbA1c goal attainment and larger HbA1c reduction than patients initiated on dapagliflozin 10 mg.

Transparency

Declaration of funding

This study was supported by Janssen Scientific Affairs, LLC. Canagliflozin has been developed by Janssen Research & Development, LLC, in collaboration with Mitsubishi Tanabe Pharma Corporation.

Author contributions: L.B., C.P., B.B., M.P., Y.C. and B.W. were responsible for study design and data interpretation. Y.C. and B.W. performed the analyses. All authors contributed to the development of this manuscript and have fulfilled all International Committee of Medical Journal Editor (ICMJE) authorship requirements.

Declaration of financial/other relationships

L.B. has disclosed that he has served as an investigator for AstraZeneca, Janssen Pharmaceuticals Inc., Lexicon Pharmaceuticals Inc., Merck & Co., Novo Nordisk and Sanofi; has served as a speaker for AstraZeneca, Janssen Pharmaceuticals Inc., Novo Nordisk and Sanofi; and has served as a consultant for Intarcia Therapeutics Inc., Janssen Pharmaceuticals Inc., Merck & Co., Novo Nordisk and Sanofi. C.P., B.B., M.P., Y.C. and B.W. have disclosed that they are full-time employees of Janssen Scientific Affairs LLC. B.B. and M.P. have disclosed that they own Johnson & Johnson stock.

CMRO peer reviewers on this manuscript have received an honorarium from CMRO for their review work, but have no relevant financial or other relationships to disclose.

Acknowledgements

The authors thank Titilayo Kazeem and Chris Pericone of Janssen Scientific Affairs, LLC, for their contributions to the study design, analyses and data interpretation. Data programming support was provided by Kamal Kant Mangla and Ankur Mishra of Mu Sigma Business Solutions Pvt Ltd. The manuscript, including writing support provided by Dana Tabor, PhD, of MedErgy, was funded by Janssen Scientific Affairs, LLC.

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