Five-year PFS from the AETHERA trial of brentuximab vedotin for Hodgkin lymphoma at high risk of progression or relapse

Craig H. Moskowitz, Jan Walewski, Auayporn Nademanee, Tamas Masszi, Edward Agura, Jerzy Holowiecki, Muneer H. Abidi, Andy I. Chen, Patrick Stiff, Simonetta Viviani, Veronika Bachanova, Anna Sureda, Teresa McClendon, Connie Lee, Julie Lisano, John Sweetenham

Research output: Contribution to journalArticlepeer-review

50 Scopus citations

Abstract

The phase 3 AETHERA trial established brentuximab vedotin (BV) as a consolidative treatment option for adult patients with classical Hodgkin lymphoma (cHL) at high risk of relapse or progression after autologous hematopoietic stem-cell transplantation (auto-HSCT). Results showed that BV significantly improved progression-free survival (PFS) vs placebo plus best supportive care alone. At 5-year follow-up, BV continued to provide patients with sustained PFS benefit; 5-year PFS was 59% (95% confidence interval [CI], 51-66) with BV vs 41% (95% CI, 33-49) with placebo (hazard ratio [HR], 0.521; 95% CI, 0.379-0.717). Similarly, patients with ‡2 risk factors in the BV arm experienced significantly higher PFS at 5 years than patients in the placebo arm (HR, 0.424; 95% CI, 0.302-0.596). Upfront consolidation with BV significantly delayed time to second subsequent therapy, an indicator of ongoing disease control, vs placebo. Peripheral neuropathy, the most common adverse event in patients receiving BV, continued to improve and/or resolve in 90% of patients. In summary consolidation with BV in adult patients with cHL at high risk of relapse or progression after auto-HSCT confers a sustained PFS benefit and is safe and well tolerated. Physicians should consider each patient's HL risk factor profile when making treatment decisions.

Original languageEnglish (US)
Pages (from-to)2639-2642
Number of pages4
JournalBlood
Volume132
Issue number25
DOIs
StatePublished - Dec 20 2018

Bibliographical note

Funding Information:
Conflict-of-interest disclosure: C.H.M. reports receiving research support from Seattle Genetics and SAB; M.H.A. reports receiving honoraria for speaker engagements from Seattle Genetics; V.B. reports receiving funding from Gamida Cell and scientific advisory fees from Kite Pharma, Inc.; S.V. reports receiving research funding from Takeda and advisory honoraria from Takeda International, Takeda Italia, and Italfarmaco; J.W. reports receiving advisory fees from Takeda, Janssen-Cilag, Roche, Celgene, Amgen, Bristol-Myers Squibb, and Incyte, research/educational grants to his institution from Roche, Janssen-Cilag, Takeda, and GlaxoSmithKline/Novartis, honoraria for speaker engagements from Roche, Takeda, Celgene, Servier, and Janssen-Cilag, and travel grants from Roche and Gilead; T. Masszi reports receiving consultancy fees from AbbVie, Bristol-Myers Squibb, Janssen-Cilag, Novartis, Pfizer, and Takeda; A.S. reports receiving honoraria for speaker engagements from Takeda and scientific advisory honoraria from MSD Pharmaceuticals and Bristol-Myers Squibb; T. McClendon was a paid consultant for Seattle Genetics, Inc., at the time of this writing; J.L. is an employee of Seattle Genetics, Inc.; and C.L. was an employee of Takeda Pharmaceuticals Ltd during development of this manuscript. The remaining authors declare no competing financial interests.

Publisher Copyright:
© 2018 by The American Society of Hematology

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