Time to Resolution of Axitinib-Related Adverse Events After Treatment Interruption in Patients With Advanced Renal Cell Carcinoma.


Journal

Clinical genitourinary cancer
ISSN: 1938-0682
Titre abrégé: Clin Genitourin Cancer
Pays: United States
ID NLM: 101260955

Informations de publication

Date de publication:
10 2021
Historique:
received: 11 12 2020
revised: 19 03 2021
accepted: 27 03 2021
pubmed: 6 5 2021
medline: 28 10 2021
entrez: 5 5 2021
Statut: ppublish

Résumé

Combined axitinib and immuno-oncology (IO) therapy is approved for first-line advanced renal cell carcinoma. Overlapping toxicities represent a clinical challenge. Calculating the time to resolution (TTR) of common axitinib-related adverse events (AEs) after treatment interruption may help to identify AE etiology and determine appropriate management strategies. Data from 5 randomized or single-arm axitinib monotherapy or combination studies were analyzed. Patients with histologically confirmed clear cell advanced renal cell carcinoma were pooled into 3 cohorts based on treatment received: axitinib monotherapy, axitinib + IO, and other tyrosine kinase inhibitor (TKI). Any grade and grade ≥3 treatment-emergent diarrhea, fatigue, hypertension, nausea, and palmar-plantar erythrodysesthesia syndrome were assessed. TTR was defined as the time from treatment interruption/discontinuation to resolution. The axitinib monotherapy cohort comprised 532 patients, the axitinib + IO cohort 541 patients, and the other TKI cohort 882 patients. Median TTR for all AEs (any grade) in the axitinib monotherapy cohort ranged from 1 to 3 days, except for fatigue (8 days). For diarrhea, hypertension, nausea, and palmar-plantar erythrodysesthesia syndrome, median TTRs were longer in the axitinib + IO (4-11 days) and other TKI (7-8 days) cohorts versus the monotherapy cohort. Results were similar when only AEs of grade ≥3 were considered. The TTR of monotherapeutic axitinib-related AEs is ≤3 days, except for fatigue, and generally shorter than for other single-agent TKIs and axitinib + IO. This has important implications for identifying AE etiology with combined axitinib-IO therapy and implementation of appropriate management strategies. ClinicalTrials.org identifiers: NCT00678392, NCT00920816, NCT02493751, NCT02684006, NCT02853331.

Identifiants

pubmed: 33947608
pii: S1558-7673(21)00082-3
doi: 10.1016/j.clgc.2021.03.019
pii:
doi:

Substances chimiques

Protein Kinase Inhibitors 0
Axitinib C9LVQ0YUXG

Banques de données

ClinicalTrials.gov
['NCT02493751', 'NCT02853331', 'NCT02684006', 'NCT00920816']

Types de publication

Journal Article Randomized Controlled Trial Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e306-e312

Informations de copyright

Copyright © 2021 Pfizer. Published by Elsevier Inc. All rights reserved.

Auteurs

Brian I Rini (BI)

Division of Hematology/Oncology, Vanderbilt University Medical Center, and Vanderbilt-Ingram Cancer Center, Nashville, TN. Electronic address: brian.rini@vumc.org.

Michael B Atkins (MB)

Georgetown-Lombardi Comprehensive Cancer Center, Washington, DC.

Toni K Choueiri (TK)

Dana-Farber Cancer Institute, Boston, MA.

Despina Thomaidou (D)

Pfizer Hellas, Athens, Greece.

Brad Rosbrook (B)

Pfizer Global Product Development-Oncology, San Diego, CA 92121.

Maghull Thakur (M)

Pfizer, Discovery Park, Sandwich, UK.

Thomas E Hutson (TE)

Baylor Sammons Cancer Center-Texas Oncology, Dallas, TX.

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Classifications MeSH