Deep, rapid, and durable prostate-specific antigen decline with apalutamide plus androgen deprivation therapy is associated with longer survival and improved clinical outcomes in TITAN patients with metastatic castration-sensitive prostate cancer.


Journal

Annals of oncology : official journal of the European Society for Medical Oncology
ISSN: 1569-8041
Titre abrégé: Ann Oncol
Pays: England
ID NLM: 9007735

Informations de publication

Date de publication:
05 2023
Historique:
received: 18 08 2022
revised: 17 02 2023
accepted: 20 02 2023
medline: 2 5 2023
pubmed: 2 3 2023
entrez: 1 3 2023
Statut: ppublish

Résumé

The first interim analysis of the phase III, randomized, double-blind, placebo-controlled, multinational TITAN study demonstrated improved overall survival (OS) and radiographic progression-free survival (rPFS) with apalutamide added to ongoing androgen deprivation therapy (ADT) in patients with metastatic castration-sensitive prostate cancer. The final analysis confirmed improvement in OS and other long-term outcomes. We evaluated prostate-specific antigen (PSA) kinetics and the association between PSA decline and outcomes in patients with metastatic castration-sensitive prostate cancer from TITAN. Patients received apalutamide (240 mg/day) or placebo plus ADT (1 : 1). This post hoc exploratory analysis evaluated PSA kinetics and decline in relation to rPFS (22.7 months' follow-up) and OS, time to PSA progression, and time to castration resistance (44.0 months' follow-up) in patients with or without confirmed PSA decline using a landmark analysis, the Kaplan-Meier method, and Cox proportional hazards model. One thousand and fifty-two patients (apalutamide, 525; placebo, 527) were enrolled. Best confirmed PSA declines (≥50% or ≥90% from baseline or to ≤0.2 ng/ml) were achieved at any time during the study in 90%, 73%, and 68% of apalutamide-treated versus 55%, 29%, and 32% of placebo-treated patients, respectively. By 3 months of apalutamide treatment, best deep PSA decline of ≥90% or to ≤0.2 ng/ml occurred in 59% and 51% of apalutamide- and in 13% and 18% of placebo-treated patients, respectively. Achievement of deep PSA decline at landmark 3 months of apalutamide treatment was associated with longer OS [hazard ratio (HR) 0.35; 95% confidence interval (CI) 0.25-0.48), rPFS (HR 0.44; 95% CI 0.30-0.65), time to PSA progression (HR 0.31; 95% CI 0.22-0.44), and time to castration resistance (HR 0.38; 95% CI 0.27-0.52) compared with no decline (P < 0.0001 for all). Similar results were observed at landmark 6 and 12 months of apalutamide treatment. Apalutamide plus ADT demonstrated a robust (rapid, deep, and durable) PSA decline that was associated with improved clinical outcomes, including long-term survival.

Sections du résumé

BACKGROUND
The first interim analysis of the phase III, randomized, double-blind, placebo-controlled, multinational TITAN study demonstrated improved overall survival (OS) and radiographic progression-free survival (rPFS) with apalutamide added to ongoing androgen deprivation therapy (ADT) in patients with metastatic castration-sensitive prostate cancer. The final analysis confirmed improvement in OS and other long-term outcomes. We evaluated prostate-specific antigen (PSA) kinetics and the association between PSA decline and outcomes in patients with metastatic castration-sensitive prostate cancer from TITAN.
PATIENTS AND METHODS
Patients received apalutamide (240 mg/day) or placebo plus ADT (1 : 1). This post hoc exploratory analysis evaluated PSA kinetics and decline in relation to rPFS (22.7 months' follow-up) and OS, time to PSA progression, and time to castration resistance (44.0 months' follow-up) in patients with or without confirmed PSA decline using a landmark analysis, the Kaplan-Meier method, and Cox proportional hazards model.
RESULTS
One thousand and fifty-two patients (apalutamide, 525; placebo, 527) were enrolled. Best confirmed PSA declines (≥50% or ≥90% from baseline or to ≤0.2 ng/ml) were achieved at any time during the study in 90%, 73%, and 68% of apalutamide-treated versus 55%, 29%, and 32% of placebo-treated patients, respectively. By 3 months of apalutamide treatment, best deep PSA decline of ≥90% or to ≤0.2 ng/ml occurred in 59% and 51% of apalutamide- and in 13% and 18% of placebo-treated patients, respectively. Achievement of deep PSA decline at landmark 3 months of apalutamide treatment was associated with longer OS [hazard ratio (HR) 0.35; 95% confidence interval (CI) 0.25-0.48), rPFS (HR 0.44; 95% CI 0.30-0.65), time to PSA progression (HR 0.31; 95% CI 0.22-0.44), and time to castration resistance (HR 0.38; 95% CI 0.27-0.52) compared with no decline (P < 0.0001 for all). Similar results were observed at landmark 6 and 12 months of apalutamide treatment.
CONCLUSIONS
Apalutamide plus ADT demonstrated a robust (rapid, deep, and durable) PSA decline that was associated with improved clinical outcomes, including long-term survival.

Identifiants

pubmed: 36858151
pii: S0923-7534(23)00086-8
doi: 10.1016/j.annonc.2023.02.009
pii:
doi:

Substances chimiques

Prostate-Specific Antigen EC 3.4.21.77
apalutamide 0
Androgen Antagonists 0
Androgens 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

477-485

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.

Auteurs

S Chowdhury (S)

Department of Urological Cancer, Guy's, King's and St Thomas' Hospitals, London; Sarah Cannon Research Institute, London, UK. Electronic address: simonchowdhuryuk@yahoo.co.uk.

A Bjartell (A)

Department of Urology, Skåne University Hospital, Lund University, Malmö, Sweden.

N Agarwal (N)

Department of Genitourinary Oncology, Huntsman Cancer Institute, University of Utah, Salt Lake City, USA.

B H Chung (BH)

Department of Urology, Yonsei University College of Medicine and Gangnam Severance Hospital, Seoul, South Korea.

R W Given (RW)

Department of Urology, Urology of Virginia, Eastern Virginia Medical School, Norfolk, USA.

A J Pereira de Santana Gomes (AJ)

Department of Clinical Oncology, Liga Norte Riograndense Contra O Cancer, Natal, Brazil.

A S Merseburger (AS)

Department of Urology, University Hospital Schleswig-Holstein, Campus Lübeck, Lübeck, Germany.

M Özgüroğlu (M)

Department of Oncology, Cerrahpaşa School of Medicine, Istanbul University-Cerrahpaşa, Istanbul, Turkey.

Á Juárez Soto (Á)

Department of Urology, Hospital Universitario de Jerez de la Frontera, Cadiz, Spain.

H Uemura (H)

Department of Medicine, Kindai University Faculty of Medicine, Osaka, Japan.

D Ye (D)

Department of Urology, Fudan University Shanghai Cancer Center, Shanghai, People's Republic of China.

S D Brookman-May (SD)

Janssen Research & Development, Spring House, USA; Ludwig-Maximilians-University (LMU), Munich, Germany.

A Londhe (A)

Janssen Research & Development, Titusville.

A Bhaumik (A)

Janssen Research & Development, Titusville.

S D Mundle (SD)

Janssen Research & Development, Raritan.

J S Larsen (JS)

Janssen Research & Development, Los Angeles, USA.

S A McCarthy (SA)

Janssen Research & Development, Raritan.

K N Chi (KN)

Department of Medicine, BC Cancer and Vancouver Prostate Centre, Vancouver, Canada.

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