Derazantinib (ARQ 087) in advanced or inoperable FGFR2 gene fusion-positive intrahepatic cholangiocarcinoma.


Journal

British journal of cancer
ISSN: 1532-1827
Titre abrégé: Br J Cancer
Pays: England
ID NLM: 0370635

Informations de publication

Date de publication:
01 2019
Historique:
received: 29 06 2018
accepted: 23 10 2018
revised: 19 10 2018
pubmed: 14 11 2018
medline: 21 9 2019
entrez: 14 11 2018
Statut: ppublish

Résumé

Next-generation sequencing has identified actionable genetic aberrations in intrahepatic cholangiocarcinomas (iCCA), including the fibroblast growth factor receptor 2 (FGFR2) fusions. Derazantinib (ARQ 087), an orally bioavailable, multi-kinase inhibitor with potent pan-FGFR activity, has shown preliminary therapeutic activity against FGFR2 fusion-positive iCCA. This multicentre, phase 1/2, open-label study enrolled adult patients with unresectable iCCA with FGFR2 fusion, who progressed, were intolerant or not eligible to first-line chemotherapy (NCT01752920). Subjects received derazantinib in continuous daily doses. Tumour response was assessed according to RECIST 1.1 every 8 weeks. Twenty-nine patients (18 women/11 men; median age, 58.7 years), 2 treatment-naive and 27 who progressed after at least one prior systemic therapy, were enrolled. Overall response rate was 20.7%, disease control rate was 82.8%. Estimated median progression-free survival was 5.7 months (95% CI: 4.04-9.2 months). Treatment-related adverse events (AE) were observed in 27 patients (93.1%, all grades), including asthenia/fatigue (69.0%), eye toxicity (41.4%), and hyperphosphatemia (75.9%). Grade ≥ 3 AEs occurred in 8 patients (27.6%). Derazantinib demonstrated encouraging anti-tumour activity and a manageable safety profile in patients with advanced, unresectable iCCA with FGFR2 fusion who progressed after chemotherapy. A pivotal trial of derazantinib in iCCA is ongoing (NCT03230318).

Sections du résumé

BACKGROUND
Next-generation sequencing has identified actionable genetic aberrations in intrahepatic cholangiocarcinomas (iCCA), including the fibroblast growth factor receptor 2 (FGFR2) fusions. Derazantinib (ARQ 087), an orally bioavailable, multi-kinase inhibitor with potent pan-FGFR activity, has shown preliminary therapeutic activity against FGFR2 fusion-positive iCCA.
METHODS
This multicentre, phase 1/2, open-label study enrolled adult patients with unresectable iCCA with FGFR2 fusion, who progressed, were intolerant or not eligible to first-line chemotherapy (NCT01752920). Subjects received derazantinib in continuous daily doses. Tumour response was assessed according to RECIST 1.1 every 8 weeks.
RESULTS
Twenty-nine patients (18 women/11 men; median age, 58.7 years), 2 treatment-naive and 27 who progressed after at least one prior systemic therapy, were enrolled. Overall response rate was 20.7%, disease control rate was 82.8%. Estimated median progression-free survival was 5.7 months (95% CI: 4.04-9.2 months). Treatment-related adverse events (AE) were observed in 27 patients (93.1%, all grades), including asthenia/fatigue (69.0%), eye toxicity (41.4%), and hyperphosphatemia (75.9%). Grade ≥ 3 AEs occurred in 8 patients (27.6%).
CONCLUSION
Derazantinib demonstrated encouraging anti-tumour activity and a manageable safety profile in patients with advanced, unresectable iCCA with FGFR2 fusion who progressed after chemotherapy. A pivotal trial of derazantinib in iCCA is ongoing (NCT03230318).

Identifiants

pubmed: 30420614
doi: 10.1038/s41416-018-0334-0
pii: 10.1038/s41416-018-0334-0
pmc: PMC6342954
doi:

Substances chimiques

Alkaloids 0
Oncogene Proteins, Fusion 0
Protein Kinase Inhibitors 0
dercitin 115141-47-4
FGFR2 protein, human EC 2.7.10.1
Receptor, Fibroblast Growth Factor, Type 2 EC 2.7.10.1

Banques de données

ClinicalTrials.gov
['NCT03230318']

Types de publication

Clinical Study Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

165-171

Commentaires et corrections

Type : CommentIn

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Auteurs

Vincenzo Mazzaferro (V)

Department of Surgery and Oncology, Istituto Nazionale Tumori IRCCS, Milan, Italy. vincenzo.mazzaferro@istitutotumori.mi.it.
University of Milan, Milan, Italy. vincenzo.mazzaferro@istitutotumori.mi.it.

Bassel F El-Rayes (BF)

Winship Cancer Institute, Emory University, Atlanta, GA, USA. belraye@emory.edu.

Michele Droz Dit Busset (M)

Department of Surgery and Oncology, Istituto Nazionale Tumori IRCCS, Milan, Italy.

Christian Cotsoglou (C)

Department of Surgery and Oncology, Istituto Nazionale Tumori IRCCS, Milan, Italy.

William P Harris (WP)

Seattle Cancer Care Alliance, Seattle, WA, USA.

Nevena Damjanov (N)

Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA, USA.

Gianluca Masi (G)

Department of Oncology, Pisa University Hospital, Pisa, Italy.

Lorenza Rimassa (L)

Humanitas Cancer Center, Humanitas Clinical and Research Center, Rozzano, Milan, Italy.

Nicola Personeni (N)

Humanitas Cancer Center, Humanitas Clinical and Research Center, Rozzano, Milan, Italy.
Department of Medical Biosciences, Humanitas University, Pieve Emanuele, Milan, Italy.

Fadi Braiteh (F)

Medical Oncology, Comprehensive Cancer Centers of Nevada, Las Vegas, NV, USA.

Vittorina Zagonel (V)

Veneto Institute of Oncology IOV - IRCCS, Padua, Italy.

Kyriakos P Papadopoulos (KP)

South Texas Accelerated Research Therapeutics, San Antonio, TX, USA.

Terence Hall (T)

ArQule, Inc, Burlington, MA, USA.

Yunxia Wang (Y)

ArQule, Inc, Burlington, MA, USA.

Brian Schwartz (B)

ArQule, Inc, Burlington, MA, USA.

Julia Kazakin (J)

ArQule, Inc, Burlington, MA, USA.

Sherrie Bhoori (S)

Department of Surgery and Oncology, Istituto Nazionale Tumori IRCCS, Milan, Italy.

Filippo de Braud (F)

Department of Surgery and Oncology, Istituto Nazionale Tumori IRCCS, Milan, Italy.
University of Milan, Milan, Italy.

Walid L Shaib (WL)

Winship Cancer Institute, Emory University, Atlanta, GA, USA.

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Classifications MeSH