Faculty, Staff and Student Publications

Language

English

Publication Date

2-27-2026

DOI

10.1093/oncolo/oyag071

PMID

41761573

Abstract

Background: Dual mitogen-activated protein kinase (MAPK) pathway and autophagy inhibition shows synergistic antitumor activity in preclinical models of RAS-mutant cancers. We hypothesized that autophagy blockade with hydroxychloroquine (HCQ) could overcome resistance to MEK inhibition with binimetinib (BINI) and provide clinical benefit in previously treated, KRAS-mutated, metastatic pancreatic ductal adenocarcinoma (PDAC).

Methods: This investigator-led, single-arm, open-label, phase I dose escalation/expansion trial evaluated the safety and tolerability of BINI + HCQ in patients with previously treated, metastatic PDAC (NCT04132505). Key eligibility criteria: ECOG 0-1, adequate organ function, ≥ 1 prior line of therapy for metastatic disease, and presence of KRAS mutation. Dose escalation followed a Bayesian optimal interval (BOIN) design. The primary endpoint was the maximum tolerated dose (MTD). Secondary endpoints included safety, objective response rate (ORR), disease control rate (DCR), progression-free survival (PFS), and overall survival (OS).

Results: From December 2019 to August 2024, 34 patients were enrolled in dose escalation (n = 17) and dose expansion (n = 17). Two dose-limiting toxicities occurred among the first 3 patients treated at dose level 1 (BINI 45 mg + HCQ 600 mg): grade 3 creatine phosphokinase elevation with renal impairment (BINI) and grade 3 QT prolongation (HCQ). Following dose de-escalation due to poor tolerance, the MTD was determined to be BINI 30 mg + HCQ 600 mg twice daily and used in expansion. Out of 31 response-evaluable patients, 2 patients achieved a partial response and 9 patients achieved stable disease, yielding ORR 6.5% and DCR 35.5%, respectively. Median PFS was 1.9 months, and median OS was 5.3 months.

Conclusion: The combination of BINI + HCQ demonstrated a challenging toxicity profile and limited clinical activity in patients with chemorefractory metastatic PDAC.

Keywords

KRAS, MEK inhibition, autophagy, hydroxychloroquine, pancreatic cancer

Published Open-Access

yes

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