ArticleThe oncologist2026
Phase I trial of binimetinib plus hydroxychloroquine in patients with previously treated metastatic pancreatic cancer.
Article in The oncologist, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04132505 (Binimetinib Plus Hydroxychloroquine in KRAS Mutant Metastatic Pancreatic Cancer), which is not on this map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Binimetinib Plus Hydroxychloroquine in KRAS Mutant Metastatic Pancreatic Cancer
Who cites it
4 citing papers in PubMed.
- Lysosomal metabolism in pancreatic cancer and its crosstalk with host physiology.Genes & development · 2026Review
- Overcoming cancer resistance in pancreatic cancer: toward dynamic precision oncology.Molecular biology reports · 2026Review
- Autophagy inhibition in pancreatic cancer: hope or hype?Autophagy reports · 2026Article
- Bracing for the storm: emerging resistance mechanisms to KRAS inhibitors in pancreatic cancer and strategies to overcome them.Cancer drug resistance (Alhambra, Calif.) · 2026Review
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
backgroundDual mitogen-activated protein kinase (MAPK) pathway and autophagy inhibition show 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).
methodsThis 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 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, and overall survival (OS).
resultsFrom 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 the 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 progression-free survival was 1.9 months, and median OS was 5.3 months.
conclusionThe combination of BINI + HCQ demonstrated a challenging toxicity profile and limited clinical activity in patients with chemorefractory metastatic PDAC.
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