Evidence map›Paper›PMID 42396524›Full record

ArticleResearch square2026

Alirocumab Plus Cemiplimab in Immunorefractory NSCLC: A Single Arm Phase 2 Study.

Eziafa Oduah, Jhanelle Gray, Thomas Stinchcombe, Steven Wolf, Xiaodi Qin, Abbie Ireland, Joel Rivera-Concepcion, Jeffrey Clarke, Jeffrey Crawford, Laura Alder and 10 more

Abstract readPreprint
In one paragraph

Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors.

Eziafa OduahDuke Cancer Institute, Duke University School of Medicine.
Jhanelle GrayMoffitt Cancer Center.
Thomas StinchcombeDuke Cancer Institute.ORCID 0000-0002-3595-8011
Steven WolfDuke Cancer Institute, Duke University.
Abbie IrelandDuke Cancer Institute, Duke University School of Medicine.
Joel Rivera-ConcepcionDuke Cancer Institute, Duke University Health System.
Jeffrey ClarkeDuke Cancer Institute.
Jeffrey CrawfordDuke Cancer Institute, Duke university School of Medicine.
Laura AlderDuke Cancer Institute, Duke university School of Medicine.
Cameron OswaltDuke Cancer Institute, Duke university School of Medicine.
Alan ChenDuke Cancer Institute, Duke university School of Medicine.
Liliana LynivDuke Cancer Institute, Duke university School of Medicine.
Aamna AbbasiDuke Cancer Institute, Duke University.
Andreas SaltosH. Lee Moffitt Cancer Center and Research Institute.
Sin-Ho JungDuke University.ORCID 0000-0002-1473-7236
Kouros OwzarDuke University.
Neal ReadyDuke Cancer Institute, Duke University.
Trudy OliverDuke Cancer Institute, Duke University.
Scott AntoniaMoffitt Cancer Center.

Funding

Women's Cancer Research ProgramP30CA014236 · NCI · DUKE UNIVERSITY · PI Shannon Jones McCall · 1985 to 2026
$174.8M
Coordinating center for the NCI small cell lung cancer research consortiumU24CA213274 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI Lauren Averett Byers, JOHN D. MINNA · 2017 to 2026
$12.9M
Construction of A Lung Cancer Preclinical Model Cross-comparison PlatformR01CA285336 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI Ling Cai · 2024 to 2026
$3.1M
Pro-tumor functions of neutrophils in squamous cell lung cancerR01CA244841 · NCI · UNIVERSITY OF UTAH · PI OLIVER, TRUDY GALE · 2020 to 2024
$2.0M
Mechanisms of Arginine Deprivation in Small Cell Lung CancerR01CA251147 · NCI · UNIVERSITY OF UTAH · PI OLIVER, TRUDY GALE · 2021 to 2025
$1.9M
NEUROD1 function in SCLC fate and plasticityR01CA262134 · NCI · DUKE UNIVERSITY · PI Trudy Gale Oliver · 2024 to 2026
$1.6M
NEUROD1 and cell fate plasticity in olfactory neuroblastomaR01CA294607 · NCI · DUKE UNIVERSITY · PI Bradley J Goldstein, Trudy Gale Oliver · 2026 to 2026
$610k
NCI NIH HHS P30 CA014236NCI NIH HHS R01 CA244841NCI NIH HHS R01 CA251147NCI NIH HHS R01 CA262134NCI NIH HHS R01 CA285336NCI NIH HHS R01 CA294607NCI NIH HHS U24 CA213274
6 · The paper itself

Abstract

In preclinical models, PCSK9 mediates cancer immunotherapy resistance and may serve as a novel immuno-inhibitory target. Herein, we report the results from a multi-center, single arm, phase II study evaluating the clinical activity and safety of the PCSK9 inhibitor alirocumab, in combination with the anti-PD1 antibody cemiplimab, in non-small cell lung cancer (NSCLC) patients with disease progression after previous immune checkpoint blockade. The primary endpoint was objective response rate (ORR). Secondary endpoints were progression-free survival (PFS), overall survival (OS), duration of response (DOR), disease control rate (DCR) and safety, and an exploratory objective was to analyze potential biomarkers of response. Sixty patients were enrolled, and 58 were evaluable for ORR. The ORR was 14.78% (90% CI, 5.30, 25.43), the median PFS was 2.5 months (95% CI, 1.5-3), and the median OS was 7.3 months (95% CI, 5.4 - 12.3). The most common treatment related adverse events (all grades) were anemia and fatigue. Grade 3 adverse events occurred in seven (12%) patients and were anemia, Guillain-Barre Syndrome and elevated amino transferase. There were no treated related adverse events of grade 4 or greater in the study population. Biomarker analysis identified superior outcomes in NSCLC harboring PIK3CA, PTEN, or AKT1 alterations. The ORR in patients with PIK3CA, PTEN, or AKT1 alterations (n=17) was 29.4% (95% CI, 10.3% - 56.0%). No objective responses were observed in the absence of PIK3CA, PTEN or AKT1 alterations (n=39). The presence of PIK3CA, PTEN or AKT1 alterations was significantly associated with response, p 0.0032 (two-sided, Fisher's exact test). Further translational studies revealed the impact of PIK3CA, PTEN or AKT1 alterations on intratumoral PCSK9, providing a biological rationale for the pattern of response and clinical benefit. These findings provide clinical proof-of-principle that PCSK9 inhibition can overcome immunotherapy resistance in a subset of patients and suggest that PIK3CA/PTEN/AKT1 pathway plays a significant role in PCSK9 mediated immune evasion and could be a biomarker of response. These findings warrant further investigation in larger confirmatory studies.

Indexed as

immune checkpoint blockadeImmunotherapyimmunotherapy resistanceNSCLCPCSK9

Identifiers

PMID42396524
PMCPMC13321338

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.