Evidence map›Paper›PMID 37945606›Full record

ArticleNature communications2023

Sphingomyelin-derived nanovesicles for the delivery of the IDO1 inhibitor epacadostat enhance metastatic and post-surgical melanoma immunotherapy.

Zhiren Wang, Wenpan Li, Yanhao Jiang, Tuyen Ba Tran, Leyla Estrella Cordova, Jinha Chung, Minhyeok Kim, Georg Wondrak, Jennifer Erdrich, Jianqin Lu

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.6field-weighted citation impact, top 6% of its field
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

23 citing papers in PubMed, 33 citations in OpenAlex.

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  17. Nanoimmunotherapy: the smart trooper for cancer therapy.Exploration of targeted anti-tumor therapy · 2025
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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

10 authors at 1 institution in 1 country.

Zhiren WangSkaggs Pharmaceutical Sciences Center, Department of Pharmacology & Toxicology, R. Ken Coit College of Pharmacy, The University of Arizona, Tucson, AZ, 85721, USA.ORCID 0000-0002-2016-0517
Wenpan LiSkaggs Pharmaceutical Sciences Center, Department of Pharmacology & Toxicology, R. Ken Coit College of Pharmacy, The University of Arizona, Tucson, AZ, 85721, USA.ORCID 0000-0002-8546-7384
Yanhao JiangSkaggs Pharmaceutical Sciences Center, Department of Pharmacology & Toxicology, R. Ken Coit College of Pharmacy, The University of Arizona, Tucson, AZ, 85721, USA.ORCID 0009-0006-2403-0601
Tuyen Ba TranSkaggs Pharmaceutical Sciences Center, Department of Pharmacology & Toxicology, R. Ken Coit College of Pharmacy, The University of Arizona, Tucson, AZ, 85721, USA.
Leyla Estrella CordovaSkaggs Pharmaceutical Sciences Center, Department of Pharmacology & Toxicology, R. Ken Coit College of Pharmacy, The University of Arizona, Tucson, AZ, 85721, USA.ORCID 0009-0009-3992-7157
Jinha ChungSkaggs Pharmaceutical Sciences Center, Department of Pharmacology & Toxicology, R. Ken Coit College of Pharmacy, The University of Arizona, Tucson, AZ, 85721, USA.
Minhyeok KimSkaggs Pharmaceutical Sciences Center, Department of Pharmacology & Toxicology, R. Ken Coit College of Pharmacy, The University of Arizona, Tucson, AZ, 85721, USA.ORCID 0009-0007-0766-3869
Georg WondrakSkaggs Pharmaceutical Sciences Center, Department of Pharmacology & Toxicology, R. Ken Coit College of Pharmacy, The University of Arizona, Tucson, AZ, 85721, USA.ORCID 0000-0003-4799-8608
Jennifer ErdrichDepartment of Surgery, Division of Surgical Oncology, The University of Arizona College of Medicine, Tucson, AZ, 85721, USA.ORCID 0000-0003-0585-0402
Jianqin LuSkaggs Pharmaceutical Sciences Center, Department of Pharmacology & Toxicology, R. Ken Coit College of Pharmacy, The University of Arizona, Tucson, AZ, 85721, USA. lu6@arizona.edu.ORCID 0000-0002-5877-619X
University of Arizona · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Teri L Bankhead · 1985 to 2026
$110.2M
SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI DEAN BILLHEIMER · 1994 to 2026
$36.7M
A fortified lipid bilayer platform for improved drug packaging and therapeutic deliveryR35GM147002 · NIGMS · UNIVERSITY OF ARIZONA · PI Jianqin Lu · 2022 to 2026
$1.9M
Repurposing Clinical ACT Antimalarials for Experimental Melanoma InterventionR01CA229418 · NCI · UNIVERSITY OF ARIZONA · PI WONDRAK, GEORG T · 2019 to 2023
$1.7M
A Phospholipid-Derived Nanotherapeutic Platform for Improved Colorectal Cancer ImmunochemotherapyR01CA272487 · NCI · UNIVERSITY OF ARIZONA · PI Jianqin Lu · 2023 to 2026
$1.4M
A Nutrition and Exercise Prehabilitation Intervention on Inflammatory Biomarkers in American Indian Cancer PatientsK08CA276137 · NCI · UNIVERSITY OF ARIZONA · PI JENNIFER A ERDRICH · 2023 to 2026
$1.1M
NCI NIH HHS K08 CA276137NCI NIH HHS P30 CA023074NCI NIH HHS R01 CA229418NCI NIH HHS R01 CA272487NIEHS NIH HHS P30 ES006694NIGMS NIH HHS R35 GM147002
6 · The paper itself

Abstract

Epacadostat (EPA), the most advanced IDO1 inhibitor, in combination with PD-1 checkpoint inhibitor, has failed in a recent Phase III clinical trial for treating metastatic melanoma. Here we report an EPA nanovesicle therapeutic platform (Epacasome) based on chemically attaching EPA to sphingomyelin via an oxime-ester bond highly responsive to hydrolase cleavage. Via clathrin-mediated endocytosis, Epacasome displays higher cellular uptake and enhances IDO1 inhibition and T cell proliferation compared to free EPA. Epacasome shows improved pharmacokinetics and tumour accumulation with efficient intratumoural drug release and deep tumour penetration. Additionally, it outperforms free EPA for anticancer efficacy, potentiating PD-1 blockade with boosted cytotoxic T lymphocytes (CTLs) and reduced regulatory T cells and myeloid-derived suppressor cells responses in a B16-F10 melanoma model in female mice. By co-encapsulating immunogenic dacarbazine, Epacasome further enhances anti-tumor effects and immune responses through the upregulation of NKG2D-mediated CTLs and natural killer cells responses particularly when combined with the PD-1 inhibitor in the late-stage metastatic B16-F10-Luc2 model in female mice. Furthermore, this combination prevents tumour recurrence and prolongs mouse survival in a clinically relevant, post-surgical melanoma model in female mice. Epacasome demonstrates potential to synergize with PD-1 blockade for improved response to melanoma immunotherapy.

Indexed as

Melanoma, ExperimentalSphingomyelinsAnimalsFemaleImmunotherapyLymphocyte ActivationMiceOximesProgrammed Cell Death 1 ReceptorSulfonamidesepacadostatOximesProgrammed Cell Death 1 ReceptorSphingomyelinsSulfonamides

Identifiers

PMID37945606
PMCPMC10636136
OpenAlexW4388530050

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.