Evidence map›Paper›PMID 28521261›Full record

ArticleEuropean journal of medicinal chemistry2017

Novel anti-inflammatory agents targeting CXCR4: Design, synthesis, biological evaluation and preliminary pharmacokinetic study.

Renren Bai, Zhongxing Liang, Younghyoun Yoon, Eric Salgado, Amber Feng, Saumya Gurbani, Hyunsuk Shim

Open access · greenAbstract read
In one paragraph

Article in European journal of medicinal chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

4 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Development of CXCR4 modulators based on the lead compound RB-108.European journal of medicinal chemistry · 2019
    Article
  4. Article
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

7 authors at 1 institution in 1 country.

Renren BaiDepartment of Radiation Oncology, School of Medicine, Emory University, Atlanta, GA, USA.
Zhongxing LiangDepartment of Radiation Oncology, School of Medicine, Emory University, Atlanta, GA, USA.
Younghyoun YoonDepartment of Radiation Oncology, School of Medicine, Emory University, Atlanta, GA, USA.
Eric SalgadoDepartment of Radiation Oncology, School of Medicine, Emory University, Atlanta, GA, USA.
Amber FengDepartment of Radiation Oncology, School of Medicine, Emory University, Atlanta, GA, USA.
Saumya GurbaniDepartment of Radiation Oncology, School of Medicine, Emory University, Atlanta, GA, USA.
Hyunsuk ShimDepartment of Radiation Oncology, School of Medicine, Emory University, Atlanta, GA, USA; Winship Cancer Institute, Emory University, Atlanta, GA, USA; Department of Radiology and Imaging Science, School of Medicine, Emory University, Atlanta, USA; Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta, GA 30322, USA. Electronic address: hshim@emory.edu.
Emory University · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM008169 · NIGMS · EMORY UNIVERSITY · PI GROSS, ROBERT E · 1987 to 2021
$20.3M
Graduate Training in the Pharmacological StudiesT32GM008602 · NIGMS · EMORY UNIVERSITY · PI HALL, RANDY A. · 1996 to 2021
$5.1M
Development of anti-CXCR4 compounds to block breast cancer metastasisR01CA165306 · NCI · EMORY UNIVERSITY · PI SHIM, HYUNSUK · 2012 to 2016
$1.7M
NCI NIH HHS R01 CA165306NIGMS NIH HHS T32 GM008169NIGMS NIH HHS T32 GM008602
6 · The paper itself

Abstract

CXCR4 plays a crucial role in the inflammatory disease process, providing an attractive means for drug targeting. A series of novel amide-sulfamide derivatives were designed, synthesized and comprehensively evaluated. This new scaffold exhibited much more potent CXCR4 inhibitory activity, with more than 70% of the compounds showed notably better binding affinity than the reference drug AMD3100 in the binding assay. Additionally, in the Matrigel invasion assay, most of our compounds significantly blocked the tumor cell invasion, demonstrating superior efficacy compared to AMD3100. Furthermore, compound IIj blocked mice ear inflammation by 75% and attenuated ear edema and damage substantially in an in vivo model of inflammation. Western blot analyses revealed that CXCR4 modulator IIj significantly blocked CXCR4/CXCL12-mediated phosphorylation of Akt. Moreover, compound IIj had no observable cytotoxicity and displayed a favourable plasma stability in our preliminary pharmacokinetic study. The preliminary structure-activity relationships were also summarized. In short, this novel amide-sulfamide scaffold exhibited potent CXCR4 inhibitory activity both in vitro and in vivo. These results also confirmed that developing modulators targeting CXCR4 provides an exciting avenue for treatment of inflammation.

Indexed as

Drug DesignAnti-Inflammatory Agents, Non-SteroidalCell Line, TumorCell SurvivalDose-Response Relationship, DrugFemaleHumansMolecular StructureReceptors, CXCR4Structure-Activity RelationshipAnti-Inflammatory Agents, Non-SteroidalCXCR4 protein, humanReceptors, CXCR4Amide-sulfamideCXCR4InflammationPharmacokinetic studyStructure–activity relationship

Identifiers

PMID28521261
PMCPMC5521218
OpenAlexW2613487043

What OpenQuestion holds

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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.