Evidence map›Paper›PMID 29152046›Full record

ArticleACS medicinal chemistry letters2017

Design and Synthesis of N1-Modified Imidazoquinoline Agonists for Selective Activation of Toll-like Receptors 7 and 8.

Peter Larson, Tamara A Kucaba, Zhengming Xiong, Michael Olin, Thomas S Griffith, David M Ferguson

Open access · greenAbstract read
In one paragraph

Article in ACS medicinal chemistry letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
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

6 authors at 1 institution in 1 country.

Peter LarsonDepartment of Medicinal Chemistry, Department of Urology, Department of Pediatrics, Masonic Cancer Center, Center for Immunology, Microbiology, Immunology, and Cancer Biology Graduate Program, and Center for Drug Design, University of Minnesota, Minneapolis, Minnesota 55455, United States.
Tamara A KucabaDepartment of Medicinal Chemistry, Department of Urology, Department of Pediatrics, Masonic Cancer Center, Center for Immunology, Microbiology, Immunology, and Cancer Biology Graduate Program, and Center for Drug Design, University of Minnesota, Minneapolis, Minnesota 55455, United States.
Zhengming XiongDepartment of Medicinal Chemistry, Department of Urology, Department of Pediatrics, Masonic Cancer Center, Center for Immunology, Microbiology, Immunology, and Cancer Biology Graduate Program, and Center for Drug Design, University of Minnesota, Minneapolis, Minnesota 55455, United States.
Michael OlinDepartment of Medicinal Chemistry, Department of Urology, Department of Pediatrics, Masonic Cancer Center, Center for Immunology, Microbiology, Immunology, and Cancer Biology Graduate Program, and Center for Drug Design, University of Minnesota, Minneapolis, Minnesota 55455, United States.
Thomas S GriffithDepartment of Medicinal Chemistry, Department of Urology, Department of Pediatrics, Masonic Cancer Center, Center for Immunology, Microbiology, Immunology, and Cancer Biology Graduate Program, and Center for Drug Design, University of Minnesota, Minneapolis, Minnesota 55455, United States.
David M FergusonDepartment of Medicinal Chemistry, Department of Urology, Department of Pediatrics, Masonic Cancer Center, Center for Immunology, Microbiology, Immunology, and Cancer Biology Graduate Program, and Center for Drug Design, University of Minnesota, Minneapolis, Minnesota 55455, United States.
University of Minnesota · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A series of N1-modified imidazoquinolines were synthesized and screened for Toll-like receptors (TLR) 7 and 8 activities to identify recognition elements that confer high affinity binding and selectivity. These receptors are key targets in the development of immunomodulatory agents that signal the NF-κB mediated transcription of pro-inflammatory chemokines and cytokines. Results are presented showing both TLR7/8 activations are highly correlated to N1-substitution, with TLR8 selectivity achieved through inclusion of an ethyl-, propyl-, or butylamino group at this position. While the structure-activity relationship analysis indicates TLR7 activity is less sensitive to N1-modification, extension of the aminoalkyl chain length to pentyl and

Identifiers

PMID29152046
PMCPMC5683703
OpenAlexW2765445021

What OpenQuestion holds

Textmetadata
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.