Evidence map›Paper›PMID 35340932›Full record

ArticleChemical science2021

Targeted 1,3-dipolar cycloaddition with acrolein for cancer prodrug activation.

Ambara R Pradipta, Peni Ahmadi, Kazuki Terashima, Kyohei Muguruma, Motoko Fujii, Tomoya Ichino, Satoshi Maeda, Katsunori Tanaka

Abstract read
In one paragraph

Article in Chemical science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Therapeutic efficacy ofChemical science · 2023
    Article
  7. Cancer Cell-Specific Fluorescent Prodrug Delivery Platforms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
  8. Click chemistry and drug delivery: A bird's-eye view.Acta pharmaceutica Sinica. B · 2023
    Review
  9. 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

8 authors.

Ambara R PradiptaDepartment of Chemical Science and Engineering, School of Materials and Chemical Technology, Tokyo Institute of Technology 2-12-1 Ookayama, Meguro 152-8552 Tokyo Japan pradipta.a.aa@m.titech.ac.jp tanaka.k.dg@m.titech.ac.jp.ORCID https://orcid.org/0000-0002-9056-447X
Peni AhmadiBiofunctional Synthetic Chemistry Laboratory, Cluster for Pioneering Research, RIKEN 2-1 Hirosawa, Wako 351-1098 Saitama Japan.
Kazuki TerashimaDepartment of Chemical Science and Engineering, School of Materials and Chemical Technology, Tokyo Institute of Technology 2-12-1 Ookayama, Meguro 152-8552 Tokyo Japan pradipta.a.aa@m.titech.ac.jp tanaka.k.dg@m.titech.ac.jp.
Kyohei MugurumaDepartment of Chemical Science and Engineering, School of Materials and Chemical Technology, Tokyo Institute of Technology 2-12-1 Ookayama, Meguro 152-8552 Tokyo Japan pradipta.a.aa@m.titech.ac.jp tanaka.k.dg@m.titech.ac.jp.
Motoko FujiiDepartment of Chemical Science and Engineering, School of Materials and Chemical Technology, Tokyo Institute of Technology 2-12-1 Ookayama, Meguro 152-8552 Tokyo Japan pradipta.a.aa@m.titech.ac.jp tanaka.k.dg@m.titech.ac.jp.
Tomoya IchinoDepartment of Chemistry, Faculty of Science, Hokkaido University Kita 10 Nishi 8, Kita 060-0815 Sapporo Japan.
Satoshi MaedaDepartment of Chemistry, Faculty of Science, Hokkaido University Kita 10 Nishi 8, Kita 060-0815 Sapporo Japan.ORCID https://orcid.org/0000-0001-8822-1147
Katsunori TanakaDepartment of Chemical Science and Engineering, School of Materials and Chemical Technology, Tokyo Institute of Technology 2-12-1 Ookayama, Meguro 152-8552 Tokyo Japan pradipta.a.aa@m.titech.ac.jp tanaka.k.dg@m.titech.ac.jp.ORCID https://orcid.org/0000-0001-6932-4802

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytotoxic anticancer drugs used in chemotherapy are often antiproliferative agents that preferentially kill rapidly growing cancer cells. Their mechanism relies mainly on the enhanced proliferation rate of cancer cells and is not genuinely selective for cancer cells. Therefore, these drugs can also significantly affect healthy cells. Prodrug therapy provides an alternative approach using a less cytotoxic form of anticancer drug. It involves the synthesis of inactive drug derivatives which are converted to an active form inside the body and, preferably, only at the site of cancerous tissues, thereby reducing adverse drug reaction (ADR) events. Herein, we demonstrate a prodrug activation strategy by utilizing the reaction between aryl azide and endogenous acrolein. Since acrolein is generally overproduced by most cancer cells, we anticipate our strategy as a starting point for further applications in mouse models with various cancers. Furthermore, cancer drugs that have had therapeutic index challenges might be reconsidered for application by utilizing our strategy.

Identifiers

PMID35340932
PMCPMC8873552

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.