Evidence map›Paper›PMID 35579105›Full record

ArticleCancer science2022

Development of a potent small-molecule degrader against oncogenic BRAF

Nobumichi Ohoka, Masanori Suzuki, Takuya Uchida, Yoshinori Tsukumo, Masayuki Yoshida, Takao Inoue, Hitoshi Ohki, Mikihiko Naito

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Review
  3. BRAFClinical and translational medicine · 2025
    Article
  4. Review
  5. Review
  6. 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 at 2 institutions in 1 country.

Nobumichi OhokaDivision of Molecular Target and Gene Therapy Products, National Institute of Health Sciences, Kawasaki, Kanagawa, Japan.ORCID https://orcid.org/0000-0002-0533-0610
Masanori SuzukiModality Research Laboratories, Biologics Division, Daiichi Sankyo Co., Ltd., Tokyo, Japan.
Takuya UchidaMedicinal Chemistry Research Laboratories, R&D Division, Daiichi Sankyo Co., Ltd., Tokyo, Japan.
Yoshinori TsukumoDivision of Molecular Target and Gene Therapy Products, National Institute of Health Sciences, Kawasaki, Kanagawa, Japan.ORCID https://orcid.org/0000-0002-4470-2392
Masayuki YoshidaModality Research Laboratories, Biologics Division, Daiichi Sankyo Co., Ltd., Tokyo, Japan.
Takao InoueDivision of Molecular Target and Gene Therapy Products, National Institute of Health Sciences, Kawasaki, Kanagawa, Japan.
Hitoshi OhkiModality Research Laboratories, Biologics Division, Daiichi Sankyo Co., Ltd., Tokyo, Japan.
Mikihiko NaitoDivision of Molecular Target and Gene Therapy Products, National Institute of Health Sciences, Kawasaki, Kanagawa, Japan.ORCID https://orcid.org/0000-0003-0451-1337
Daiichi-Sankyo (Japan) · JPNational Institute of Health Sciences · JP

Funding

Japan Agency for Medical Research and Development JP19cm0106136Japan Agency for Medical Research and Development JP20ak0101073Japan Agency for Medical Research and Development JP21ak0101073Japan Agency for Medical Research and Development JP21mk0101197Japan Society for the Promotion of Science JP18H05502Japan Society for the Promotion of Science JP18K06567Japan Society for the Promotion of Science JP21H02777Japan Society for the Promotion of Science JP21K06490Princess Takamatsu Cancer Research Fund
6 · The paper itself

Abstract

BRAF mutations are frequently observed in melanoma and hairy-cell leukemia. Currently approved rapidly accelerated fibrosarcoma (RAF) kinase inhibitors targeting oncogenic BRAF V600 mutations have shown remarkable efficacy in the clinic, but their therapeutic benefits are occasionally hampered by acquired resistance due to RAF dimerization-dependent reactivation of the downstream MAPK pathway, which is known as paradoxical activation. There is also a concern that paradoxical activation of the MAPK pathway may trigger secondary cancer progression. In this study, we developed chimeric compounds, proteolysis targeting chimeras (PROTACs), that target BRAF

Indexed as

MelanomaProtein Kinase InhibitorsProto-Oncogene Proteins B-rafCell Line, TumorHumansMAP Kinase Signaling SystemMutationBRAF protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins B-rafBRAFdrug discoveryMAPKPROTACubiquitination

Identifiers

PMID35579105
PMCPMC9357609
OpenAlexW4280609867

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.