Evidence map›Paper›PMID 36970199›Full record

ArticleActa pharmaceutica Sinica. B2023

A novel IRAK4/PIM1 inhibitor ameliorates rheumatoid arthritis and lymphoid malignancy by blocking the TLR/MYD88-mediated NF-

Sae-Bom Yoon, Hyowon Hong, Hee-Jong Lim, Ji Hye Choi, Yoon Pyo Choi, Seong Wook Seo, Hyuk Woo Lee, Chong Hak Chae, Woo-Kyu Park, Hyun Young Kim and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Acta pharmaceutica Sinica. B, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

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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

14 authors at 2 institutions in 1 country.

Sae-Bom YoonTherapeutics & Biotechnology Division, Korea Research Institute of Chemical Technology, Yuseong-gu, Daejeon 34114, Republic of Korea.
Hyowon HongTherapeutics & Biotechnology Division, Korea Research Institute of Chemical Technology, Yuseong-gu, Daejeon 34114, Republic of Korea.
Hee-Jong LimTherapeutics & Biotechnology Division, Korea Research Institute of Chemical Technology, Yuseong-gu, Daejeon 34114, Republic of Korea.
Ji Hye ChoiTherapeutics & Biotechnology Division, Korea Research Institute of Chemical Technology, Yuseong-gu, Daejeon 34114, Republic of Korea.
Yoon Pyo ChoiFuture Medicine Co., Ltd. Rm616 LH-Business Growth Center, Seongnam, Gyeonggido 13449, Republic of Korea.
Seong Wook SeoFuture Medicine Co., Ltd. Rm616 LH-Business Growth Center, Seongnam, Gyeonggido 13449, Republic of Korea.
Hyuk Woo LeeFuture Medicine Co., Ltd. Rm616 LH-Business Growth Center, Seongnam, Gyeonggido 13449, Republic of Korea.
Chong Hak ChaeTherapeutics & Biotechnology Division, Korea Research Institute of Chemical Technology, Yuseong-gu, Daejeon 34114, Republic of Korea.
Woo-Kyu ParkTherapeutics & Biotechnology Division, Korea Research Institute of Chemical Technology, Yuseong-gu, Daejeon 34114, Republic of Korea.
Hyun Young KimTherapeutics & Biotechnology Division, Korea Research Institute of Chemical Technology, Yuseong-gu, Daejeon 34114, Republic of Korea.
Daeyoung JeongTherapeutics & Biotechnology Division, Korea Research Institute of Chemical Technology, Yuseong-gu, Daejeon 34114, Republic of Korea.
Tran Quang DeTherapeutics & Biotechnology Division, Korea Research Institute of Chemical Technology, Yuseong-gu, Daejeon 34114, Republic of Korea.
Chang-Seon MyungDepartment of Pharmacology, Chungnam National University College of Pharmacy, Yuseong-gu, Daejeon 34134, Republic of Korea.
Heeyeong ChoTherapeutics & Biotechnology Division, Korea Research Institute of Chemical Technology, Yuseong-gu, Daejeon 34114, Republic of Korea.
Korea Research Institute of Chemical Technology · KRChungnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin-1 receptor-associated kinase 4 (IRAK4) is a pivotal enzyme in the Toll-like receptor (TLR)/MYD88 dependent signaling pathway, which is highly activated in rheumatoid arthritis tissues and activated B cell-like diffuse large B-cell lymphoma (ABC-DLBCL). Inflammatory responses followed by IRAK4 activation promote B-cell proliferation and aggressiveness of lymphoma. Moreover, proviral integration site for Moloney murine leukemia virus 1 (PIM1) functions as an anti-apoptotic kinase in propagation of ABC-DLBCL with ibrutinib resistance. We developed a dual IRAK4/PIM1 inhibitor KIC-0101 that potently suppresses the NF-

Indexed as

ABC-DLBCLDrug discoveryDual inhibitorIbrutinib resistanceIRAK4NF-κB pathwayPIM1Rheumatoid arthritis

Identifiers

PMID36970199
PMCPMC10031381
OpenAlexW4311564107

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.