Evidence map›Paper›PMID 15753951›Full record

ArticleBritish journal of pharmacology2005

A selective novel low-molecular-weight inhibitor of IkappaB kinase-beta (IKK-beta) prevents pulmonary inflammation and shows broad anti-inflammatory activity.

Karl Ziegelbauer, Florian Gantner, Nicholas W Lukacs, Aaron Berlin, Kinji Fuchikami, Toshiro Niki, Katsuya Sakai, Hisayo Inbe, Keisuke Takeshita, Mina Ishimori and 4 more

Open access · greenAbstract read
In one paragraph

Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

80 citing papers in PubMed, 145 citations in OpenAlex.

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  17. Targeting the Canonical Nuclear Factor-κB Pathway with a High-Potency IKK2 Inhibitor Improves Outcomes in a Mouse Model of Idiopathic Pneumonia Syndrome.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2017
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20 more citing papers are in PubMed but not listed here.

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 1 institution in 3 countries.

Karl ZiegelbauerBayer Yakuhin, Ltd, Research Center Kyoto, Kyoto, Japan. karl.ziegelbauer@bayerhealthcare.com
Florian Gantner
Nicholas W Lukacs
Aaron Berlin
Kinji Fuchikami
Toshiro Niki
Katsuya Sakai
Hisayo Inbe
Keisuke Takeshita
Mina Ishimori
Hiroshi Komura
Toshiki Murata
Timothy Lowinger
Kevin B Bacon
Bayer (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1 Pulmonary inflammatory diseases such as asthma are characterized by chronic, cell-mediated inflammation of the bronchial mucosa. 2 Recruitment and activation of inflammatory cells is orchestrated by a variety of mediators such as cytokines, chemokines, or adhesion molecules, the expression of which is regulated via the transcription factor nuclear factor kappa B (NF-kappaB). 3 NF-kappaB signaling is controlled by the inhibitor of kappa B kinase complex (IKK), a critical catalytic subunit of which is IKK-beta. 4 We identified COMPOUND A as a small-molecule, ATP-competitive inhibitor selectively targeting IKK-beta kinase activity with a K(i) value of 2 nM. 5 COMPOUND A inhibited stress-induced NF-kappaB transactivation, chemokine-, cytokine-, and adhesion molecule expression, and T- and B-cell proliferation. 6 COMPOUND A is orally bioavailable and inhibited the release of LPS-induced TNF-alpha in rodents. 7 In mice COMPOUND A inhibited cockroach allergen-induced airway inflammation and hyperreactivity and efficiently abrogated leukocyte trafficking induced by carrageenan in mice or by ovalbumin in a rat model of airway inflammation. 8 COMPOUND A was well tolerated by rodents over 3 weeks without affecting weight gain. 9 Furthermore, in mice COMPOUND A suppressed edema formation in response to arachidonic acid, phorbol ester, or edema induced by delayed-type hypersensitivity. 10 These data suggest that IKK-beta inhibitors offer an effective therapeutic approach for inhibiting chronic pulmonary inflammation.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalCell Adhesion MoleculesCell Line, TumorCell MovementCell ProliferationEdemaFemaleHumansI-kappa B KinaseI-kappa B ProteinsLeukocytesMaleMiceMice, Inbred BALB CNF-kappa B7-(2-(cyclopropylmethoxy)-6-hydroxyphenyl)-5-(3-piperidinyl)-1,4-dihydro-2H-pyrido(2,3-d)(1,3)oxazin-2-oneAnti-Inflammatory Agents, Non-SteroidalCell Adhesion MoleculesCHUK protein, humanChuk protein, mouseI-kappa B KinaseI-kappa B ProteinsIKBKB protein, humanIkbkb protein, mouseIKBKE protein, humanIkbke protein, mouseNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanNfkbia protein, mouseNfkbia protein, ratOxazinesProtein Serine-Threonine KinasesPyridinesTumor Necrosis Factor-alpha

Identifiers

PMID15753951
PMCPMC1576128
OpenAlexW1968730445

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.