Evidence map›Paper›PMID 31832202›Full record

ArticlePharmacology research & perspectives2019

Janus kinase inhibitors for the treatment of rheumatoid arthritis demonstrate similar profiles of in vitro cytokine receptor inhibition.

Martin E Dowty, Tsung H Lin, Michael I Jesson, Martin Hegen, David A Martin, Vaibhav Katkade, Sujatha Menon, Jean-Baptiste Telliez

Open access · goldAbstract read
In one paragraph

Article in Pharmacology research & perspectives, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
10.5field-weighted citation impact, top 1% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. Interferon-JAK-STAT Axis in Bone Metabolism.Current osteoporosis reports · 2026
    Review
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  18. Neutrophils in Atopic Dermatitis.Clinical reviews in allergy & immunology · 2024
    Review
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  20. 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 1 institution in 1 country.

Martin E DowtyPfizer Inc Cambridge MA USA.ORCID 0000-0003-1393-6388
Tsung H LinPfizer Inc Cambridge MA USA.
Michael I JessonPfizer Inc Cambridge MA USA.
Martin HegenPfizer Inc Cambridge MA USA.
David A MartinPfizer Inc Cambridge MA USA.
Vaibhav KatkadePfizer Inc Collegeville PA USA.
Sujatha MenonPfizer Inc Groton CT USA.
Jean-Baptiste TelliezPfizer Inc Cambridge MA USA.
Pfizer (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Janus kinase (JAK) inhibitors have emerged as an effective class of therapies for various inflammatory diseases such as rheumatoid arthritis (RA). JAK inhibitors function intracellularly by modulating the catalytic activity of JAKs and disrupting the receptor-mediated signaling of multiple cytokines and growth factors, including those with pro-inflammatory activity. Understanding the inhibition profiles of different JAK inhibitors, based on the associated cytokine receptors and downstream inflammatory pathways affected, is important to identify the potential mechanisms for observed differences in efficacy and safety. This study applied an integrated modeling approach, using in vitro whole blood cytokine inhibition potencies and plasma pharmacokinetics, to determine JAK-dependent cytokine receptor inhibition profiles, in the context of doses estimated to provide a similar clinical response in RA clinical trials. The calculated profiles of cytokine receptor inhibition for the JAK inhibitors tofacitinib, baricitinib, upadacitinib, and filgotinib and its metabolite, were generally similar when clinically efficacious doses for RA were considered. Only minor numerical differences in percentage cytokine receptor inhibition were observed, suggesting limited differentiation of these inhibitors based on JAK pharmacology, with each showing a differential selectivity for JAK1 heterodimer inhibition. Nevertheless, only robust clinical testing involving head-to-head studies will ultimately determine whether there are clinically meaningful differences between these JAK inhibitors. Furthermore, ongoing and future research into inhibitors with alternative JAK selectivity remains of clinical importance. Thus, all JAK inhibitors should be characterized via thorough preclinical, metabolic and pharmacological evaluation, adequate long-term clinical data, and when available, real-world experience.

Indexed as

Antirheumatic AgentsArthritis, RheumatoidAzetidinesCell LineCytokinesEnzyme AssaysFemaleHealthy VolunteersHeterocyclic Compounds, 3-RingHumansInhibitory Concentration 50Janus Kinase 1Janus Kinase InhibitorsMalePiperidinesPurinesAntirheumatic AgentsAzetidinesbaricitinibCytokinesGLPG0634Heterocyclic Compounds, 3-RingJAK1 protein, humanJanus Kinase 1Janus Kinase InhibitorsPiperidinesPurinesPyrazolesPyridinesPyrimidinesPyrrolesReceptors, CytokineSulfonamidestofacitinibTriazolesupadacitinibcytokine receptorsimmunopharmacologyinhibitionJAK‐STATrheumatoid arthritis

Identifiers

PMID31832202
PMCPMC6857076
OpenAlexW2988722150

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.