Evidence map›Paper›PMID 27714763›Full record

Trial reportBritish journal of pharmacology2017

Amiselimod, a novel sphingosine 1-phosphate receptor-1 modulator, has potent therapeutic efficacy for autoimmune diseases, with low bradycardia risk.

Kunio Sugahara, Yasuhiro Maeda, Kyoko Shimano, Akira Mogami, Hirotoshi Kataoka, Kei Ogawa, Kumiko Hikida, Hiroshi Kumagai, Mahoko Asayama, Toshinobu Yamamoto and 4 more

Open access · hybridAbstract readClinical Trial, Phase IRandomized Controlled Trial
In one paragraph

Trial report in British journal of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 83 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 5 institutions in 2 countries.

Kunio SugaharaResearch Unit/Frontier Therapeutic Sciences, Sohyaku. Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Japan.
Yasuhiro MaedaResearch Unit/Frontier Therapeutic Sciences, Sohyaku. Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Japan.
Kyoko ShimanoResearch Unit/Frontier Therapeutic Sciences, Sohyaku. Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Japan.
Akira MogamiResearch Unit/Frontier Therapeutic Sciences, Sohyaku. Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Japan.
Hirotoshi KataokaResearch Unit/Frontier Therapeutic Sciences, Sohyaku. Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Japan.
Kei OgawaDMPK Research Laboratories, Sohyaku. Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Japan.
Kumiko HikidaDMPK Research Laboratories, Sohyaku. Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Japan.
Hiroshi KumagaiDMPK Research Laboratories, Sohyaku. Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Japan.
Mahoko AsayamaSafety Research Laboratories, Sohyaku. Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Saitama, Japan.
Toshinobu YamamotoSafety Research Laboratories, Sohyaku. Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Saitama, Japan.
Tomohiko HaradaMitsubishi Tanabe Pharma Europe, Dashwood House, London, UK.
Pingping NiMitsubishi Tanabe Pharma Europe, Dashwood House, London, UK.
Shinsuke InoueData Science Department, Sohyaku. Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Tokyo, Japan.
Atsuhiro KawaguchiData Science Department, Sohyaku. Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Tokyo, Japan.
Mitsubishi Tanabe Pharma CorporationMitsubishi Chemical (Japan) · JPMitsubishi Corporation (United Kingdom) · GBMitsubishi Group (Japan) · JPMitsubishi Materials (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeWe conducted preclinical and clinical studies to examine the pharmacological, particularly cardiac, effects of amiselimod (MT-1303), a second-generation sphingosine 1-phosphate (S1P) receptor modulator, designed to reduce the bradycardia associated with fingolimod and other S1P receptor modulators. EXPERIMENTAL APPROACH: The selectivity of the active metabolite amiselimod phosphate (amiselimod-P) for human S1P receptors and activation of G-protein-coupled inwardly rectifying K KEY

resultsAmiselimod-P showed potent selectivity for S1P CONCLUSIONS AND IMPLICATIONS: Amiselimod exhibited potent therapeutic efficacy with minimal cardiac effects at the anticipated clinical dose and is unlikely to require dose titration.

Indexed as

AnimalsAutoimmune DiseasesBradycardiaCell LineDose-Response Relationship, DrugHumansMacaca fascicularisMaleMolecular StructureOrganophosphatesPropanolaminesRatsRats, Sprague-DawleyReceptors, LysosphingolipidSphingosine-1-Phosphate ReceptorsStructure-Activity Relationshipamiselimodamiselimod phosphateOrganophosphatesPropanolaminesReceptors, LysosphingolipidS1PR1 protein, humanSphingosine-1-Phosphate Receptors

Identifiers

PMID27714763
PMCPMC5221453
OpenAlexW2529362670

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.