Evidence map›Paper›PMID 28677901›Full record

Trial reportBritish journal of pharmacology2017

Big conductance calcium-activated potassium channel openers control spasticity without sedation.

David Baker, Gareth Pryce, Cristina Visintin, Sofia Sisay, Alexander I Bondarenko, W S Vanessa Ho, Samuel J Jackson, Thomas E Williams, Sarah Al-Izki, Ioanna Sevastou and 13 more

Open access · hybridAbstract readClinical Trial, Phase IRandomized Controlled Trial
PubMed Full text at PMC Publisher
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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Activation of BKCurrent issues in molecular biology · 2026
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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

23 authors at 7 institutions in 3 countries.

David BakerNeuroimmunology Unit, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.ORCID http://orcid.org/0000-0002-8872-8711
Gareth PryceNeuroimmunology Unit, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Cristina VisintinDepartment of Neuroinflammation, UCL Institute of Neurology, University College London, London, UK.
Sofia SisayNeuroimmunology Unit, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Alexander I BondarenkoInstitute of Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria.
W S Vanessa HoVascular Biology Research Centre. St. George's, University of London, London, UK.
Samuel J JacksonNeuroimmunology Unit, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Thomas E WilliamsNeuroimmunology Unit, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Sarah Al-IzkiNeuroimmunology Unit, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Ioanna SevastouDepartment of Medicinal Chemistry, UCL Wolfson Institute for Biomedical Research, University College London, London, UK.
Masahiro OkuyamaDepartment of Medicinal Chemistry, UCL Wolfson Institute for Biomedical Research, University College London, London, UK.
Wolfgang F GraierInstitute of Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria.
Lesley A StevensonVascular Biology Research Centre. St. George's, University of London, London, UK.
Carolyn TannerDepartment of Biomedical Sciences, Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
Ruth RossDepartment of Biomedical Sciences, Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
Roger G PertweeDepartment of Biomedical Sciences, Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
Christopher M HenstridgeNeurosciences Institute, Division of Pathology and Neuroscience, Ninewells Hospital and Medical School, University of Dundee, Dundee, UK.
Andrew J IrvingNeurosciences Institute, Division of Pathology and Neuroscience, Ninewells Hospital and Medical School, University of Dundee, Dundee, UK.
Jesse SchulmanCanbex Therapeutics Ltd, London BioScience Innovation Centre, London, UK.
Keith PowellCanbex Therapeutics Ltd, London BioScience Innovation Centre, London, UK.
Mark D BakerNeuroimmunology Unit, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Gavin GiovannoniNeuroimmunology Unit, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
David L SelwoodDepartment of Medicinal Chemistry, UCL Wolfson Institute for Biomedical Research, University College London, London, UK.
Queen Mary University of London · GBWolfson Foundation · GBUniversity of Aberdeen · GBCanbex Therapeutics (United Kingdom) · GBMedical University of Graz · ATSt George's, University of London · GBUniversity of Dundee · GB

Funding

Medical Research Council MC_PC_13037Wellcome Trust
6 · The paper itself

Abstract

background and purposeOur initial aim was to generate cannabinoid agents that control spasticity, occurring as a consequence of multiple sclerosis (MS), whilst avoiding the sedative side effects associated with cannabis. VSN16R was synthesized as an anandamide (endocannabinoid) analogue in an anti-metabolite approach to identify drugs that target spasticity. EXPERIMENTAL APPROACH: Following the initial chemistry, a variety of biochemical, pharmacological and electrophysiological approaches, using isolated cells, tissue-based assays and in vivo animal models, were used to demonstrate the activity, efficacy, pharmacokinetics and mechanism of action of VSN16R. Toxicological and safety studies were performed in animals and humans. KEY

resultsVSN16R had nanomolar activity in tissue-based, functional assays and dose-dependently inhibited spasticity in a mouse experimental encephalomyelitis model of MS. This effect occurred with over 1000-fold therapeutic window, without affecting normal muscle tone. Efficacy was achieved at plasma levels that are feasible and safe in humans. VSN16R did not bind to known CB CONCLUSIONS AND IMPLICATIONS: We identified the neuronal form of the BK

Indexed as

BenzamidesEncephalomyelitis, Autoimmune, ExperimentalLarge-Conductance Calcium-Activated Potassium ChannelsMuscle SpasticityAnimalsDogsDouble-Blind MethodEndocannabinoidsFemaleHepatocytesHumansIsomerismMacacaMaleMesenteric ArteriesMice3-(5-dimethylcarbamoylpent-1-enyl)-N-(2-hydroxy-1-methylethyl)benzamideBenzamidesEndocannabinoidsGPR55 protein, mouseLarge-Conductance Calcium-Activated Potassium ChannelsReceptor, Cannabinoid, CB1Receptors, Cannabinoid

Identifiers

PMID28677901
PMCPMC5522996
OpenAlexW2731853540

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.