Evidence map›Paper›PMID 23202314›Full record

ReviewToxins2012

Conotoxins targeting neuronal voltage-gated sodium channel subtypes: potential analgesics?

Oliver Knapp, Jeffrey R McArthur, David J Adams

Open access · goldAbstract readReview
In one paragraph

Review in Toxins, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Journal of Zhejiang University. Science. B · 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

3 authors at 1 institution in 1 country.

Oliver KnappHealth Innovations Research Institute, RMIT University, Melbourne, Victoria 3083, Australia. oliver.knapp@rmit.edu.au
Jeffrey R McArthur
David J Adams
RMIT University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Voltage-gated sodium channels (VGSC) are the primary mediators of electrical signal amplification and propagation in excitable cells. VGSC subtypes are diverse, with different biophysical and pharmacological properties, and varied tissue distribution. Altered VGSC expression and/or increased VGSC activity in sensory neurons is characteristic of inflammatory and neuropathic pain states. Therefore, VGSC modulators could be used in prospective analgesic compounds. VGSCs have specific binding sites for four conotoxin families: μ-, μO-, δ- and ί-conotoxins. Various studies have identified that the binding site of these peptide toxins is restricted to well-defined areas or domains. To date, only the μ- and μO-family exhibit analgesic properties in animal pain models. This review will focus on conotoxins from the μ- and μO-families that act on neuronal VGSCs. Examples of how these conotoxins target various pharmacologically important neuronal ion channels, as well as potential problems with the development of drugs from conotoxins, will be discussed.

Indexed as

Drug DiscoveryAmino Acid SequenceAnalgesicsAnimalsBinding SitesConotoxinsConus SnailHumansModels, MolecularMolecular Sequence DataNeuralgiaNeuronsVoltage-Gated Sodium Channel BlockersVoltage-Gated Sodium ChannelsAnalgesicsConotoxinsVoltage-Gated Sodium Channel BlockersVoltage-Gated Sodium Channels

Identifiers

PMID23202314
PMCPMC3509706
OpenAlexW2158996595

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.