Evidence map›Paper›PMID 23831344›Full record

ReviewNeuroscience letters2013

Challenging the catechism of therapeutics for chronic neuropathic pain: Targeting CaV2.2 interactions with CRMP2 peptides.

Polina Feldman, Rajesh Khanna

Open access · greenAbstract readReview
In one paragraph

Review in Neuroscience letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Noradrenergic αMolecular neurobiology · 2025
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Partners in Crime: Towards New Ways of Targeting Calcium Channels.International journal of molecular sciences · 2019
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
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  18. Review
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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

2 authors at 1 institution in 1 country.

Polina FeldmanSophia Therapeutics LLC, 351 West 10th Street, Indianapolis, IN 46202, USA.
Rajesh Khanna
University of Indianapolis · US

Funding

Quality Assurance and Quality Control Project Management: Improving Submissions and Study Conduct in the Human Subjects Research Prior Approval ProcessUL1TR002529 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI MOE, SHARON M, WIEHE, SARAH ELIZABETH · 2018 to 2022
$27.2M
Indiana Clinical and Translational Sciences InstituteUL1TR001108 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI DENNE, SCOTT C., SHEKHAR, ANANTHA · 2013 to 2017
$23.3M
INDIANA CLINICAL AND TRANSLATIONAL SCIENCE INSTITUTE (UL1): BPCAUL1RR025761 · NCRR · INDIANA UNIVERSITY INDIANAPOLIS · PI SHEKHAR, ANANTHA · 2008 to 2011
$21.0M
Mechanisms of Neuropathic Pain in Demylenated NervesR01NS049136 · NINDS · LOYOLA UNIVERSITY CHICAGO · PI WHITE, FLETCHER A · 2006 to 2010
$1.3M
NCATS NIH HHS UL1 TR001108NCRR NIH HHS RR025761NCRR NIH HHS UL1 RR025761NINDS NIH HHS R01 NS049136
6 · The paper itself

Abstract

Chronic neuropathic pain management is a worldwide concern. Pharmaceutical companies globally have historically targeted ion channels as the therapeutic catechism with many blockbuster successes. Remarkably, no new pain therapeutic has been approved by European or American regulatory agencies over the last decade. This article will provide an overview of an alternative approach to ion channel drug discovery: targeting regulators of ion channels, specifically focusing on voltage-gated calcium channels. We will highlight the discovery of an anti-nociceptive peptide derived from a novel calcium channel interacting partner - the collapsin response mediator protein 2 (CRMP2). In vivo administration of this peptide reduces pain behavior in a number of models of neuropathic pain without affecting sympathetic-associated cardiovascular activity, memory retrieval, sensorimotor function, or depression. A CRMP2-derived peptide analgesic, with restricted access to the CNS, represents a completely novel approach to the treatment of severe pain with an improved safety profile. As peptides now represent one of the fastest growing classes of new drugs, it is expected that peptide targeting of protein interactions within the calcium channel complex may be a paradigm shift in ion channel drug discovery.

Indexed as

AnalgesicsAnimalsCalcium Channel BlockersCalcium Channels, N-TypeChronic DiseaseHumansIntercellular Signaling Peptides and ProteinsMiceNerve Tissue ProteinsNeuralgiaPeptidesSignal TransductionAnalgesicsCalcium Channel BlockersCalcium Channels, N-Typecollapsin response mediator protein-2Intercellular Signaling Peptides and ProteinsNerve Tissue ProteinsPeptidesAnti-nociceptiveBBBblood brain barrierCa(2+) channel binding domaincalcitonin gene related peptideCalcium channelsCaV2.2CBDcell penetrating peptidecentral nervous systemCGRPCNScollapsin response mediator protein 2conotoxinCPPCRMP2CTXdays in vitroDIVdorsal root ganglionDRGHIV-1 transactivator of transcription domainLPClysophosphotidylcholineNeuropathic painnona-arginineNRTIN-type voltage-gated Ca(2+) channelnucleoside reverse transcriptase inhibitoromega-conotoxinpaw withdrawal thresholdPeptidePWTR9sEPSCsSophia Therapeuticsspontaneous excitatory postsynaptic currentsSTTATtibial nerve injuryTNIω-CTX

Identifiers

PMID23831344
PMCPMC3849117
OpenAlexW2060274276

What OpenQuestion holds

Textmetadata
LicenceTDM
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.