Evidence map›Paper›PMID 21031168›Full record

ArticleDrug news & perspectives2010

The rise and fall of Dimebon.

Ilya Bezprozvanny

Registry-linked trialAbstract read
In one paragraph

Article in Drug news & perspectives, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03683394 (Multidomain Alzheimers Risk Reduction Study), which is not on this map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
8.3field-weighted citation impact, top 2% 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.

NCT03683394 nacompletednot on this mapstarted 2018, after this paper: background citation

Multidomain Alzheimers Risk Reduction Study (MARRS) Pilot

TypeinterventionalSponsorKaiser PermanenteRan2018 to 2022Enrolled172ConditionsDementia, Alzheimer DiseaseArmsSMARRT Intervention, Health Education Intervention
3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 94 citations in OpenAlex.

  1. Trial
  2. Trial
  3. PolyfunctionalizedInternational journal of molecular sciences · 2026
    Article
  4. Review
  5. Latrepirdine (Dimebon), a potent 5-HTFrontiers in pharmacology · 2026
    Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Multitargeting the Action of 5-HTInternational journal of molecular sciences · 2022
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Old Drugs as New Treatments for Neurodegenerative Diseases.Pharmaceuticals (Basel, Switzerland) · 2018
    Review
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

1 author at 1 institution in 1 country.

Ilya BezprozvannyDepartment of Physiology, University of Texas Southwestern Medical Center, Dallas, TX, USA. Ilya.Bezprozvanny@UTSouthwestern.edu
The University of Texas Southwestern Medical Center · US

Funding

Deranged calcium signaling and polyglutamine expansion disordersR01NS056224 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI BEZPROZVANNY, ILYA B · 2008 to 2020
$3.5M
Presenilins and neuronal calcium signalingR01AG030746 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI BEZPROZVANNY, ILYA B · 2009 to 2010
$785k
NIA NIH HHS R01 AG030746NIA NIH HHS R01AG030746NINDS NIH HHS R01 NS056224
6 · The paper itself

Abstract

Dimebon (latrepirdine) was developed and used in Russia as an over-the-counter oral antihistamine for allergy treatment. In the early 1990s, Dimebon was characterized as a low-affinity NMDA receptor antagonist by Dr. Sergey Bachurin and his colleagues. An initial small-scale, open-label trial of Dimebon in 14 Alzheimer's disease (AD) patients demonstrated potential efficacy. Dimebon was then patented for the treatment of neurodegenerative disorders and licensed by Medivation. Extremely promising results were obtained in a double-blind, placebo-controlled, phase II AD trial in 183 patients; however, a phase II trial of Dimebon in 91 Huntington's disease patients was much less successful. Recently, a phase III AD trial of Dimebon in 598 patients failed to result in any significant improvement in primary or secondary outcomes. The failure of Dimebon may be in large part due to insufficient understanding of its mechanism of action. The NMDA receptor blocking activity of Dimebon is too weak to be physiologically relevant, while the proposed "novel mitochondrial mechanism of action" lacks credible scientific evidence or a molecular target. Independent studies indicate that the clinical effects of Dimebon most likely result from inhibition of histamine H₁ and serotonin 5-HT₆ receptors. Careful preclinical studies of novel potential therapies are needed to minimize chances of making similar costly mistakes in the future.

Indexed as

Product Recalls and WithdrawalsAlzheimer DiseaseAnimalsControlled Clinical Trials as TopicHumansHuntington DiseaseIndolesReceptors, Histamine H1Receptors, SerotoninRussiaTreatment FailureIndoleslatrepirdineReceptors, Histamine H1Receptors, Serotoninserotonin 6 receptor

Identifiers

PMID21031168
PMCPMC3922928
OpenAlexW150733228

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.