Delving into the Latest Updates on Dimebolin hydrochloride with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Dimebolin, Dimebon, Latrepirdine

+ [5]

Target

H1 receptor

Action

antagonists

Mechanism

H1 receptor antagonists(Histamine H1 receptor antagonists)

Therapeutic Areas

Immune System DiseasesInfectious DiseasesOtorhinolaryngologic Diseases+ [2]

Active Indication

HypersensitivityRhinitis, AllergicDementia due to Alzheimer's disease (disorder)

Inactive Indication

Huntington Diseaseliver function failure

Originator Organization-

Active Organization

Bigespas Ltd.

Inactive Organization

Pfizer Inc.MediVation, Inc.

License Organization-

Drug Highest PhaseApproved

First Approval Date

Russia (01 Jan 1983),

HypersensitivityRhinitis, Allergic

RegulationOrphan Drug (United States)

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Structure/Sequence

Molecular FormulaC21H27Cl2N3

InChIKeyGTWLIQOLGOZTLF-UHFFFAOYSA-N

CAS Registry97657-92-6

The goal of this clinical study is to learn if the study drug DMB-I (INN: Latrepirdine) works to treat Alzheimer type dementia in adults. It will also learn about the safety of DMB-I (INN: Latrepirdine).
The main questions it aims to answer are:
* Does DMB-I improve cognitive functions in patients with dementia associated with Alzheimer's disease, and how sigificant the improvement is?
* What medical problems do participants have when taking DMB-I? Researchers will compare DMB-I to a placebo (a look-alike substance that contains no drug) to see if the study drug works to treat Alzheimer type dementia.
* Is DMB-I effective and safe when taken long-term?
Participants will:
Take the study drug or a placebo (with or without Akatinol Memantine®) every day for 26 weeks at Stage 1 of the study, and take the study drug (with or without Akatinol Memantine®) every day for 26 weeks at Stage 2 of the study.
Visit the clinic 13 times for checkups and tests Keep a diary of their symptoms

Start Date11 Sep 2025

Sponsor / Collaborator

Bigespas Ltd.

NCT06292351

/ CompletedPhase 2

Multicenter Randomized Double-blind Placebo-controlled Three-arm Parallel-group Clinical Study to Evaluate the Efficacy and Safety of DMB-I in the Treatment of Dementia Associated With Alzheimer's Disease

The purpose of this study is to assess the efficacy and safety of DMB-I for the treatment of patients with Alzheimer type dementia.

Start Date27 Dec 2023

Sponsor / Collaborator

Bigespas Ltd.

EUCTR2009-018123-32-DE

/ Not yet recruitingNot Applicable

HORIZON-Plus: An Open-Label Extension of the HORIZON Protocol (DIM20) Evaluating the Safety of Dimebon (Latrepirdine) in Subjects with Huntington Disease - HORIZON-Plus

Start Date07 Jun 2010

Sponsor / Collaborator-

100 Clinical Results associated with Dimebolin hydrochloride

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100 Translational Medicine associated with Dimebolin hydrochloride

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100 Patents (Medical) associated with Dimebolin hydrochloride

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181

Literatures (Medical) associated with Dimebolin hydrochloride

01 Jun 2025·Current computer-aided drug design

In-silico Design, ADMET Screening, Prime MM-GBSA Binding Free Energy Calculation and MD Simulation of Some Novel Phenothiazines as 5HT₆R Antagonists Targeting Alzheimer’s Disease

Article

Author: Natarajan, Ramalakshmi ; Arumugam, Meena ; Vediappan, Prema

Background::

Alzheimer's disease is a type of dementia that affects neuronal function, leading to a decline in cognitive functions. Serotonin-6 (5HT6) receptors are implicated in the etiology of neurological diseases. 5HT6 receptor antagonists act as anti-dementia agents. PDB ID: 7YS6 represents a membrane protein, and amplification and overexpression of this protein are associated with Alzheimer's disease. Coumarin-fused phenothiazines are significant anti-Alzheimer's agents due to their inhibitory activity on the Serotonin- 6 receptor.

Objectives::

Numerous previously unreported Coumarin-substituted Phenothiazines [A2 to A50] were designed using in-silico methods to evaluate their 5HT6 receptor antagonistic activity. Molecular modeling techniques were employed to study the ligands [A2 to A50] in interaction with the Serotonin-6 receptor (PDB ID: 7YS6) using Schrödinger Suite 2019-4.

Methods::

Molecular modeling studies of the designed ligands [A2 to A50] were conducted using the Glide module. In-silico ADMET screening was performed using the QikProp module, and binding free energy calculations were carried out using the Prime MM-GBSA module within the Schrödinger Suite. The binding affinity of the designed ligands [A2 to A50] towards 5HT6 receptors was determined based on Glide scores. Subsequently, ligand A31 underwent a 100 ns molecular dynamics simulation using the Desmond module of Schrödinger Suite 2020-1, which is based in New York, NY.

Results::

The majority of the designed ligands exhibited strong hydrogen bonding interactions and hydrophobic associations with the serotonin-6 receptor, which hinder its activity. These ligands achieved remarkable Glide scores within the range of -4.2859 to -7.7128, in comparison to reference standards such as Idalopirdine (-7.78149), Intepirdine (-5.20103), Latrepirdine (-5.54853), and the co-crystallized ligand (-7.02889). In-silico ADMET properties for these ligands fell within the recommended values for drug-likeness. It is worth noting that the MMGBSA binding free energy of the most potent inhibitor was positive, indicating a strong binding interaction. Additionally, the dynamic behavior of the protein (7YS6)-ligand (A31) complex was studied by subjecting ligand A31 to a 100 ns molecular dynamics simulation.

Conclusion::

The results of this study reveal strong evidence supporting the potential of coumarin- substituted phenothiazine derivatives as effective Serotonin-6 receptor antagonists. Ligands [A2 to A50], which exhibited noteworthy Glide scores, hold promise for significant anti- Alzheimer activity. Further in-vitro and in-vivo investigations are warranted to explore and confirm their therapeutic potential.

01 Dec 2024·FOOD CHEMISTRY

In situ fortification of cereal by-products with vitamin B12: An eco-sustainable approach for food fortification

Article

Author: Odochean, Răzvan ; Martău, Gheorghe-Adrian ; Mitrea, Laura ; Nemes, Silvia Amalia ; Călinoiu, Lavinia Florina ; Ștefănescu, Bianca-Eugenia ; Vodnar, Dan Cristian

Vitamin B12 deficiency poses significant health risks, especially among populations with limited access to animal-based foods. This study explores the utilisation of cereal bran by-products, wheat (WB) and oat bran (OB), as substrates for in situ vitamin B12 fortification through solid-state fermentation (SSF) using Propionibacterium freudenreichii. The impact of various precursors addition, including riboflavin, cobalt, nicotinamide and DMBI on vitamin B12 production, along with changes in microbial growth, chemical profiles, and vitamin B12 yields during fermentation was evaluated. Results showed that WB and OB possess favourable constituents for microbial growth and vitamin B12 synthesis. The substrates supplemented with riboflavin, cobalt, and DMBI demonstrated enhanced B12 production. In addition, pH levels are essential in microbial viability and cobalamin biosynthesis. Monosaccharides and organic acids play a crucial role, with maltose showing a strong positive association with B12 production in OB, while in WB, citric acid exhibits significant correlations with various factors.

01 May 2023·Current neuropharmacology

Mitochondrial Medicine: A Promising Therapeutic Option Against Various Neurodegenerative Disorders

Review

Author: Almikhlafi, Mohannad A. ; Alqurashi, Thamer M. ; Karami, Mohammed M. ; Alghamdi, Badrah S. ; Majrashi, Mohammed ; Ashraf, Ghulam Md. ; Jana, Ankit

Abstract::

Abnormal mitochondrial morphology and metabolic dysfunction have been observed in many neurodegenerative disorders (NDDs). Mitochondrial dysfunction can be caused by aberrant mitochondrial DNA, mutant nuclear proteins that interact with mitochondria directly or indirectly, or for unknown reasons. Since mitochondria play a significant role in neurodegeneration, mitochondriatargeted therapies represent a prosperous direction for the development of novel drug compounds that can be used to treat NDDs. This review gives a brief description of how mitochondrial abnormalities lead to various NDDs such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. We further explore the promising therapeutic effectiveness of mitochondria- directed antioxidants, MitoQ, MitoVitE, MitoPBN, and dimebon. We have also discussed the possibility of mitochondrial gene therapy as a therapeutic option for these NDDs.

100 Deals associated with Dimebolin hydrochloride

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External Link

KEGG	Wiki	ATC	Drug Bank
-	Dimebolin hydrochloride	R	DB11725

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Hypersensitivity	Russia	-	01 Jan 1983
Rhinitis, Allergic	Russia	-	01 Jan 1983

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Dementia due to Alzheimer's disease (disorder)	Phase 3	Russia	Bigespas Ltd.	11 Sep 2025
Huntington Disease	Phase 3	United States	MediVation, Inc.	01 Jul 2009
Huntington Disease	Phase 3	United States	Pfizer Inc.	01 Jul 2009
Huntington Disease	Phase 3	Australia	Pfizer Inc.	01 Jul 2009
Huntington Disease	Phase 3	Australia	MediVation, Inc.	01 Jul 2009
Huntington Disease	Phase 3	Canada	MediVation, Inc.	01 Jul 2009
Huntington Disease	Phase 3	Canada	Pfizer Inc.	01 Jul 2009
Huntington Disease	Phase 3	Denmark	MediVation, Inc.	01 Jul 2009
Huntington Disease	Phase 3	Denmark	Pfizer Inc.	01 Jul 2009
Huntington Disease	Phase 3	Germany	MediVation, Inc.	01 Jul 2009

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT00975481 (CTgov)	Phase 1	Alzheimer Disease \| Huntington Disease	36	placebo (Placebo)	npfivrcgkh(jyuwjipuwt) = zfgslmwbaz akelauhavs (iqzsplivdd, 10.03) View more	-	02 Apr 2013
				alprazolam (Alprazolam 1 mg)	npfivrcgkh(jyuwjipuwt) = jefjylkkjx akelauhavs (iqzsplivdd, 17.53) View more
NCT00838110 (CTgov)	Phase 3	Alzheimer Disease	742	dimebon (latrepirdine) (Dimebon (Cohort 1))	lhkxvmhzgg = taafqgdccs nfpyxckvew (wynxzlmkba, quptovhysi - vszingrcel) View more	-	08 Feb 2013
				Placebo (Placebo (Cohort 1))	lhkxvmhzgg = ctfayaarqm nfpyxckvew (wynxzlmkba, ymzvjztpbl - kbnwyvubzf) View more
NCT00920946 (Pubmed \| JAMA Neurol)	Phase 3	Huntington Disease	403	Latrepirdine 20 mg	ghylhilxqx(xjfqytuvou) = ydcvdhncbn xngxifuyeb (odlaiwjiuz )	Negative	01 Jan 2013
				Placebo	ghylhilxqx(xjfqytuvou) = xdoelkmjad xngxifuyeb (odlaiwjiuz )
NCT00939783 (CTgov)	Phase 3	Alzheimer Disease	649	Dimebon (latrepirdine)	abfyzbrecq = elqsrgwefi uxrmycfhwu (tnvnbazxcz, aovmoysnal - avdejyryjs) View more	-	14 Nov 2012
NCT01066546 (CTgov)	Phase 3	Alzheimer Disease	5	Dimebon	jevwlqasvf = fmgbrwywvd hoaoeoqjjj (vytfpxvxpd, uzrizhmuaf - azzasyoqym) View more	-	02 Oct 2012
NCT00912288 (CTgov)	Phase 3	Alzheimer Disease	86	Dimebon 20 mg po TID (Dimebon)	vcknfjzoow = qzdgzkemgw tdexdigdwq (ecbjzjhxhm, jkvfpbkkwf - nabirpydul) View more	-	02 Oct 2012
				Placebo po TID (Placebo)	vcknfjzoow = hsqygfitcr tdexdigdwq (ecbjzjhxhm, sdbkdcqyxc - ypdubixgkr) View more
NCT00497159 (Pubmed)	Phase 2	Huntington Disease	91	Latrepirdine 20 mg	mpazpdngdt(tmrgesvejz): treatment effect = 0.97 (95% CI, 0.1 - 1.85)	-	01 Feb 2010
				Placebo