Delving into the Latest Updates on Clemastine Fumarate with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

(+)-(2R)-2-(2-(((R)-p-chloro-α-methyl-α-phenylbenzyl)oxy)ethyl)-1-methylpyrrolidine, (+)-(2R)-2-[2-[[(R)-p-chloro-α-methyl-α-phenylbenzyl]oxy]ethyl]-1-methylpyrrolidine, Clemastine

+ [9]

Target

H1 receptor

Action

antagonists

Mechanism

H1 receptor antagonists(Histamine H1 receptor antagonists)

Therapeutic Areas

Immune System DiseasesInfectious DiseasesEye Diseases+ [3]

Active Indication

Conjunctivitis, AllergicCommon ColdDermatitis+ [4]

Inactive Indication

Rhinitis, Allergic, Seasonal

Originator Organization

Novartis Pharma AG

Active Organization

NISSIN Pharmaceutical Co., Ltd.

Shandong Linuo Pharmaceutical Co. Ltd.

Shandong Keyuan Pharmaceutical Co., Ltd.

Inactive Organization

Novartis Pharmaceuticals Corp.

NovaDel Pharma, Inc.

Drug Highest PhaseApproved

First Approval Date

Japan (17 Jan 1970),

Common ColdDermatitisEczema+ [3]

Regulation-

Login to view timeline

Structure/Sequence

Molecular FormulaC25H30ClNO5

InChIKeyPMGQWSIVQFOFOQ-YKVZVUFRSA-N

CAS Registry14976-57-9

View All Structures (2)

The goal of this study is to find out if the antihistamine, clemastine, can make the white matter in the brain better in older adults with depression. The study will also determine whether this improvement can make antidepressant treatment work better, reduce depressive symptoms, and improve memory and thinking.

Start Date01 Apr 2025

Sponsor / Collaborator

University of Illinois

[+1]

NCT06065670

/ Not yet recruitingPhase 1/2IIT

A Randomized, Double-Blind, Delayed Treatment, Placebo-Controlled Trial to Assess the Changes in Multi-parametric MRI in Patients With Acute Demyelinating Lesions Taking Clemastine Fumarate as a Myelin Repair Therapy

The clinical trial is intended to assess for clinical evidence of Clemastine Fumarate as a myelin repair therapy in patients with acute inflammatory injury-causing demyelination as measured by multi-parametric MRI assessments.
No reparative therapies exist for the treatment of acute demyelinating lesions. Clemastine fumarate was identified along with a series of other antimuscarinic medications as a potential remyelinating agent using the micropillar screen (BIMA) developed at the University of California, San Francisco (UCSF). Following in vivo validation, an FDA IND exemption was granted to investigate clemastine for the treatment of multiple sclerosis in the context of chronic optic neuropathy. That pilot study was recently completed and is the first randomized control trial documenting efficacy for a putative remyelinating agent for the treatment of MS. The preselected primary efficacy endpoint (visual evoked potential) was met and a strong trend to benefit was seen for the principal secondary endpoint assessing function (low contrast visual acuity). That trial number was 13-11577.
This study seeks to follow up on that study and examine clemastine fumarate's protective and reparative effects in the context of acute demyelinating brain lesions as imaged by multi-parametric MRI assessments. The investigators will be assessing the effects of clemastine fumarate as a remyelinating therapy and assessing its effect on MRI metrics of lesions found in patients with a confirmed diagnosis of acute inflammatory injury-causing demyelination.
In addition to using conventional multi-parametric MRI assessments, this study will also evaluate a new MRI technique called Ultrashort Echo Time (UTE) MRI to assess the effects of clemastine fumarate as a remyelinating therapy of acute lesions found in patients with a confirmed diagnosis of acute inflammatory injury-causing demyelination and compare it to the other assessments.

Start Date15 Sep 2024

Sponsor / Collaborator

The University of California, San Francisco

NCT06087757

/ RecruitingPhase 3IIT

Clemastine Treatment in Individuals With Williams Syndrome- a Double-blind Placebo Control to Assess the Safety and Efficacy

This study explores the neurobiological etiology of Williams syndrome and potential therapeutic targets for associated social, motor, and cognitive abnormalities. The main translational objective will be to test the effectiveness of Clemasntine on neurocognitive and other associated abnormalities in individuals with Williams syndrome.

Start Date01 Apr 2024

Sponsor / Collaborator

Sheba Medical Center

[+1]

100 Clinical Results associated with Clemastine Fumarate

Login to view more data

100 Translational Medicine associated with Clemastine Fumarate

Login to view more data

100 Patents (Medical) associated with Clemastine Fumarate

Login to view more data

1,105

Literatures (Medical) associated with Clemastine Fumarate

01 Mar 2025·International Immunopharmacology

Clemastine fumarate alleviates endoplasmic reticulum stress through the Nur77/GFPT2/CHOP pathway after ischemia/reperfusion in rat hearts

Article

Author: Wang, Yuansheng ; Song, Caixuan ; Sun, Fan ; Liu, Yongxin ; Wang, Yingmeng ; Juan, Zhaodong ; Wang, Rouguo ; Sun, Xiaotong ; He, Yuling

BACKGROUND AND PURPOSEClemastine fumarate (CLE) is an H1 receptor (H1R) antagonist that is used clinically to treat various allergic disorders. It blocks histamine release from mast cells and inhibits H1R. Preliminary studies have shown that CLE can reduce myocardial ischemia/reperfusion (I/R) injury. In this study, we confirmed the efficacy of CLE against myocardial I/R injury using in vivo and in vitro examinations.EXPERIMENTAL APPROACHTo test the efficacy of CLE against myocardial I/R injury, we established a rat model of myocardial hypoxia/reperfusion injury. A series of assessments were conducted to determine cardiac function, measure areas of myocardial infarction, and analyze the histopathological changes. Additionally, we developed a rat model of cardiomyocyte hypoxia/reoxygenation (H/R); in both models, we quantified the expression levels of key markers and cardiac injury-specific proteins to assess the biochemical milieu influenced by CLE treatment.KEY RESULTSOur findings demonstrated that CLE reduced the expression of nerve growth factor-induced gene B (Nur77), glutamine-fructose-6-phosphate transaminase 2 (GFPT2), and C/EBP homologous protein (CHOP) and decreased the area of myocardial infarction and the degree of endoplasmic reticulum stress. CLE pretreatment ameliorated abnormal fibers and myocardial edema and reduced the inflammatory cell infiltration caused by I/R injury. While Nur77 overexpression aggravated cardiac function, these effects were ameliorated by the downregulation of Nur77.CONCLUSION AND IMPLICATIONSWe anticipate that these results validate the hypothesis that CLE mitigates apoptosis and reduces endogenous stress within myocardial cells by modulating Nur77, GFPT2, and CHOP expression. These findings elucidate the therapeutic mechanisms by which CLE alleviates myocardial I/R injury. In addition, they will serve as a new theoretical foundation for developing future treatment strategies and enhancing clinical applications in cardiac care.

01 Feb 2025·Brain, Behavior, and Immunity

Demyelination of the amygdala mediates psychological stress-induced emotional disorders partially contributed by activation of P2X7R/NLRP3 cascade

Article

Author: Li, Yanning ; Fu, Xiaoliang ; Lin, Dandan ; Jing, Chenchen ; Zhang, Yi

Psychological stress can lead to emotional disorders, such as anxiety and depression; however, the underlying mechanisms are complicated and remain unclear. In this study, we established a mouse psychological stress model using an improved communication box, in which the psychologically stressed mice received visual, auditory, and olfactory emotional stimuli from the mice receiving electric foot shock, thus avoiding physical stress interference. After the 14-day psychological stress paradigm, our mice exhibited a significant increase in depressive and anxious behaviors. We then performed proteomic liquid chromatography-tandem mass spectrometry for proteomic data analysis of the amygdala, and the results demonstrated that differentially expressed proteins were more enriched in myelin-related biological processes, cellular components, and molecular functions, indicating a correlation between psychological stress-induced emotional disorders and amygdala myelin damage. Molecular and morphological evidence further confirmed that psychological stress damages myelin ultrastructure, downregulated myelin basic protein and proteolipid protein expression, and reduced oligodendrocyte proliferation in the amygdala. Moreover, clemastine, an antimuscarinic and antihistaminic compound that has been shown to enhance oligodendrocyte differentiation and myelination, rescued depressive behaviors accompanied by increased oligodendrogenesis. In the amygdala, psychological stress was also noted to activate microglia and increase the levels of NOD-like receptor protein 3 (NLRP3) and the proinflammatory cytokines interleukin 1β and tumor necrosis factor α, as indicated by ELISA and Western blot analyses. Moreover, in stressed mice, the administration of Brilliant Blue G, a purinergic ligand-gated ion channel 7 receptor (P2X7R) antagonist, completely reversed the increases in NLRP3 and cleaved caspase-1 levels and partially prevented amygdala myelin damage. In conclusion, amygdala demyelination may mediate psychological stress-induced emotional disorders, and P2X7R/NLRP3 cascade activation partially contributes to amygdala myelin damage after psychological stress.

01 Jan 2025·Brain Research

Clemastine enhances exercise-induced motor improvement in hypoxic ischemic rats

Article

Author: Komaki, Yuji ; Tsurugizawa, Tomokazu ; Iwaki, Sunao ; Goto, Taichi ; Takashima, Ichiro ; Kunori, Nobuo

Neonatal hypoxic ischemia (HI) occurs owing to reduced cerebral oxygen levels and perfusion during the perinatal period. Brain injury after HI triggers neurological manifestations such as motor impairment, and the improvement of impaired brain function remains challenging. Recent studies suggest that cortical myelination plays a role in motor learning, but its involvement in motor improvement after HI injury is not well understood. This study aimed to investigate the impact of myelination on motor improvement following neonatal HI injury. We employed a modified Rice-Vannucci model; the right common carotid artery of postnatal day 7 (P7) Wistar rats was isolated and divided, and the rats were then exposed to hypoxic condition (90 min, 8 % O2). A total of 101 rats (66 males) were divided into four groups: trained-HI (n = 38), trained-Sham (n = 16), untrained-HI (n = 31), and untrained-Sham (n = 16). The trained groups underwent rotarod-based exercise training from P22 to P41 (3 days per week). Structural analysis using magnetic resonance imaging and immunohistochemistry (n = 6 per group) revealed increased fractional anisotropy and myelin density in the primary somatosensory cortex of the trained-HI group. We further evaluated the effect of myelination promotion on rotarod performance by administering clemastine, a myelination-promoting drug, via daily intraperitoneal injections. Clemastine did not enhance motor improvement in untrained-HI rats. However, clemastine-administered trained-HI rats (n = 7) exhibited significantly improved motor performance compared to both saline-administered trained-HI rats (n = 11) and clemastine-administered untrained-HI rats (n = 7). These findings suggest that myelination may be a key mechanism in motor improvement after HI injury and that combining exercise training with clemastine administration could be an effective therapeutic strategy for motor improvement following HI injury.

100 Deals associated with Clemastine Fumarate

Login to view more data

External Link

KEGG	Wiki	ATC	Drug Bank
D00666	Clemastine Fumarate	R06AA04 D04AA14	DB00283

R&D Status

Approved

10 top approved records.

Login

to view more data

Indication	Country/Location	Organization	Date
Conjunctivitis, Allergic	China	Shandong Linuo Pharmaceutical Co. Ltd.	01 Jan 1991
Conjunctivitis, Allergic	China	Shandong Keyuan Pharmaceutical Co., Ltd.	01 Jan 1991
Common Cold	Japan	NISSIN Pharmaceutical Co., Ltd.	17 Jan 1970
Dermatitis	Japan	NISSIN Pharmaceutical Co., Ltd.	17 Jan 1970
Eczema	Japan	NISSIN Pharmaceutical Co., Ltd.	17 Jan 1970
Pruritus	Japan	NISSIN Pharmaceutical Co., Ltd.	17 Jan 1970
Rhinitis, Allergic	Japan	NISSIN Pharmaceutical Co., Ltd.	17 Jan 1970
Urticaria	Japan	NISSIN Pharmaceutical Co., Ltd.	17 Jan 1970

Developing

10 top R&D records.

Login

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Rhinitis, Allergic, Seasonal	Preclinical	United States	NovaDel Pharma, Inc.	-

Login to view more data

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


TRAP-MS (ACTRIMS2024)	Not Applicable	Multiple Sclerosis, Chronic Progressive	9	Clemastine Fumarate	srksjcvdpq(gesvhpjrmt) = imlkiapbdr mquueiosav (aiawvzlqwx )	Negative	29 Feb 2024
NCT02040298 (ReBUILD, CTgov)	Phase 2	Multiple Sclerosis, Relapsing-Remitting	50	Clemastine (Clemastine)	kafwrtfgwe(vkjojdejue) = yrdttwgids awnksauapd (mygnenbwxq, kmnacijynk - juntmndaqn) View more	-	15 Jul 2021
				Placebo+clemastine (Placebo)	kafwrtfgwe(vkjojdejue) = rnnsfwfqta awnksauapd (mygnenbwxq, islrlkwzij - cnfhuillbk) View more
SABCS2020	Not Applicable	Breast Cancer Adjuvant estrogen receptor	-	Desloratadine	-	Positive	15 Feb 2020
				Loratadine