Siagoside(Siagoside) - _专利_临床

概要

基本信息

药物类型

化学药

别名

Sygen

靶点-

作用机制-

治疗领域

神经系统疾病心血管疾病内分泌与代谢疾病+ [1]

在研适应症-

非在研适应症

阿尔茨海默症帕金森病脊髓损伤+ [1]

原研机构

Fidia Pharma USA, Inc.

在研机构-

非在研机构

Fidia Farmaceutici SpA

Fidia Pharma USA, Inc.

最高研发阶段终止临床1期

首次获批日期-

最高研发阶段(中国)-

特殊审评-

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结构

分子式C73H129N3O30

InChIKeyWVHBJHLTCHODOA-UHFFFAOYSA-N

CAS号100345-64-0

关联

2

项与 Siagoside 相关的临床试验

NCT04976127 / Active, not recruiting临床1期

Safety Evaluation of Intravenous Talineuren (TLN) in Parkinson's Disease-affected Patients

This study is an open-label, single ascending dose escalation followed by a multiple administration dose at the maximal suitable dose (MSD). The investigational Medicinal Product (IMP) is given as an add-on therapy.
Talineuren consists of GM1 (monosialotetrahexosylganglioside), the pharmacologically active ingredient, associated with a proprietary lipid formulation assembled as liposomes.
The primary objective is to demonstrate the safety of TLN administration intravenously in Parkinson patients.
Secondary objectives are the determination of the maximal suitable dose based on the safety profile and preliminary efficacy, as well as the determination of the pharmacokinetics (PK) profile.

开始日期2021-12-07

申办/合作机构

InnoMedica Schweiz AG

NCT01884987 / Unknown statusN/AIIT

Phase II Study of Monosialotetrahexosylganglioside for Cerebral Radiation Necrosis

Cerebral radiation necrosis (CRN) is a well-documented late complication of radiation therapy for cancers, and may have a devastating effect on the patient's quality of life (QOL). However,CRN was once regarded as a progressive and irreversible disease, no standard therapy has been suggested for CRN. In our clinical practice, we have used monosialotetrahexosylganglioside (GM1)to treat CRN, and found that GM1 can successfully reverse CRN. So we carried out this prospective study to test the efficacy of GM1 for CRN.

开始日期2012-01-01

申办/合作机构

复旦大学

100 项与 Siagoside 相关的临床结果

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100 项与 Siagoside 相关的转化医学

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100 项与 Siagoside 相关的专利（医药）

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975

项与 Siagoside 相关的文献（医药）

2024-10-01·Molecular Neurobiology

Correction to: Protective Effect of GM1 Attenuates Hippocampus and Cortex Apoptosis After Ketamine Exposure in Neonatal Rat via PI3K/AKT/GSK3β Pathway

作者: Jin, Xiaodi ; Bai, Hui ; Li, Rouqian ; Shen, Meilun ; Gao, Li ; Ma, Xiangying ; Liu, Wenhan ; Zhang, Zhiheng

2024-08-28·ACS Central Science

Probing the Origin of Affinity in the GM1-Cholera Toxin Complex through Site-Selective Editing with Fluorine

Article

作者: Hayashi, Taiki ; Löbbert, Arnelle ; Siebold, Kathrin ; Aufiero, Marialuisa ; Gilmour, Ryan ; Köhnke, Jesko ; Bussmann, Kathrin ; Bergander, Klaus ; Gossert, Alvar D. ; Jordan, Christina ; Pape, Felix ; Teschers, Charlotte S. ; Axer, Alexander ; Fan, Jingran ; Campbell, Emma

Carbohydrates regulate an inimitable spectrum of biological functions, yet successfully leveraging this therapeutic avenue continues to be frustrated by low affinities with glycan-specific proteins. A conspicuous exception is the interaction of monosialotetrahexosylganglioside (GM1) with the carbohydrate-recognition domain of cholera toxin from Vibrio cholerae: this is one of the strongest protein-carbohydrate interactions known. To establish the importance of a long-discussed key hydrogen bond between C2 of the terminal galactose of GM1 and the B subunit pentamer of cholera toxin (CTB₅), the total synthesis of a selectively fluorinated GM1 epitope was conducted in 19 steps. This process of molecular editing (O^δ-H → F^δ-) strategically deletes the hydrogen bond donor while retaining the localized partial charge of the substituent. Comparison of the binding affinity of F-GM1/CTB₅ with native GM1, the GM1 carbohydrate epitope, and meta-mononitrophenyl-α-galactoside (MNPG) revealed a trend that fully supports the importance of this key interaction. These NMR data suggest that F-GM1 binds in a closely similar conformation as native GM1. Crystallographic analyses of the complex also confirm that the OH → F bioisosteric exchange at C2 of the terminal galactose induces a ring conformation that eliminates key hydrogen bonds: these interactions are compensated for by inter- and intramolecular fluorine-specific interactions.

2024-07-01·Neuroscience

GM1 Ameliorates Neuronal Injury in Rats after Cerebral Ischemia and Reperfusion: Potential Contribution of Effects on SPTBN1-mediated Signaling

Article

作者: Sun, Chun-Yan ; Liu, Jia-Xing ; Wang, Cai-Ping ; Shi, Yun-Wei ; Liu, Dong ; Zhao, Shu-Yong ; Fan, Xing-Juan ; Xu, Chun-Cheng

Monosialoganglioside GM1 (GM1) has long been used as a therapeutic agent for neurological diseases in the clinical treatment of ischemic stroke. However, the mechanism underlying the neuroprotective function of GM1 is still obscure until now. In this study, we investigated the effects of GM1 in ischemia and reperfusion (I/R) brain injury models. Middle cerebral artery occlusion and reperfusion (MCAO/R) rats were treated with GM1 (60 mg·kg^-1·d^-1, tail vein injection) for 2 weeks. The results showed that GM1 substantially attenuated the MCAO/R-induced neurological dysfunction and inhibited the inflammatory responses and cell apoptosis in ischemic parietal cortex. We further revealed that GM1 inhibited the activation of NFκB/MAPK signaling pathway induced by MCAO/R injury. To explore its underlying mechanism of the neuroprotective effect, transcriptome sequencing was introduced to screen the differentially expressed genes (DEGs). By function enrichment and PPI network analyses, Sptbn1 was identified as a node gene in the network regulated by GM1 treatment. In the MCAO/R model of rats and oxygen-glucose deprivation and reperfusion (OGD/R) model of primary culture of rat cortical neurons, we first found that SPTBN1 was involved in the attenuation of I/R induced neuronal injury after GM1 administration. In SPTBN1-knockdown SH-SY5Y cells, the treatment with GM1 (20 μM) significantly increased SPTBN1 level. Moreover, OGD/R decreased SPTBN1 level in SPTBN1-overexpressed SH-SY5Y cells. These results indicated that GM1 might achieve its potent neuroprotective effects by regulating inflammatory response, cell apoptosis, and cytomembrane and cytoskeleton signals through SPTBN1. Therefore, SPTBN1 may be a potential target for the treatment of ischemic stroke.

100 项与 Siagoside 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB12351

研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
帕金森病	临床3期	-	Fidia Pharma USA, Inc.	-
阿尔茨海默症	临床1期	-	Fidia Pharma USA, Inc.	-
脊髓损伤	临床1期	-	Fidia Pharma USA, Inc.	-
脑卒中	临床1期	-	Fidia Pharma USA, Inc.	-