Amyotrophic Lateral Sclerosis Riluzole Powder Pharmaceutical Riluzolepurity Riluzole

• Customization: Available
• CAS No.: 1744-22-5
• Formula: C8h5f3n2OS
• Model NO.: QS-Riluzole
• EINECS: 605-724-6
• Packaging Material: Negotiable
• Storage Method: Normal
• Shelf Life: 2year
• Nutrient Composition: Riluzole
• Resource: Riluzole
• The content of active substances: 99%
• Product Name: Riluzole
• Name: Riluzole Powder
• Appearance: White Powder
• Color: White
• Grade: Pharmaceutical Grade
• Assay: HPLC 99%
• Application: Pharmaceutical Grade
• Specific: COA
• Test Method: HPLC
• CAS No: 1744-22-5
• MW: 234
• Mf: C8h5f3n2OS
• Density: 1.572
• Melting Point: 296.3
• Boiling Point: 116
• Transport Package: Negotiabie
• Specification: 99%
• Trademark: QS
• Origin: Xi′an Shaanxi
• Production Capacity: 500kg/Month

Product Description

Amyotrophic Lateral Sclerosis Riluzole Powder Pharmaceutical Riluzolepurity Riluzole

Product Description

Product Detials

Product Name	Riluzole
Apperance	White Powder
CAS	1744-22-5
MF	C8H5F3N2OS
MW	234.196

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Riluzole is a neuroprotective agent and the first FDA-approved medication for the treatment of amyotrophic lateral sclerosis (ALS), a progressive neurodegenerative disorder. Chemically designated as *2-amino-6-(trifluoromethoxy)benzothiazole*, its molecular formula is CC8H5F3N2OS. Approved in 1995, riluzole is available as 50 mg oral tablets and an oral suspension (Tiglutik®), designed to slow disease progression and extend survival in ALS patients. It is classified as a glutamate modulator, targeting excitotoxic pathways implicated in motor neuron degeneration.

Application&Function

Riluzole exerts its therapeutic effects through multimodal mechanisms aimed at mitigating glutamate-mediated excitotoxicity, a key driver of motor neuron death in ALS. It inhibits voltage-gated sodium channels on glutamatergic neurons, reducing the presynaptic release of glutamate. Additionally, riluzole enhances glutamate uptake by astrocytes via upregulation of excitatory amino acid transporters (EAATs), thereby lowering extracellular glutamate concentrations. Secondary mechanisms include antagonism of NMDA and kainate receptors, inhibition of protein kinase C, and promotion of neurotrophic factor synthesis. Collectively, these actions attenuate neuronal hyperexcitability and oxidative stress, preserving motor function.

Specification

Certificate of Analysis