104632-27-1
Chemical Structure
Dexpramipexole dihydrochloride
Synonym(s): (R)-Pramipexole dihydrochloride; R-(+)-Pramipexole dihydrochloride; KNS-760704 dihydrochloride
- CAS No.: 104632-27-1
- Formula:C10H19Cl2N3S
- Molecular Weight:284.26
IUPAC Name: (R)-N6-propyl-4,5,6,7-tetrahydrobenzo[d]thiazole-2,6-diamine dihydrochloride
InChIKey: QMNWXHSYPXQFSK-XCUBXKJBSA-N
SMILES: NC(S1)=NC2=C1C[C@H](NCCC)CC2.[H]Cl.[H]Cl
Biological Activity: Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more[1][2][3][4][5][6].
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Dexpramipexole dihydrochloride | 99.94% | Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more. | ||||||||||||||||||||
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Dexpramipexole dihydrochloride (Standard) | ≥98% | Dexpramipexole ((R)-Pramipexole) dihydrochloride (Standard) is the analytical standard of Dexpramipexole (dihydrochloride). This product is intended for research and analytical applications. Dexpramipexole dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more. | ||||||||||||||||||||
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Dexpramipexole-d3 dihydrochloride | Dexpramipexole-d3 ((R)-Pramipexole-d3) dihydrochloride is the deuterium labeled Dexpramipexole. Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more. | |||||||||||||||||||||
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- [1]. Tang L, et al. Dexpramipexole attenuates myocardial ischemia/reperfusion injury through upregulation of mitophagy. Eur J Pharmacol. 2021;899:173962. [Content Brief]
- [2]. Wang B, et al. Dexpramipexole Attenuates White Matter Injury to Facilitate Locomotion and Motor Coordination Recovery via Reducing Ferroptosis after Intracerebral Hemorrhage. Oxid Med Cell Longev. 2022;2022:6160701. Published 2022 Aug 4. [Content Brief]
- [3]. Zhang Y, et al. Dexpramipexole ameliorates cognitive deficits in sepsis-associated encephalopathy through suppressing mitochondria-mediated pyroptosis and apoptosis. Neuroreport. 2023;34(4):220-231. [Content Brief]
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[4]. Cusack RP, Sulaiman I, Gauvreau GM. Refashioning dexpramipexole: A new horizon in eosinophilic asthma? J Allergy Clin Immunol. 2023 Nov;152(5):1092-1094.
[Content Brief] -
[5]. Urru M, et al. Dexpramipexole blocks Nav1.8 sodium channels and provides analgesia in multiple nociceptive and neuropathic pain models. Pain. 2020 Apr;161(4):831-841.
[Content Brief] - [6]. Panch SR, et al. Dexpramipexole as an oral steroid-sparing agent in hypereosinophilic syndromes. Blood. 2018;132(5):501-509. [Content Brief]