Squalamine phosphate
Based on 1 publication(s) in Google Scholar
Squalamine phosphate (Compound ENT-01) is an orally active neuroprotective agent. Squalamine phosphate can displace α-Syn that is bound electrostatically to nerve cell membranes and prevent aggregation of α-Syn. Squalamine phosphate can be used for the research of neurological disease, such as Parkinson’s disease.
For research use only. We do not sell to patients.
- CAS No.: 1309370-82-8
- Formula: C34H68N3O9PS
- Molecular Weight:725.96
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) Squalamine phosphate
MoreAll α-synuclein Isoforms
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Biological Activity
Description
Chemical Information
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CAS No. 1309370-82-8
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Molecular Weight 725.96
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Formula C34H68N3O9PS
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SMILES
O=P(O)(O)O.O[C@H]1[C@]2([H])[C@@](CC[C@]3([C@@]2([H])CC[C@]3([H])[C@H](C)CC[C@H](C(C)C)OS(=O)(O)=O)C)([H])[C@@]4([C@@](C[C@H](CC4)NCCCNCCCCN)([H])C1)C
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Synonyms
ENT 01; MSI-1256 phosphate
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (1)
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Journal Impact Factor
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Most Recent
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J Enzyme Inhib Med Chem
Identification of chemical scaffolds for targeting ubiquitin-specific protease 11 (USP11) through high-throughput virtual screening. [Abstract]2025 Dec;40(1):2518191. PMID: 40588719
Protocols
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Research Protocol for Neurological Diseases
PINK1/Parkin-mediated mitophagy pathway is a mitochondrial quality-control signaling axis in which mitochondrial depolarization stabilizes PINK1 on damaged mitochondria, activates Parkin recruitment and E3 ubiquitin ligase activity, promotes ubiquitination of outer mitochondrial membrane proteins, recruits selective autophagy adaptors, and drives lysosomal degradation of damaged mitochondria. In neurological disease research, this pathway is experimentally important because neurons, especially dopaminergic neurons, are highly dependent on mitochondrial integrity, and defective mitochondrial turnover can lead to mitochondrial dysfunction, oxidative stress, impaired neuronal survival, α-synuclein accumulation, and neuroinflammatory damage-associated signals. The genetic disease link is strongest in Parkinson’s disease because mutations in PRKN/parkin cause autosomal recessive juvenile parkinsonism, mutations in PINK1 cause hereditary early-onset Parkinson’s disease, and Drosophila studie
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)