Nalanthalide
Nalanthalide is a voltage-gated potassium channel Kv1.3 blocker (IC50=3.9 µM) and a potential immunosuppressant. Nalanthalide can be used for research on inflammatory immune diseases, such as neuroinflammation.
For research use only. We do not sell to patients.
- CAS No.: 145603-76-5
- Formula: C30H44O5
- Molecular Weight:484.67
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
IC50: 3.9 µM (Kv1.3)[1].
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| T-cell | EC50 |
500 nM
Compound: 7
|
Depolarization of human T cells by electrophysiological method
Depolarization of human T cells by electrophysiological method
|
[PMID: 19042133] |
Chemical Information
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CAS No. 145603-76-5
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Molecular Weight 484.67
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Formula C30H44O5
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SMILES
O=C1C(C[C@@H]2C(CC[C@@]3([H])[C@@](CC/C=C(C)/C)(C)[C@@H](OC(C)=O)CC[C@]23C)=C)=C(OC)OC(C)=C1C
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Structure Classification
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Initial Source
Nalanthamala sp.
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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.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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)