Sophoranol
Based on 1 Customer Validation
Sophoranol is an alkaloid that can be isolated from S. flavescens, with antiviral activity. Sophoranol has anti-HBV (hepatitis B virus) activity. Sophoranol shows potent antiviral activities against respiratory syncytial virus (RSV) with an IC50 of 10.4 μg/mL.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Reinheit : 96.08%
- CAS. Nr.: 3411-37-8
- Formel: C15H24N2O2
- Molecular Weight:264.36
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Speicherung:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
Biologische Aktivität
Beschreibung
IC50 & Target
IC50: 10.4 μg/mL (RSV)[2]
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| Vero | IC50 |
252.18 μM
Compound: 11
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Antiviral activity against coxsackievirus B3 infected in African green monkey Vero cells assessed as inhibition of virus-induced cytopathogenic effect dosed 1 hr after viral adsorption
Antiviral activity against coxsackievirus B3 infected in African green monkey Vero cells assessed as inhibition of virus-induced cytopathogenic effect dosed 1 hr after viral adsorption
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[PMID: 26132528] |
In Vitro
Sophoranol has a remarkable inhibitory effect on the secretion of HBsAg and HBeAg in 2.2.15 cell line[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS. Nr. 3411-37-8
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Appearance Solid
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Molecular Weight 264.36
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Formel C15H24N2O2
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Color White to off-white
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SMILES
O=C1CCC[C@]2([H])[C@@]3([H])CCCN4[C@@]3([H])[C@](CCC4)(O)CN21
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Structure Classification
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Initial Source
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Protokoll
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Reinheit & Dokumentation
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Data Sheet (273 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
Verweise
[1]. Guan Ye, et al. LC-MS characterization of efficacy substances in serum of experimental animals treated with Sophora flavescens extracts. Biomed Chromatogr. 2007 Jun;21(6):655-60. [Content Brief]
[2]. Shuang-Cheng Ma, et al. Antiviral Chinese medicinal herbs against respiratory syncytial virus. J Ethnopharmacol. 2002 Feb;79(2):205-11. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)