Procumbenoside I
Procumbenoside I is a naturally derived broad-spectrum antiviral agent targeting the SFTSV glycoprotein Gn. Procumbenoside I binds to the conserved B domain of SFTSV Gn, blocking the binding and internalization steps during viral entry. Procumbenoside I inhibits the entry of VSV, H5N1, and SARS-CoV-2 pseudoviral particles, while exhibiting antiviral activity against bunyaviruses such as LCMV and WELV. Procumbenoside I protects mice against lethal SFTSV challenge, reducing mortality and alleviating pathological damage. Procumbenoside I is useful for research related to viral infections.
For research use only. We do not sell to patients.
- CAS No.: 2243471-10-3
- Formula: C26H24O12
- Molecular Weight:528.47
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| Huh-7 | IC50 |
0.583 μM
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Inhibition of SFTSV infection in human Huh7 cells assessed by reduction in viral load in cell culture supernatants quantified by qRT-PCR at 48 h post-infection.
Inhibition of SFTSV infection in human Huh7 cells assessed by reduction in viral load in cell culture supernatants quantified by qRT-PCR at 48 h post-infection.
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42425227 |
| A549 | EC50 |
0.014 μM
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Antiviral activity against VSVpp in A549 human lung epithelial cells assessed by inhibition of pseudovirus infection.
Antiviral activity against VSVpp in A549 human lung epithelial cells assessed by inhibition of pseudovirus infection.
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33818100 |
| A549 | EC50 |
0.0063 μM
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Antiviral activity against H5N1pp in A549 human lung epithelial cells assessed by inhibition of pseudovirus infection.
Antiviral activity against H5N1pp in A549 human lung epithelial cells assessed by inhibition of pseudovirus infection.
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33818100 |
| A549 | CC50 |
1.13 μM
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Cytotoxicity against A549 human lung epithelial cells.
Cytotoxicity against A549 human lung epithelial cells.
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33818100 |
| HEK-293T | EC50 |
1.13 μM
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Antiviral activity against SARS-CoV-2pp in HEK-293T-hACE2 cells assessed by luciferase assay after 72 hrs infection.
Antiviral activity against SARS-CoV-2pp in HEK-293T-hACE2 cells assessed by luciferase assay after 72 hrs infection.
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33818100 |
| HEK-293T | CC50 |
2.15 μM
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Cytotoxicity against HEK-293T-hACE2 cells.
Cytotoxicity against HEK-293T-hACE2 cells.
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33818100 |
In Vitro
Procumbenoside I (2.5-10 μM; 48 h) effectively inhibits SFTSV infection in Huh7 cells with an IC50 of 0.583 μM and a CC50 of >20 μM[1].
Procumbenoside I does not exert a direct virucidal effect on SFTSV particles[1].
Procumbenoside I (10 μM; 1 h before infection, 2 h infection, 24 h collection) inhibits SFTSV infection at the viral entry stage, with maximal effect when present before and during infection[1].
Procumbenoside I (5-20 μM; 1 h pretreatment, 15 min cooling, 2 h binding) inhibits the binding of SFTSV to Huh7 cells and the entry of SFTSV into Huh7 cells[1].
Procumbenoside I (compound 5) (25 μM) exhibits potent antiviral activity against VSVpp and H5N1pp in A549 cells, with EC50 values of 0.014 μM and 0.0063 μM, respectively[2].
Procumbenoside I (72 h) exhibits moderate antiviral activity against SARS-CoV-2pp in HEK-293T-hACE2 cells with an EC50 of 1.13 μM[2][3].
Procumbenoside I (100 μM; 1 h incubation, 5 min heating) directly interacts with and stabilizes SFTSV Gn but not Gc in Huh7 cell lysates[1].
Procumbenoside I (5-400 μM; 1 h incubation, 5 min heating) stabilizes SFTSV Gn in a dose-dependent manner[1].
Procumbenoside I (100 μM; 1 h incubation, 20 min pronase treatment) binds to SFTSV Gn, thereby protecting it from pronase-mediated degradation[1].
Procumbenoside I directly binds to SFTSV-Gn with a KD of 5.73 × 10-5 M[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Huh7 cells
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Concentration:2.5, 10 μM
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Incubation Time:48 h
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Result:Inhibited SFTSV infection with an IC50 of 0.583 μM.
Exhibited a CC50 of >20 μM.
Yielded a selection index (SI) of >34.
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Cell Line:Huh7 cells
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Concentration:10 μM
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Incubation Time:1 h (pre-infection); 2 h (infection); 24 h (collection)
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Result:Reduced vRNA levels when present prior to and during infection.
Showed a more limited inhibitory effect upon post-infection addition.
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Cell Line:Huh7 cells
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Concentration:5, 10, 20 μM
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Incubation Time:1 h (pre-treatment); 15 min (chilling); 2 h (binding)
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Result:Reduced vRNA levels compared to the control group.
Reduced intracellular vRNA levels compared to the control group.
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Cell Line:Huh7 cell lysates
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Concentration:5, 25, 50, 100, 200, 400 μM
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Incubation Time:1 h (incubation); 5 min (heating)
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Result:Stabilized Gn in a dose-dependent manner.
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Cell Line:Huh7 cell lysates
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Concentration:100 μM
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Incubation Time:1 h (incubation); 20 min (pronase treatment)
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Result:Reduced pronase-mediated degradation of SFTSV Gn.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J (male, six-week-old, pretreated with anti-IFNAR1 blocking antibody and challenged intraperitoneally with SFTSV, infected with 100 μL of SFTSV solution (1.5 × 105 PFU/mL))[1]
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Dosage:1, 5 mg/kg/day
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Administration:i.p.; daily; 5 consecutive days
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Result:Reduced fatality rates with survival rates of 66.7% at 1 mg/kg/day and 83.3% at 5 mg/kg/day.
Significantly reduced serum viral loads and splenic viral titers at both doses.
Confirmed inhibitory effect on viral infection by immunohistochemical analysis of spleen sections using anti-SFTSV NP antibody.
Alleviated splenic pathological damage such as attenuating the loss of white pulp by H&E staining.
Chemical Information
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CAS No. 2243471-10-3
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Molecular Weight 528.47
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Formula C26H24O12
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SMILES
O=C1C2=C(C=3C(C(O[C@@H]4O[C@H](CO)[C@@H](O)[C@H](O)[C@H]4O)=C2CO1)=CC(OC)=C(O)C3)C=5C=C6C(=CC5)OCO6
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Structure Classification
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Initial Source
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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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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Procumbenoside I Related Classifications
HY-N21657 Related Classifications
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