Arcapillin
Arcapillin is a flavonoid that can be isolated from Artemisia capillaris Thunb. Arcapillin induces dose-dependent relaxation of ileum and pulmonary artery smooth muscle, causes slight urinary bladder smooth muscle contraction at highest tested concentrations. Arcapillin binds to the active site of SARS-CoV-2 Mpro via interactions with Gln139, His163, and His164, exhibits antiviral activity against SARS-CoV-2 and MERS-CoV. Arcapillin can be used for the research of gastrointestinal disorders, COVID-19, and Middle East respiratory syndrome (MERS).
For research use only. We do not sell to patients.
- CAS No.: 83162-82-7
- Formula: C18H16O8
- Molecular Weight:360.31
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
PTP1B[1]
In Vitro
Arcapillin binds to the SARS-CoV-2 main protease (PDB: 7L0D) with a docking score of -6.16 kcal mol−1, indicating favorable interactions with the enzyme's active site[2].
Arcapillin (72 h) exhibits antiviral activity against SARS-CoV-2 in Vero E6 cells with an IC50 of 190.8 μg mL−1, and has a low cytotoxic profile in the same cell line with a CC50 of 1228 μg mL−1, yielding a selectivity index of 6.40[2].
Arcapillin (72 h) exhibits potent antiviral activity against MERS-CoV in Vero E6 cells with an IC50 of 16.58 μg mL−1, and has a CC50 of 54.17 μg mL−1 in the same cell line, yielding a selectivity index of 3.26[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
-
CAS No. 83162-82-7
-
Molecular Weight 360.31
-
Formula C18H16O8
-
SMILES
O=C1C=C(C2=CC(OC)=C(O)C=C2O)OC3=CC(OC)=C(OC)C(O)=C13
-
Structure Classification
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
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)