Suraxavir marboxil
Suraxavir marboxil (GP681; Cap-dependent endonuclease-IN-3) is a PA subunit cap-dependent endonuclease inhibitor with antiviral activity. Suraxavir marboxil inhibits PA subunit cap-dependent endonuclease activity and inhibits influenza A and/or influenza B viral replication. Suraxavir marboxil can be used alone or in combination with other anti-influenzal agents for the prevention of influenza A and/or influenza B viral infectious diseases. Suraxavir marboxil can be used for the research of influenza A and/or influenza B viral infectious diseases.
For research use only. We do not sell to patients.
- CAS No.: 2364589-86-4
- Formula: C29H25F2N3O7S
- Molecular Weight:597.59
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Parmacokinetics
| Species | Dose | Route | T1/2 | Tmax | Cmax | AUC0-t | F |
|---|---|---|---|---|---|---|---|
| Rat[1] | 3.0 mg/kg | i.g. | 3.32 h | 1.67 h | 253 ng/mL | 1377 ng·h/mL | 47.2 % |
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:BALB/c mice infected with A/WS/33 (H1N1) virus[1]
-
Dosage:15 mg/kg
-
Administration:P.o.; daily for 5 days
-
Result:Achieved a statistically significant reduction in lung influenza virus titers.
Increased survival rate to 100%.
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
-
CAS No. 2364589-86-4
-
Molecular Weight 597.59
-
Formula C29H25F2N3O7S
-
SMILES
O=C1N2[C@](COC3(CC3)C2)([H])N([C@@]4([H])C5=CC=C(F)C(F)=C5CSC6=CC=CC=C64)N7C1=C(C(C=C7)=O)OCOC(OC)=O
-
Synonyms
GP681; Cap-dependent endonuclease-IN-3
-
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)