Antiviral agent 74
Antiviral agent 74 is an antiviral agent consisting of Cidofovir (HY-17438) prodrug and lipid chain. Antiviral agent 74 can inhibit the activity of viral DNA polymerase by transforming into Cidofovir.Antiviral agent 74 demonstrates potent antiviral activity against vacciniavirus (VACV) (EC50 = 0.156 μM) comparable to Brincidofovir (HY-14532). Antiviral agent 74 shows superior potency against monkeypox virus (MPXV) with an EC50 vales of 0.202 μM. Antiviral agent 74 can be used for the research of virus infection.
For research use only. We do not sell to patients.
- CAS No.: 3059641-72-1
- Formula: C28H54N3O8PS
- Molecular Weight:623.78
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All DNA/RNA Synthesis Isoforms
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Biological Activity
Description
In Vitro
Antiviral agent 74 (Compound 13f) demonstrates potent antiviral activity against vacciniavirus (VACV) and monkeypox virus (MPXV) in Vero cells with EC50 values of 0.156 and 0.202 μM and[1].
Antiviral agent 74 demonstrates low cytotoxicity in Vero cells with a CC50 of 11.36 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
| Species | Dose | Route | Cmax | Tmax | AUClast | F | T1/2 |
|---|---|---|---|---|---|---|---|
| Rat | 3 mg/kg | i.v. | 5.63.5 ng/mL | / | 1873.9 ng·h/mL | / | 0.19 h |
| Rat | 15 mg/kg | p.o. | 668.4 ng/mL | 0.83 h | 1607.4 ng·h/mL | 17.16 % | 1.89 h |
Chemical Information
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CAS No. 3059641-72-1
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Molecular Weight 623.78
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Formula C28H54N3O8PS
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SMILES
OP(OCCS(CCCCCCCCCCCCCCCCCC)(=O)=O)(CO[C@H](CO)CN1C=CC(N)=NC1=O)=O
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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)