MMT5-14
MMT5-14 is a remdesivir analogue with a higher antiviral activity in four variants of SARS-CoV-2 than Remdesivir (HY-104077). MMT5-14 inhibits SARS-CoV-2, α, β, γ and δ variants with EC50s of 0.4, 2.5, 15.9, 1.7 and 5.6 μM, respectively. MMT5-14 can be used for the research of COVID-19.
For research use only. We do not sell to patients.
- CAS No.: 2719679-31-7
- Formula: C39H55N6O8P
- Molecular Weight:766.86
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
MMT5-14 (10 μM; 0-12 h) increases epithelial cell uptake[1]. MMT5-14 (5 μM; 2 d) shows a better in vitro antiviral activity than remdesivir[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:Vero-E6 cell line
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Concentration:5 μM
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Incubation Time:2 days
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Result:Inhibited SARS-CoV-2, alpha, beta, gamma and delta variants with EC50s of 0.4, 2.5, 15.9, 1.7 and 5.6 μM, respectively.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Catheterized female hamsters[1]
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Dosage:10 mg/kg
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Administration:Intravenous injection; 10 mg/kg once
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Result:Showed higher intact prodrugs concentration than remdesivir in lungs after 4 hours injection, increased tissue exposure in most of the tissues and showed 5- to 10-fold higher tissue selectivity in lungs compared to remdesivir.
Chemical Information
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CAS No. 2719679-31-7
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Molecular Weight 766.86
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Formula C39H55N6O8P
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SMILES
C[C@@H](C(OCCCCCCCC/C=C\C/C=C\CCCCC)=O)NP(OC1=CC=CC=C1)(OC[C@H]2O[C@@](C#N)(C3=CC=C4C(N)=NC=NN43)[C@H](O)[C@@H]2O)=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)