DMA-155
DMA-155 is an antiviral agent with binding activity against SARS-CoV-2 5'-terminal stem-loop RNAs, with affinities of 51.1 μM (SL1), 61.1 μM (SL4), 54.5 μM (SL5a), 66.9 μM (SL5b) and 48.6 μM (SL6), respectively. DMA-155 inhibits SARS-CoV-2 viral replication and reduces SARS-CoV-2 viral RNA levels. DMA-155 is applicable to the research of COVID-19.
For research use only. We do not sell to patients.
- CAS No.: 2237925-69-6
- Formula: C20H21N7O
- Molecular Weight:375.43
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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
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Biological Activity
Description
In Vitro
DMA-155 (50-100 μM; 24 h) significantly inhibits human coronavirus OC43 replication in Vero E6 cells when administered at 50 μM or 100 μM for 24 hours[1].
DMA-155 (24-72 h) potently inhibits SARS-CoV-2 replication in Vero E6 cells with an IC50 of 16 μM at 24 hours post-infection, with sustained dose-dependent activity through 72 hours[1].
DMA-155 (10 μM; 72 h) inhibits SARS-CoV-2 replication in Vero E6 cells at 10 μM for 72 hours without significant cellular toxicity[1].
DMA-155 (0.1-100 μM; 2 days) specifically inhibits SARS-CoV-2 5'-UTR-dependent translation in Vero E6 cells, with a ~90% reduction in FLuc activity at 10 μM after 2 days of incubation, without non-specific effects on translation[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 2237925-69-6
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Molecular Weight 375.43
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Formula C20H21N7O
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SMILES
O=C(C1=C(N)N=C(N(C)C)C(C2=CC=C(C3=CC=CC=C3)C=C2)=N1)NC(N)=N
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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)
DMA-155 Related Classifications
HY-179334 Related Classifications
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Keywords
- DMA-155
- 2237925-69-6
- DMA155
- DMA 155
- SARS-CoV
- DNA/RNA Synthesis
- Vero E6 cells
- SARS-CoV-2 5'-end stem loop RNAs
- SARS-CoV-2 viral RNA
- SARS-CoV-2 5'-UTR-dependent translation
- SARS-CoV-2 5'-end SL4 RNA
- human coronavirus OC43
- SARS-CoV-2 5'-end SL5a RNA
- SARS-CoV-2 5'-end SL1 RNA
- SARS-CoV-2
- SARS-CoV-2 5'-end SL6 RNA
- Inhibitor
- inhibitor
- inhibit