ML416
ML416 is a broad-spectrum antiviral agent. ML416 inhibits host de novo pyrimidine biosynthesis, and induces a variety of interferon-stimulated genes (ISGs). ML416 can be used for the research of viral infections including alphaviruses, influenza virus, and HIV-1.
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- No. CAS: 2043014-84-0
- Fòrmula: C14H15FN2OS2
- Peso molecular:310.41
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Almacenamiento:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Actividad biológica
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Chemical Information
- Protocolo
- Pureza y Documentación
- Referencias
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Help & FAQs
Actividad biológica
Descripciòn
IC50 & Target
[1]|
HIV-1 |
In Vitro
ML416 (Compound 1) (10 μM; 24 h) potently inhibits HIV-1 infectivity in TZM-bl cells, achieving 94% inhibition at a 10 μM concentration[1].
ML416 (1 μM; 2 h pretreatment + 18 h post-infection incubation) potently inhibits V3526-luc and pVSV-luc replication in HEK 293T cells, and its antiviral activity is reversed by exogenous pyrimidines (cytidine, uridine), confirming its mechanism of action involves inhibition of pyrimidine biosynthesis[1].
ML416 (48-96 h) shows low cytotoxicity against Vero 76 cells, with CC50 values ranging from 31.0 to 74.1 μM across 48 to 96 hours of exposure[1].
ML416 (5 μM; 8 h pre-treatment) reduces progeny virus titers by 1.3 to 4.768 log at 5 μM in Vero 76 cells across a broad range of viruses[2].
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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No. CAS 2043014-84-0
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Peso molecular 310.41
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Fòrmula C14H15FN2OS2
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SMILES
O=C(N(C1=NC2=C(S1)CCCC2)C)CC=3SC=CC3F
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocolo
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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.
Pureza y Documentación
Referencias
[1]. Chung DH, et al. Discovery of a Broad-Spectrum Antiviral Compound That Inhibits Pyrimidine Biosynthesis and Establishes a Type 1 Interferon-Independent Antiviral State. Antimicrob Agents Chemother. 2016;60(8):4552-4562. Published 2016 Jul 22. [Content Brief]
[2]. Jennifer E. Golden, et al. Inhibitors of viruses. WO2016183093A1. 2017-11-11
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
ML416 Related Classifications
HY-125613 Related Classifications
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