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.
商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- CAS 番号: 2043014-84-0
- 分子式: C14H15FN2OS2
- 分子量:310.41
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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生物活性
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化学情報
- プロトコル
- 純度とドキュメンテーション
- 参考文献
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Help & FAQs
生物活性
製品説明
IC50 & Target
[1]|
HIV-1 |
体外実験
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.
化学情報
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CAS 番号 2043014-84-0
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分子量 310.41
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分子式 C14H15FN2OS2
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SMILES
O=C(N(C1=NC2=C(S1)CCCC2)C)CC=3SC=CC3F
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
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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.
純度とドキュメンテーション
参考文献
[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
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)
ML416 関連分類
HY-125613 関連分類
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