CHVB-066
CHVB-066 is an alphavirus non-structural protein nsP1 inhibitor that exhibits varying degrees of inhibitory activity against nsP1 of CHIKV and VEEV. CHVB-066 inhibits MTase and GTase activities and disrupts the capping process of viral RNA, including inhibiting CHIKV replication, reducing progeny viruses, and preventing cytopathic effects. It shows varying degrees of inhibitory activity against nsP1 of CHIKV and VEEV but lacks anti-SFV replication activity, displays cross-resistance with MADTP series compounds, and requires nsP2/nsP3 mutations to develop complete drug resistance. This inhibitor with varying inhibitory activity against nsP1 of CHIKV and VEEV can be widely applied to relevant studies on chikungunya virus infection and chikungunya fever.
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- CAS. Nr.: 1309199-94-7
- Formel: C19H25N5O
- Molecular Weight:339.43
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
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Biologische Aktivität
Beschreibung
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| Vero | CC50 |
203 μM
Compound: 31f
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Cytotoxicity against African green monkey Vero cells assessed as reduction in overall metabolic activity incubated for 5 days by MTS reagent based absorbance method
Cytotoxicity against African green monkey Vero cells assessed as reduction in overall metabolic activity incubated for 5 days by MTS reagent based absorbance method
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[PMID: 38104375] |
In Vitro
CHVB-066 (Serial dilutions; 96 h) potently inhibits CHIKV replication in Vero E6 cells with an EC50 of 0.6 μM and has a CC50 of 25 μM, with no activity against SFV[1].
CHVB-066 (0.5-32 μM; 30 min) dose-dependently inhibits the combined methyltransferase and guanylyltransferase enzymatic activity of purified wild-type CHIKV nsP1 at concentrations ranging from 0.5 to 32 μM[1].
CHVB-066 (0.16-5.00 μM; 48 h) induces a dose-dependent reduction in CHIKV 899 viral RNA and infectious progeny production in Vero cells, with a significant >4-log10 reduction at 5.00 μM after 48 h[2].
CHVB-066 (0-12.5 μM; 4 days) inhibits wild-type rCHIKV LS3 replication in Vero E6 cells with an EC50 of 0.65 μM; resistance requires the combined nsP1S454G and nsP1W456R mutations, with maximum resistance (18.5-fold) achieved when combined with nsP2M703T and nsP3L494P mutations[2].
CHVB-066 (0.5-1000 μM) potently inhibits the guanylyltransferase activity of purified VEEV nsP1 with an IC50 of <0.5 μM[2].
CHVB-066 (0.001-100 μM) inhibits the methyltransferase activity of purified VEEV nsP1 with an IC50 of 1.9 μM[2].
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 cells
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Concentration:Serial dilutions
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Incubation Time:96 h
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Result:Inhibited CHIKV-induced CPE with a 50% effective concentration (EC50) of 0.6 μM.
Exhibited a 50% cytotoxic concentration (CC50) of 25 μM.
Showed no antiviral activity against Semliki Forest virus (SFV).\nRendered CHIKV nsP1-P34S and CHIKV nsP1-S454G+W456R mutants completely resistant, with an EC50 of >12.5 μM and a fold resistance of 20.8 compared to wild-type CHIKV.
Maintained activity against CHIKV nsP1-G230R+K299E mutant, with an EC50 of 0.3 μM and a fold resistance <1.
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Cell Line:Vero cells
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Concentration:0.16-5.00 μM
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Incubation Time:48 h
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Result:Caused a marked dose-dependent reduction in CHIKV 899 viral genome copies and infectious virus progeny.
Induced a significant >4-log10 reduction in both viral RNA and infectious virus yield at 5.00 μM compared to untreated controls.
Chemical Information
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CAS. Nr. 1309199-94-7
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Molecular Weight 339.43
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Formel C19H25N5O
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SMILES
O=C(N1CCN(CC1)C2=NC(NCC)=NC(C)=C2)C3=CC=C(C)C=C3
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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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.
Reinheit & Dokumentation
Verweise
[1]. Besztercei B, et al. Three nitrogen atoms turn old kinase inhibitors into new targetable remedy[J]. bioRxiv, 2026: 2026.04. 11.717649. [Content Brief]
[2]. Abdelnabi R, Kovacikova K, Moesslacher J, et al. Novel class of chikungunya virus small molecule inhibitors that targets the viral capping machinery[J]. Antimicrobial Agents and Chemotherapy, 2020, 64(7): 10.1128/aac. 00649-20. [Content Brief]
[4]. Kovacikova K, van Hemert M J. Small-molecule inhibitors of chikungunya virus: mechanisms of action and antiviral drug resistance[J]. Antimicrobial agents and chemotherapy, 2020, 64(12): 10.1128/aac. 01788-20. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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