RSV-IN-15
RSV-IN-15 is a selective inhibitor of the RSV RNA-dependent RNA polymerase PRNTase domain. RSV-IN-15 blocks polymerase-dependent RNA synthesis through allosteric binding. RSV-IN-15 exhibits antiviral EC50 = 37 nM against the RSV‑A Long strain in Hep‑2 cells, reduces polymerase-dependent reporter gene activity, and inhibits RSV RNA synthesis. RSV-IN-15 can be used for research on respiratory syncytial virus infection.
For research use only. We do not sell to patients.
- CAS No.: 3136661-66-7
- Formula: C25H25FN4O4
- Molecular Weight:464.49
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All DNA/RNA Synthesis Isoforms
More
Biological Activity
Description
IC50 & Target
[1]|
RNA Polymerase |
Cellular Effect
|
Cell Line
|
Type | Value | Description | References |
|---|---|---|---|---|
| HEp-2 | EC50 |
0.037 μM
|
Antiviral activity against respiratory syncytial virus A Long strain in HEp-2 cells assessed by cytopathic effect reduction using MTS after 4 days post-infection.
Antiviral activity against respiratory syncytial virus A Long strain in HEp-2 cells assessed by cytopathic effect reduction using MTS after 4 days post-infection.
|
42641470 |
| HEp-2 | CC50 |
>50 μM
|
Cytotoxicity against HEp-2 cells assessed by MTS after 4 days; CC50 >50 µM; no 50% cytotoxicity reached up to 50 µM.
Cytotoxicity against HEp-2 cells assessed by MTS after 4 days; CC50 >50 µM; no 50% cytotoxicity reached up to 50 µM.
|
42641470 |
In Vitro
RSV-IN-15 (LX1) (50 µM; 4 days post-infection) inhibits RSV-A Long in HEp-2 cells with an EC50 of 37 nM and a CC50 greater than 50 µM[1].
RSV-IN-15 reduces RSV polymerase-dependent reporter gene expression and inhibits viral RNA synthesis[1].
RSV-IN-15 (molecular docking) binds to the allosteric pocket of the RSV polymerase PRNTase and forms stable hydrogen bonds, π-π stacking, and hydrophobic interactions with key amino acid residues of the RSV-L protein[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
-
CAS No. 3136661-66-7
-
Molecular Weight 464.49
-
Formula C25H25FN4O4
-
SMILES
COC1=C(OC2CC2)C=CC(C(NNC(C3=CC(NCC)=CC(C4=CC=C(F)C=C4)=N3)=O)=O)=C1
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
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)