RSV-IN-14
RSV-IN-14 is an orally active pre-fusion F protein inhibitor of respiratory syncytial virus (RSV), with a Kd of 5.0 μM, and exhibits lung-targeted distribution properties. RSV-IN-14 binds to the central cavity of the trimeric pre-fusion F protein, locks it in the pre-fusion state, and inhibits the conformational changes required for membrane fusion to block viral entry. RSV-IN-14 suppresses respiratory syncytial virus-induced syncytium formation. RSV-IN-14 can be used in studies on respiratory syncytial virus infection.
For research use only. We do not sell to patients.
- CAS No.: 3103996-88-6
- Formula: C22H29N5O3S
- Molecular Weight:443.56
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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
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
RSV pre-fusion F protein 5.0 μM (Kd) |
In Vitro
RSV-IN-14 (compound 7d) demonstrates highly potent anti-RSV activity against the RSV-long strain and minimal cytotoxicity in HEp-2 cells, with an EC50 of 3.65 nM[1].
RSV-IN-14 (50 μM) exerts potent broad-spectrum inhibitory activity against diverse clinically isolated RSV subtype strains in in vitro[1].
RSV-IN-14 forms a stable protein-ligand complex by directly binding to the prefusion conformational epitope of the RSV F protein[1].
RSV-IN-14 (0.1-1.0 nM) effectively suppresses RSV infection, viral protein expression, and syncytium formation while restoring normal epithelial structure in aged human nasal organoids[1].
RSV-IN-14 is classified as a medium-permeability compound with good cellular uptake potential[1].
RSV-IN-14 exhibits low cardiac toxicity risk as indicated by its relatively high hERG IC50 value[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
In Vivo
RSV-IN-14 (12.5-50 mg/kg; p.o.; twice daily; 3 consecutive days) effectively inhibits pulmonary RSV replication and ameliorates RSV-induced severe lung injury in 65-week-old aged C57BL/6 mice, with the 50 mg/kg dose achieving 82% reduction in both viral titer and RSV-F gene copies[1].
RSV-IN-14 (12.5-100 mg/kg; p.o.; twice daily; 3 consecutive days) reduces RSV viral loads by over 90% and mitigates virus-induced pulmonary inflammation and tissue injury in 4-week-old juvenile C57BL/6 mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c mice (4-week-old female)[1]
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Dosage:100 mg/kg
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Administration:p.o.; twice daily; 3 consecutive days
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Result:Attenuated RSV-induced progressive body weight loss in infected mice.
Reduced the elevated lung index by 12.9% relative to the RSV-infected control group at 3 days post-infection.
Reduced pulmonary RSV-F protein mRNA expression by 92.98% at 3 days post-infection.
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Animal Model:C57BL/6 mice (4-week-old female)[1]
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Dosage:12.5 mg/kg; 50 mg/kg; 100 mg/kg
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Administration:p.o.; twice daily; 3 consecutive days
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Result:Produced greater than 90% reduction in RSV-F gene copy levels in lung tissue across all tested doses.
Resulted in only transient initial body weight decrease at 1 day post-infection followed by recovery over subsequent 2 days, in contrast to the 18.8% progressive body weight loss observed in untreated RSV-infected mice by 3 days post-infection.
Reduced lung index values, attenuated inflammatory cell infiltration and virus-induced lung tissue damage, and markedly suppressed pulmonary mRNA expression of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 across all dose groups.
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Animal Model:C57BL/6 mice (65-week-old male)[1]
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Dosage:12.5 mg/kg; 50 mg/kg
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Administration:p.o.; twice daily; 3 consecutive days
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Result:Alleviated the downward trend of body weight in RSV-infected aged mice, though body weight recovery was slower than that observed in juvenile mice.
Produced an 82% reduction in lung viral titer and an 82% reduction in RSV-F gene copies at the 50 mg/kg dose level.
Reduced the elevated lung index values by 18-32% relative to RSV-infected mice.
Alleviated the severe RSV-induced lung pathology including lymphocytic/granulocytic infiltration, alveolar septal thickening, necrotic cellular debris, alveolar/bronchial hemorrhage, perivascular lymphocytic cuffing and vascular congestion, with the 50 mg/kg dose demonstrating greater efficacy than 12.5 mg/kg.
Chemical Information
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CAS No. 3103996-88-6
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Molecular Weight 443.56
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Formula C22H29N5O3S
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SMILES
O=S1(CCN(C2=NC(NCC3(N)COC3)=C(CC(C)CC4)C4=N2)CC5=C1C=CC=C5)=O
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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)
RSV-IN-14 Related Classifications
HY-189244 Related Classifications
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