L0909
L0909 is an HCV inhibitor with an EC50 of 0.022 μM. L0909 blocks HCV replication by inhibiting E1-mediated viral entry. L0909 exhibits sensitivity to clinical resistant HCV mutants. L0909 displays synergistic effects with clinical HCV drugs. L0909 can be used for the research of hepatitis c virus (HCV) infection.
For research use only. We do not sell to patients.
- CAS No.: 2085271-43-6
- Formula: C23H30ClN5
- Molecular Weight:411.97
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| Huh-7.5 | CC50 |
121.47 μM
Compound: L0909
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Cytotoxicity against human Huh7.5 cells carrying HCV subgenomic replicons assessed as reduction in cell viability incubated for 96 hrs by MTT assay
Cytotoxicity against human Huh7.5 cells carrying HCV subgenomic replicons assessed as reduction in cell viability incubated for 96 hrs by MTT assay
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[PMID: 35050619] |
In Vitro
L0909 (72 h) potently inhibits HCV RNA replication in Huh7.5 cells (CC50 = 14.77 μM) with an EC50 of 0.022 μM[1].
L0909 (-chloro) (72 h) potently inhibits HCV replication in Huh7.5 cells (CC50 = 12.761 μM) with an EC50 of 0.083 μM and a selectivity index of 154[1].
L0909 (0.1-5 μM; 3-14 days) does not inhibit HCV replication in replicon GS4.3 cells[1].
L0909 (0.3125-12.5 μM; 4-72 h) blocks HCV entry into Huh7.5 cells, exhibiting potent, rapid, and broad-spectrum activity against both genotype 1b and 2a HCV pseudoparticles and replicating virus[1].
L0909 inhibits HCV entry via targeting the HCV E1 glycoprotein, as evidenced by the F291V E1 mutation conferring ~20-fold resistance to the compound in Huh7.5 cells[1].
L0909 (serial dilutions; 72 h) retains potent, nanomolar activity against drug-resistant HCV variants (A156T, D168V, S282T) in Huh7.5 cells, similar to its activity against wild-type HCV[1].
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:Wild-type and drug-resistant HCV mutants (A156T NS3, D168V NS3, S282T NS5B)-infected Huh7.5 cells
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Concentration:Serial dilutions
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Incubation Time:72 h
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Result:Maintained potent activity against all tested drug-resistant mutants: EC50 = 0.0019 μM (A156T NS3), 0.03 μM (D168V NS3), 0.0044 μM (S282T NS5B), compared to an EC50 of 0.003 μM against wild-type HCV.
Parmacokinetics
| Species | Dose | Route | T1/2 | Tmax | Cmax | Vz | CL | F |
|---|---|---|---|---|---|---|---|---|
| Rat[1] | 5 mg/kg | i.v. | 14.34 h | / | 616.99 ng/mL | 20057.05 mL/kg | 1088.11 mL/h/kg | / |
| Rat[1] | 15 mg/kg | p.o. | 12.83 h | 3.08 h | 500.72 ng/mL | 34834.07 mL/kg | 2246.3 mL/h/kg | 59 % |
| Dog[1] | 5 mg/kg | i.v. | 7.28 h | / | 531.93 ng/mL | 49181.42 mL/kg | 4752.98 mL/h/kg | / |
| Dog[1] | 15 mg/kg | p.o. | 12.72 h | 3 h | 94.51 ng/mL | 238116.97 mL/kg | 12025.86 mL/h/kg | 39 % |
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Kunming mice (male and female, 3 each per group)[1]
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Dosage:250 mg/kg; 500 mg/kg; 1000 mg/kg
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Administration:p.o.; single dose
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Result:Showed no mortality across all treatment groups over 7 days.
Detected no significant changes in body weight compared to the control group.
Found no significant abnormalities in blood AST, ALT, UREA, or CRE levels at any tested dose, including 1000 mg/kg.
Chemical Information
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CAS No. 2085271-43-6
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Molecular Weight 411.97
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Formula C23H30ClN5
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SMILES
N#CC1=CC=C(N(CCN(C)C)C)C=C1CN2CCN(CC2)C3=CC=C(C=C3)Cl
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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)