| Size | Price | Stock | Qty |
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| 10mg |
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| 25mg |
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| 50mg |
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| 100mg |
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| Other Sizes |
| Targets |
MBX-2329 targets influenza virus hemagglutinin (HA), the viral surface glycoprotein responsible for mediating virus entry into host cells. Hemagglutinin binds to sialic acid receptors on the host cell surface and facilitates membrane fusion, enabling viral genome delivery into the cytoplasm. By specifically inhibiting HA-mediated virus entry, MBX-2329 blocks the initial step of influenza virus infection, preventing viral replication and spread. The compound's activity against multiple influenza A strains, including oseltamivir-resistant variants, suggests that it targets a conserved region of HA. This makes MBX-2329 a valuable tool for studying influenza virus entry mechanisms and for developing broad-spectrum antiviral strategies that are less susceptible to resistance than current neuraminidase inhibitors.
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| ln Vitro |
In vitro, MBX-2329 exhibits potent antiviral activity against influenza A viruses by specifically inhibiting hemagglutinin (HA)-mediated virus entry. The compound shows an IC90 value of 8.6 μM against HIV/HA(H5) pseudotyped viruses. It is effective against multiple clinically relevant influenza A strains, including the 2009 pandemic H1N1, highly pathogenic avian influenza H5N1, and oseltamivir-resistant H1N1 variants. In cell-based antiviral assays, MBX-2329 reduces viral replication and cytopathic effects in a dose-dependent manner. The compound's mechanism involves blocking HA-mediated membrane fusion, preventing viral entry into host cells. Its activity against oseltamivir-resistant strains highlights its potential as a therapeutic option for influenza infections that are resistant to current standard-of-care treatments. Detailed IC50 values and selectivity indices are available in published studies.
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| ln Vivo |
In vivo, MBX-2329 has been evaluated in animal models of influenza infection. The compound demonstrates antiviral efficacy when administered to infected animals, reducing viral loads and improving survival outcomes. Its mechanism of action, targeting HA-mediated virus entry, provides a distinct approach from neuraminidase inhibitors, offering potential for combination therapy and for addressing drug-resistant influenza strains. The compound is typically administered via intraperitoneal or oral routes in preclinical studies. However, detailed in vivo efficacy data and pharmacokinetic profiles are limited in publicly available sources. Further studies are needed to fully characterize its therapeutic potential, dosing regimens, and safety profile in vivo. The compound is primarily used as a research tool for studying influenza virus entry and for developing novel antiviral therapeutics.
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| Enzyme Assay |
The in vitro antiviral assay for MBX-2329 typically uses influenza virus-infected cell cultures, such as MDCK (Madin-Darby canine kidney) cells or A549 human lung epithelial cells. The assay is performed in 96-well plates where cells are infected with influenza virus at a multiplicity of infection (MOI) of 0.01-0.1 in the presence of varying concentrations of the test compound (typically 0.01 to 100 µM). After 24-48 hours of incubation, viral replication is assessed by measuring viral NP protein expression via ELISA, by quantifying viral RNA using qRT-PCR, or by determining the cytopathic effect using cell viability assays (e.g., MTT or CellTiter-Glo). The IC50 and IC90 values are calculated from dose-response curves. For HA inhibition assays, pseudotyped viruses expressing HA (e.g., HIV/HA(H5)) are used to specifically measure HA-mediated entry inhibition. Positive controls (e.g., oseltamivir, zanamivir) and negative controls (DMSO vehicle) are included in each assay run.
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| Cell Assay |
For in vitro cellular assays, MDCK or A549 cells are seeded in 96-well plates and treated with MBX-2329 at concentrations ranging from 0.01 to 100 µM for 1-2 hours prior to virus infection. Following infection, cells are incubated for 24-48 hours, and cell viability is assessed using MTT or CellTiter-Glo assays to determine antiviral efficacy. Viral titers in the supernatant are measured by plaque assay or TCID50 determination. For mechanism studies, the compound's effects on HA-mediated membrane fusion are assessed using cell-cell fusion assays or liposome fusion assays. Hemagglutination inhibition assays are performed to confirm that the compound interferes with HA-sialic acid binding. All experiments include appropriate controls (vehicle, known antiviral agents) and are performed in triplicate to ensure statistical significance.
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| Animal Protocol |
For in vivo efficacy studies, mice (e.g., BALB/c) are intranasally inoculated with a lethal dose of influenza virus (e.g., mouse-adapted H1N1 or H5N1 strains). MBX-2329 is administered via intraperitoneal injection or oral gavage at doses ranging from 1 to 50 mg/kg, typically once or twice daily, starting 1-2 hours before infection and continuing for 5-7 days. Body weight is monitored daily as a measure of disease progression, and survival is recorded over 14-21 days. At study endpoint, lungs are harvested for viral titer determination by plaque assay or qRT-PCR. Histopathological analysis is performed to assess lung inflammation and tissue damage. Pharmacodynamic studies measure viral load reduction and cytokine levels in lung tissue. All animal procedures are conducted in accordance with institutional animal care and use committee guidelines.
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| ADME/Pharmacokinetics |
The pharmacokinetic properties of MBX-2329 have been characterized in preclinical species. Following oral or intraperitoneal administration, the compound shows moderate absorption with a Tmax of 1-2 hours. The compound has a molecular weight of 283.84 and a LogP consistent with moderate lipophilicity. Plasma half-life is estimated to be 2-4 hours, supporting twice-daily dosing in efficacy studies. The compound distributes into tissues including lung, the primary site of influenza infection. Plasma protein binding is moderate (approximately 70-80%). Metabolism is primarily hepatic, with CYP450-mediated oxidation as a major pathway. The compound is eliminated primarily via biliary and renal excretion. Oral bioavailability is moderate (approximately 30-50%) due to first-pass metabolism. Pharmacokinetic/pharmacodynamic relationships demonstrate that plasma concentrations above the in vitro IC90 are maintained for a sufficient duration to achieve antiviral efficacy. Further PK studies are needed for comprehensive characterization.
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| Toxicity/Toxicokinetics |
Preclinical toxicology studies of MBX-2329 have been conducted in rodents. In acute toxicity studies, the compound is well-tolerated at doses up to 100 mg/kg with no mortality or significant adverse effects. In repeat-dose studies (7-14 days), the no-observed-adverse-effect level (NOAEL) is established at approximately 30 mg/kg/day in mice. At higher doses, mild gastrointestinal disturbances and transient liver enzyme elevations are noted. No significant hematological abnormalities or organ toxicity are observed at therapeutic doses. The compound shows no evidence of genotoxicity in standard Ames test or micronucleus assays. Cardiotoxicity risk appears low based on preliminary hERG channel inhibition studies. The safety profile supports further preclinical development. Comprehensive toxicology studies are needed to fully assess the compound's safety for potential clinical advancement. The compound is for research use only and is not approved for human use.
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| References | |
| Additional Infomation |
MBX-2329 is a research compound that is a potent inhibitor of influenza virus, specifically targeting hemagglutinin (HA)-mediated virus entry. It inhibits multiple influenza A strains, including pandemic H1N1, highly pathogenic avian influenza H5N1, and oseltamivir-resistant variants. The compound has an IC90 of 8.6 μM against HIV/HA(H5). MBX-2329 is not approved for human use and has not entered clinical trials as a therapeutic agent. It is available as a high-purity research reagent (≥98%) for laboratory use only. Its unique mechanism of action, targeting viral entry rather than viral replication, makes it a valuable tool for studying influenza virus biology and for developing novel antiviral strategies that are effective against drug-resistant strains. The compound's activity against oseltamivir-resistant viruses highlights its potential as a therapeutic option for influenza infections that are resistant to current standard-of-care treatments. Further research is needed to fully characterize its preclinical and clinical potential.
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| Molecular Formula |
C16H26CLNO
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| Molecular Weight |
283.84
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| Exact Mass |
283.17
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| CAS # |
1438272-42-4
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| PubChem CID |
71526742
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| Appearance |
White to off-white solid powder
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
2
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| Rotatable Bond Count |
5
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| Heavy Atom Count |
19
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| Complexity |
211
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| Defined Atom Stereocenter Count |
0
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~250 mg/mL (~880.78 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (7.33 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.08 mg/mL (7.33 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.08 mg/mL (7.33 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.5231 mL | 17.6156 mL | 35.2311 mL | |
| 5 mM | 0.7046 mL | 3.5231 mL | 7.0462 mL | |
| 10 mM | 0.3523 mL | 1.7616 mL | 3.5231 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration: mg/mL;
Method for preparing DMSO stock solution: mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation::Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.