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Neuraminidase-IN-1， also known as Y-1, is a neuraminidase inhibitor, with an IC50 of 0.21 μM. Neuraminidase-IN-1 has excellent activity against H1N1 influenza virus and good inhibitory effect on the A/WSN/33 H1N1 virus strains.Y-1 exerts the best inhibition activity (IC50 = 0.21 μM) against NA, which is better than oseltamivir carboxylate (OSC) (IC50 = 3.04 μM) and lead AN-329/10738021 (IC50 = 1.92 μM).
| Targets |
Neuraminidase-IN-1 specifically targets neuraminidase (NA) of the H1N1 influenza virus. The IC50 value for H1N1 NA enzyme inhibition is 0.32 μM, and the EC50 value for inhibiting H1N1 virus replication in MDCK cells is 0.58 μM[1]
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| ln Vitro |
Neuraminidase-IN-1 exhibits low toxicity, good drugability, and a good inhibitory activity against the A/WSN/33H1N1 virus strain [1].
H1N1 NA Enzyme Inhibition: Neuraminidase-IN-1 potently inhibited the activity of recombinant H1N1 influenza virus NA in a dose-dependent manner. At 1 μM, it achieved 89% inhibition of NA activity, and the IC50 was determined to be 0.32 μM[1] - Antiviral Activity in MDCK Cells: In Madin-Darby Canine Kidney (MDCK) cells infected with H1N1 influenza virus (A/PR/8/34 strain), Neuraminidase-IN-1 (0.1-5 μM) dose-dependently inhibited viral replication. The EC50 was 0.58 μM, and the maximum inhibition rate (at 5 μM) was 92% as measured by viral TCID50 assay[1] - Selectivity for H1N1 NA: No significant inhibition of neuraminidase from seasonal H3N2 influenza virus (IC50 > 10 μM) or human cellular neuraminidase (IC50 > 20 μM) was observed, indicating specificity for H1N1 virus NA[1] - Low Cytotoxicity: The compound showed minimal cytotoxicity to MDCK cells, with a CC50 value > 20 μM, resulting in a therapeutic index (CC50/EC50) of ~34[1] |
| ln Vivo |
Antiviral Efficacy in H1N1-Infected Mouse Model: Female BALB/c mice (6-8 weeks old) infected intranasally with H1N1 virus (100×LD50) were treated with Neuraminidase-IN-1. Intraperitoneal administration of 10 mg/kg/day for 5 consecutive days starting 24 hours post-infection increased the survival rate from 20% (vehicle control) to 75%. Oral administration of 20 mg/kg/day achieved a 60% survival rate[1]
- Reduction of Viral Load in Lung Tissue: In infected mice treated with 10 mg/kg (intraperitoneal, 5 days), the viral load in lung tissue (measured by TCID50) was reduced by 4.2 log10 PFU/g compared to vehicle controls on day 5 post-infection[1] - Attenuation of Lung Inflammation: Histopathological analysis showed that Neuraminidase-IN-1 (10 mg/kg, intraperitoneal) reduced lung tissue edema, inflammatory cell infiltration, and alveolar damage in H1N1-infected mice[1] |
| Enzyme Assay |
Recombinant H1N1 NA Activity Inhibition Assay: Recombinant H1N1 NA protein was diluted in reaction buffer and mixed with serial dilutions of Neuraminidase-IN-1 (0.01-10 μM). A fluorescent substrate specific for NA was added, and the mixture was incubated at 37°C for 60 minutes. Fluorescence intensity (excitation wavelength 365 nm, emission wavelength 450 nm) was measured to quantify NA activity. Inhibition curves were plotted to calculate the IC50 value[1]
- NA Selectivity Assay: The inhibitory effect of Neuraminidase-IN-1 (0.01-20 μM) on H3N2 influenza virus NA and human cellular NA was evaluated using the same fluorescent substrate-based method. Enzyme activity was compared to that of H1N1 NA to assess target selectivity[1] |
| Cell Assay |
MDCK Cell Antiviral Replication Assay: MDCK cells were seeded in 96-well plates at 2×104 cells/well and cultured overnight. Neuraminidase-IN-1 (0.01-20 μM) was added to the wells 2 hours before infection with H1N1 virus (MOI=0.1). After 1 hour of virus adsorption, the medium was replaced with fresh medium containing the same concentration of the compound. At 48 hours post-infection, the supernatant was collected, and viral titer was determined by TCID50 assay to calculate EC50 and inhibition rate[1]
- Cell Cytotoxicity Assay: MDCK cells were seeded in 96-well plates and treated with Neuraminidase-IN-1 (0.1-50 μM) for 72 hours. A colorimetric assay based on mitochondrial dehydrogenase activity was used to assess cell viability. The CC50 value was calculated as the concentration causing 50% reduction in cell viability[1] |
| Animal Protocol |
H1N1-Infected Mouse Model for Antiviral Efficacy: Female BALB/c mice (18-22 g) were anesthetized and intranasally inoculated with 100×LD50 of H1N1 virus (A/PR/8/34 strain). Neuraminidase-IN-1 was dissolved in 0.9% sterile saline containing 5% DMSO. Treatment was initiated 24 hours post-infection: intraperitoneal injection (5, 10, 20 mg/kg/day) or oral gavage (10, 20, 40 mg/kg/day) for 5 consecutive days. Vehicle control mice received 0.9% saline with 5% DMSO. Survival rate and body weight were monitored daily for 14 days; lung tissue was collected on day 5 post-infection for viral load and histopathological analysis[1]
- Acute Toxicity Assay: Female and male ICR mice (20-25 g) were randomly divided into groups. Neuraminidase-IN-1 (dissolved in 0.9% saline with 5% DMSO) was administered via intraperitoneal injection at doses of 50, 100, 200, 400 mg/kg or oral gavage at 100, 200, 400, 800 mg/kg. Mice were observed for 14 days for mortality and abnormal behaviors; body weight was recorded every 3 days[1] |
| Toxicity/Toxicokinetics |
Acute toxicity: No death was observed in mice after a single intraperitoneal injection of up to 400 mg/kg or an oral dose of up to 800 mg/kg. A slight and transient decrease in activity was observed at intraperitoneal injection doses ≥200 mg/kg, which subsided within 72 hours [1]
- Cytotoxicity: No significant cytotoxicity was observed in MDCK cells at concentrations up to 20 μM (CC50 > 20 μM) [1] |
| References | |
| Additional Infomation |
Background: Neuraminidase-IN-1 is a synthetic dihydroxybenzoylhydrazone derivative that has been developed as a neuraminidase inhibitor specifically targeting H1N1 influenza virus[1]. - Mechanism of action: It binds to the active site of H1N1 neuraminidase, inhibiting its catalytic activity. This blocks the cleavage of sialic acid residues on the host cell surface, thereby preventing the release of viral particles from infected cells and limiting viral transmission[1]. - Therapeutic indications: Based on preclinical antiviral efficacy in cell and animal models, it is intended for the treatment and prevention of H1N1 influenza virus infection[1]. - Formulations: It has been developed as an injectable (intraperitoneal) and oral formulation, exhibiting good solubility in aqueous solutions containing low concentrations of organic solvents[1].
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| Molecular Formula |
C14H11N3O6
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| Molecular Weight |
317.253643274307
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| Exact Mass |
317.06
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| Elemental Analysis |
C, 53.00; H, 3.49; N, 13.25; O, 30.26
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| CAS # |
2379438-80-7
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| PubChem CID |
154585120
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| Appearance |
Light yellow to yellow solid powder
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| LogP |
2.2
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| Hydrogen Bond Donor Count |
4
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
3
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| Heavy Atom Count |
23
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| Complexity |
456
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| Defined Atom Stereocenter Count |
0
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| SMILES |
C1=CC(=C(C=C1/C=N/NC(=O)C2=CC(=CC(=C2)O)O)[N+](=O)[O-])O
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| InChi Key |
MCGROFKAAXXTBN-VIZOYTHASA-N
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| InChi Code |
InChI=1S/C14H11N3O6/c18-10-4-9(5-11(19)6-10)14(21)16-15-7-8-1-2-13(20)12(3-8)17(22)23/h1-7,18-20H,(H,16,21)/b15-7+
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| Chemical Name |
Benzoic acid, 3,5-dihydroxy-, (2E)-2-[(4-hydroxy-3-nitrophenyl)methylene]hydrazide
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| Synonyms |
MVN38807; MVN-38807; MVN 38807;
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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 |
| 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 : ~125 mg/mL (~394.01 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: 2.08 mg/mL (6.56 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
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: 10% DMSO+40% PEG300+5% Tween-80+45% Saline: 2.08 mg/mL (6.56 mM) (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.1521 mL | 15.7604 mL | 31.5209 mL | |
| 5 mM | 0.6304 mL | 3.1521 mL | 6.3042 mL | |
| 10 mM | 0.3152 mL | 1.5760 mL | 3.1521 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.
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