CD388
CD388 is an antiviral reagent-Fc conjugate formed by linking an influenza virus neuraminidase inhibitor to the CH1-Fc hybrid domain of IgG1. CD388 exerts antiviral activity extracellularly by inhibiting Neuraminidase. CD388 reduces pulmonary viral load and proinflammatory cytokine levels in influenza-infected mice, prevents death, reduces body weight loss, and prolongs median time to death. CD388 exhibits activity against influenza A and B subtypes, including highly pathogenic strains. CD388 can be used in influenza-related research.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Formel: CD388
- Molecular Weight:793.48
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Speicherung:
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Biologische Aktivität
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Chemical Information
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Biologische Aktivität
Beschreibung
In Vitro
CD388 (0.001 pM-10000 nM; 3 days (influenza A), 5 days (influenza B)) potently inhibits the cytopathic effect of MDCK/MDCK-SIAT1 cells infected with influenza A and influenza B viruses, with median EC50 values ranging from 0.80 nM to 1.72 nM and a selectivity index of >1000-fold[3].
CD388 potently neutralizes highly pathogenic avian influenza (HPAI) A/H5N1 and A/H7N9 viruses in MDCK cells, with median half-maximal effective concentrations (EC50) of 0.57 nM and 0.04 nM, respectively[3].
CD388 (0.001-1000 nM; 20 min) potently inhibits recombinant influenza neuraminidase (NA) from various A/H5N1, A/H7N9 and CDC reference strains (including NAI-resistant variants), with IC50 values ranging from 0.12 to 7.63 nM, and shows minimal loss of activity against drug-resistant variants[4].
CD388 (0.001 pM-10000 nM; 3 days for influenza A, 5 days for influenza B) potently inhibits influenza A strains A/H1N1, A/H3N2 and influenza B strains in the cytopathic effect (CPE) assay using MDCK/MDCK-SIAT1 cells, with median EC50 values of 0.80 nM, 1.27 nM and 1.72 nM, respectively[4].
CD388 (0.00001 nM-10,000 nM; 24 h-5 days) exhibits no cytotoxicity toward primary lung fibroblasts, PBMC, HEp-2 cells, and A549 cells, with a CC50 greater than 10,000 nM and a selectivity index greater than 1000[4].
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:primary human lung fibroblast (HLF) cells, peripheral blood mononuclear cells (PBMCs), HEp-2 cells, and A549 cells
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Concentration:0.00001 nM-10,000 nM
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Incubation Time:24 h (HLF/PBMCs); 5 days (HEp-2/A549 cells)
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Result:Had a half-maximal cytotoxic concentration (CC50) of >10,000 nM in all tested human cell types, resulting in a >1,000-fold selectivity index relative to its antiviral EC50 values.
Parmacokinetics
| Species | Dose | Route | Tmax | Cmax | T1/2 | AUC0-t | CL/F | Vz/F |
|---|---|---|---|---|---|---|---|---|
| Rat[2] | 146 (14C-CD388) mg/kg | s.c. | 24 h | 440.1 μg/mL | 190 h | 114700 μg·h/mL | 1.191 mL/h/kg | 326.5 mL/kg |
In Vivo
CD388 (0.03-3 mg/kg; i.m.; single dose) provides full survival protection against lethal influenza A/Puerto Rico/8/1934 (H1N1) challenge in BALB/c mice at a single 0.3 mg/kg i.m. dose, with dose-dependent reductions in lung viral burden and pro-inflammatory cytokines[3].
CD388 (1 mg/kg; i.m.; single dose; 7 days pre-challenge) provides full prophylactic survival protection against lethal challenge with multiple influenza A and B strains in BALB/c mice at a single 1 mg/kg i.m. dose administered 7 days pre-exposure[3].
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 (immune competent)[1]
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Dosage:0.3 mg/kg; 1 mg/kg
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Administration:i.m.; single dose
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Result:Provided 100% survival across all tested influenza subtypes at ≤1 mg/kg.
Achieved minimum fully protective dose of 1 mg/kg for H1N1 (7 isolates) and B (Victoria) (2 isolates), and 0.3 mg/kg for H3N2 (1 isolate) and B (Yamagata) (1 isolate).
Caused transient BW loss (5-15% of starting weight) before recovery.
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Animal Model:BALB/c SCID (female, 6-8 weeks of age, intranasal challenge with 3×LD95 of mouse-adapted influenza A/Puerto Rico/8/1934 (H1N1))[3]
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Dosage:1 mg/kg
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Administration:i.m.; single dose
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Result:Provided full survival protection.
Chemical Information
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Molecular Weight 793.48
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Formel CD388
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SMILES
[2H]C([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])([2H])[2H]
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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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.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Reinheit & Dokumentation
Verweise
[2]. Laenen A, et al. Absorption, distribution, metabolism, and excretion of an antiviral drug-Fc conjugate CD388 following subcutaneous administration of C-CD388 in the rat. Drug metabolism and disposition: the biological fate of chemicals. 2025 Jul;53(7):100103. [Content Brief]
[4]. Döhrmann S, et al. Drug-Fc conjugate CD388 targets influenza virus neuraminidase and is broadly protective in mice. Nature microbiology. 2025 Apr;10(4):912-926. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
CD388 Related Classifications
HY-185821 Related Classifications
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