KP-S54
KP-S54 is an antiviral agent derived from GS-441524 (HY-103586) and also a SARS-CoV-2 Mac1 and MERS-CoV Mac1 inhibitor. KP-S54 blocks interferon-induced reversal of ADP-ribosylation, with an IC50 value of 44 nM against SARS-CoV-2 and an IC50 value of 91 nM against MERS-CoV. KP-S54 produced no detectable antiviral efficacy in a SARS-CoV-2-infected mouse model. KP-S54 can be used for research related to SARS-CoV and MERS-CoV infection.
For research use only. We do not sell to patients.
- Formula: C30H31N9O7S
- Molecular Weight:661.69
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
KP-S54 (compound 18c) exhibits inhibitory activity against recombinant SARS-CoV-2 Mac1 (IC50 = 44 nM) and MERS-CoV Mac1 (IC50 = 91 nM)[1].
KP-S54 (1 μM) exhibited half-lives of 17, 41, and 35 min in mouse, rat, and human liver microsomes, respectively, with 32.8% remaining in mouse MLM after 15 min[1].
KP-S54 (500 μM; 5 h) exhibited a PAMPA permeability of approximately 4.72 × 10-6 cm/s[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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Molecular Weight 661.69
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Formula C30H31N9O7S
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SMILES
CN(C(CNC(C1=CN=CC(NS(=O)(C2=CC=CC=C2)=O)=C1)=O)=O)C[C@H]3O[C@@](C4=CC=C5C(N)=NC=NN54)([C@@H]6OC(C)(O[C@H]36)C)C#N
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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.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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How to Choose the Right Model Animal
Choosing the right model animal is a validity-driven decision in which the species, strain, sex, age, genetic background, disease-induction method, outcome measures, and welfare burden must match the scientific question rather than laboratory tradition or convenience. A model should be selected by judging face validity, construct validity, and predictive validity: whether it resembles the human phenotype, whether it reproduces relevant mechanisms, and whether results are likely to predict human biology or treatment response. Animal studies often fail to translate because of species differences, weak disease resemblance, poor experimental design, inadequate reporting, publication bias, and underuse of randomization, blinding, and sample-size justification. Unresolved questions include how to rank competing models objectively, how much human-disease complexity must be reproduced for a given objective, and when non-animal systems such as organoids, ex vivo tissue, or computational models
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)