Chemical Information | |
Antiviral agent ID | DrugRepV_3339 | |
Antiviral agent name | Trametinib | |
IUPAC Name | N-[3-[3-cyclopropyl-5-(2-fluoro-4-iodoanilino)-6,8-dimethyl-2,4,7-trioxopyrido[4,3-d]pyrimidin-1-yl]phenyl]acetamide | |
SMILES (canonical) | CC1=C2C(=C(N(C1=O)C)NC3=C(C=C(C=C3)I)F)C(=O)N(C(=O)N2C4=CC(=CC=C4)NC(=O)C)C5CC5 | |
Molecular Formula | C26H23FIN5O4 | |
Molecular Weight (g/mol) | 615.404 | |
InChl | InChI=1S/C26H23FIN5O4/c1-13-22-21(23(31(3)24(13)35)30-20-10-7-15(28)11-19(20)27)25(36)33(17-8-9-17)26(37)32(22)18-6-4-5-16(12-18)29-14(2)34/h4-7,10-12,17,30H,8-9H2,1-3H3,(H,29,34) | |
Common Name | Trametinib | |
Synonyms | Tramétinib | Trametinib | Trametinibum | |
Structural Information | |
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Clinical Information | |
Category | Antineoplastic and Immunomodulating Agents
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Primary Indication (Clinical trial phases) | Approved
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Biological Information | |
Primary Indication (Disease Category) | Non Infectious Disease
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Primary Indication (Disease) | Thyroid cancer
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Secondary Indication | Influenza virus (IAV) H1N1 WSN/H1N1 | |
Secondary Indication (Approaches) | Experimental | |
Secondary Indication (Methods) | In-vitro | |
Secondary Indication (Model system) [cell lines/ animal models] | HBEpC
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Secondary Indication (Mode of viral infection) | Adsorption
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Secondary Indication (Viral titer) | 0.01 MOI
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Secondary Indication (Mode of drug delivery) | Culture
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Secondary Indication (Time of drug delivery) | Pre infection
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Secondary Indication (Duration of drug delivery) | 24 hours
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Secondary Indication (Drug concentration) | 20 μM
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Secondary Indication (Cell based assay) | Plaque assay
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Secondary Indication (Change) | Decrease
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Secondary Indication (Type of Inhibition) | Percentage inhibition [ 70 % ] | |
Reference | SchrÌ_der T, Dudek SE, Schreiber A, Ehrhardt C, Planz O, Ludwig S.The clinically approved MEK inhibitor Trametinib efficiently blocks influenza A virus propagation an.Antiviral Res. 2018 Sep;157:80-92. doi: 10.1016 j.antiviral.2018.07.006. Epub 2018 Jul 7. PMID:29990517
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Comment | Trametinib efficiently blocks replication of different IAV subtypes in vitro and in vivo. The broad antiviral activity against various IAV strains was due to its ability to interfere with export of progeny vRNPs from the nucleus.
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