Chemical, Structural, Clinical and Biological details of Antiviral agents ID: DrugRepV_4318



Chemical Information
Antiviral agent IDDrugRepV_4318
Antiviral agent nameFGI-106
IUPAC Name1-N,7-N-bis[3-(dimethylamino)propyl]-3,9-dimethylquinolino[8,7-h]quinoline-1,7-diamine;tetrahydrochloride PubChem
SMILES (canonical)CC1=NC2=C(C=CC3=C2C=CC4=C3N=C(C=C4NCCCN(C)C)C)C(=C1)NCCCN(C)C.Cl.Cl.Cl.Cl PubChem
Molecular FormulaC28H42Cl4N6 PubChem
Molecular Weight (g/mol)604.486 PubChem
InChlInChI=1S/C28H38N6.4ClH/c1-19-17-25(29-13-7-15-33(3)4)23-11-10-22-21(27(23)31-19)9-12-24-26(18-20(2)32-28(22)24)30-14-8-16-34(5)6;;;;/h9-12,17-18H,7-8,13-16H2,1-6H3,(H,29,31)(H,30,32);4*1H PubChem
SynonymsQuino(8,7-H)quinoline-1,7-diamine, N1,N7-bis(3-(dimethylamino)propyl)-3,9-dimethyl-, hydrochloride | 1149348-10-6 | 76TVI971YY
Structural Information
  
Clinical Information
Biological Information
Secondary Indication Ebola virus (EBOV) NA ZaireWorld Health OrganisationCDC
Secondary Indication (Approaches)Experimental
Secondary Indication (Methods)In-vitro
Secondary Indication (Model system) [cell lines/ animal models]VeroE6
Secondary Indication (Mode of viral infection)Adsorption
Secondary Indication (Viral titer)1 MOI
Secondary Indication (Mode of drug delivery) Culture
Secondary Indication (Time of drug delivery) Post infection
Secondary Indication (Duration of drug delivery)48 hours
Secondary Indication (Drug concentration)100 nM
Secondary Indication (Cell based assay)Plaque assay
Secondary Indication (Change)Decrease
Secondary Indication (Type of Inhibition) EC50 [ 50 % ]
Secondary Indication (Cytotoxicity)10 μM
ReferenceAman MJ, Kinch MS, Warfield K, Warren T, Yunus A, Enterlein S, Stavale E, Wang P, Chang S, Tang Q, Porter K, Goldblatt M, Bavari S..Development of a broad-spectrum antiviral with activity against Ebola virus..Antiviral Res. 2009 Sep;83(3):245-51. doi: 10.1016/j.antiviral.2009.06.001. Epub 2009 Jun 10. PMID:19523489 PubMed
CommentCell-based assays identified inhibitory activity against diverge virus families, which supports a hypothesis that FGI-106 interferes with a common pathway utilized different viruses.