Drug Information

Drug (ID: DG01463) and It's Reported Resistant Information

• Name: AG1296
• Synonyms: 146535-11-7; Tyrphostin AG 1296; 6,7-dimethoxy-2-phenylquinoxaline; AG-1296; AG 1296; 6,7-Dimethoxy-3-phenylquinoxaline; ag1296; Tyrphostin AG-1296; Quinoxaline, 6,7-dimethoxy-2-phenyl-; Tyrphostin AG1296; CHEMBL71191; MFCD00270913; tyrphostin-AG1296; 6,7-Dimethoxy-2-phenylquinozaline; tyrphostin-AG-1296; BiomolKI_000055; BiomolKI2_000061; BMK1-F7; BSPBio_001422; KBioGR_000142; KBioSS_000142; SCHEMBL595944; GTPL5915; QCR-71; ZINC8082; CHEBI:93335; KBio2_000142; KBio2_002710; KBio2_005278; KBio3_000283; KBio3_000284; DTXSID70163393; Bio2_000142; Bio2_000622; HMS1361H04; HMS1791H04; HMS1989H04; HMS3229M21; HMS3402H04; HMS3653H21; BCP06928; EX-A4245; Tyrphostin AG 1296, >=98%; 6,7-Dimethoxy-2-phenyl-quinoxaline; 2090AH; 2774AH; BDBM50154227; s8024; AKOS025287463; CCG-100659; Quinozaline, 6,7-dimethoxy-2-phenyl-; Tyrphostin AG 1296 (AG 1296); IDI1_033892; NCGC00163386-01; NCGC00163386-02; NCGC00163386-03; NCGC00163386-04; AS-62520; HY-13894; CS-0008498; SW220231-1; AG-1296; ; ; 6,7-Dimethoxy-2-phenylquinoxaline; SR-03000001061; J-008233; SR-03000001061-1; AG 1296 - CAS 146535-11-7; BRD-K76064317-001-03-2; BRD-K76064317-001-04-0; Q27074335
• Indication:
  In total 1 Indication(s)
  Alzheimer disease [ICD-11: 8A20]; Investigative; [1]
• Target: Acetylcholinesterase (AChE); ACES_HUMAN; [2]
• Formula: 3
• IsoSMILES: COC1=C(C=C2C(=C1)N=CC(=N2)C3=CC=CC=C3)OC
• InChI: InChI=1S/C16H14N2O2/c1-19-15-8-12-13(9-16(15)20-2)18-14(10-17-12)11-6-4-3-5-7-11/h3-10H,1-2H3
• InChIKey: QNOXYUNHIGOWNY-UHFFFAOYSA-N
• PubChem CID: 2049
• ChEBI ID: CHEBI:93335
• TTD Drug ID: D0E6YQ

Type(s) of Resistant Mechanism of This Drug

  UAPP: Unusual Activation of Pro-survival Pathway

Drug Resistance Data Categorized by Their Corresponding Diseases

ICD-02: Benign/in-situ/malignant neoplasm

Acute myeloid leukemia [ICD-11: 2A60]

Drug Sensitivity Data Categorized by Their Corresponding Mechanisms

Unusual Activation of Pro-survival Pathway (UAPP)

Key Molecule: Receptor-type tyrosine-protein kinase FLT3 (FLT3) [2]

• Molecule Alteration: IF-deletion; p.Q569_G613 (c.1705_1837)
• Sensitive Disease: Acute myeloid leukemia [ICD-11: 2A60.0]
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Bone marrow; N.A.
• Experiment for Molecule Alteration: Immunoprecipitation and immunoblot analysis
• Experiment for Drug Resistance: MTT assay
• Mechanism Description: The if-deletion p.Q569_G613 (c.1705_1837) in gene FLT3 cause the sensitivity of AG1296 by unusual activation of pro-survival pathway.

Key Molecule: Receptor-type tyrosine-protein kinase FLT3 (FLT3) [1]

• Molecule Alteration: Missense mutation; p.D835V (c.2504A>T)
• Sensitive Disease: Acute myeloid leukemia [ICD-11: 2A60.0]
• Experimental Note: Revealed Based on the Cell Line Data
• In Vitro Model: Ba/F3 cells; Colon; Homo sapiens (Human); CVCL_0161
• Experiment for Molecule Alteration: Western blotting analysis
• Experiment for Drug Resistance: Cell proliferation Kit II XTT assay
• Mechanism Description: The missense mutation p.D835V (c.2504A>T) in gene FLT3 cause the sensitivity of AG1296 by unusual activation of pro-survival pathway

References

• Ref 1: AS602868, a dual inhibitor of IKK2 and FLT3 to target AML cellsLeukemia. 2007 May;21(5):877-85. doi: 10.1038/sj.leu.2404614. Epub 2007 Mar 1.
• Ref 2: Inhibition of the transforming activity of FLT3 internal tandem duplication mutants from AML patients by a tyrosine kinase inhibitorLeukemia. 2002 Oct;16(10):2027-36. doi: 10.1038/sj.leu.2402674.