m6A-centered Drug Response Information

General Information of the Drug (ID: M6APDG00398)
Name
4-amino-biphenyl-3-carboxylic acid amide
Synonyms
CHEMBL207940; 5-phenylanthranilamide; 2-amino-5-phenylbenzamide; SCHEMBL3781950; Amino-substituted benzamide, 8c; BDBM27462; ZINC13686738
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Status
Investigative
Structure
Formula
C13H12N2O
InChI
1S/C13H12N2O/c14-12-7-6-10(8-11(12)13(15)16)9-4-2-1-3-5-9/h1-8H,14H2,(H2,15,16)
InChIKey
KLDLPUIJJYDCEE-UHFFFAOYSA-N
PubChem CID
11600944
TTD Drug ID
D0UP6G
Target Gene(s) and Their Upstream m6A Regulator, Together with the Effect of Target Gene(s) in Drug Response
The target genes involved in drug-target interaction (such as drug-metabolizing enzymes, drug transporters and therapeutic targets) and drug-mediated cell death signaling (including modulating DNA damage and repair capacity, escaping from drug-induced apoptosis, autophagy, cellular metabolic reprogramming, oncogenic bypass signaling, cell microenvironment, cell stemness, etc.) could be regulated by m6A regulator(s) and affected their corresponding drug response. You can browse detailed information on drug-related target gene(s) mediated by m6A regulators.
Inhibitor of nuclear factor kappa-B kinase beta (IKKB)
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Inhibitor of nuclear factor kappa-B kinase beta (IKKB) is a therapeutic target for 4-amino-biphenyl-3-carboxylic acid amide. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of 4-amino-biphenyl-3-carboxylic acid amide through regulating the expression of Inhibitor of nuclear factor kappa-B kinase beta (IKKB). [1], [2]
References
Ref 1 The m(6)A methyltransferase METTL3 promotes bladder cancer progression via AFF4/NF-KappaB/MYC signaling network. Oncogene. 2019 May;38(19):3667-3680. doi: 10.1038/s41388-019-0683-z. Epub 2019 Jan 18.
Ref 2 Evolution of the thienopyridine class of inhibitors of IkappaB kinase-beta: part I: hit-to-lead strategies. J Med Chem. 2006 May 18;49(10):2898-908. doi: 10.1021/jm0510979.