m6A-centered Drug Response Information

General Information of the Drug (ID: M6APDG00519)
Name
1-(4-(methylsulfonyl)phenyl)-1H-indole
Synonyms
CHEMBL1240964; 1-(4-(methylsulfonyl)phenyl)-1H-indole; 1-[4-(Methylsulfonyl)phenyl]-1H-indole; ZINC64475267
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Status
Investigative
Structure
Formula
C15H13NO2S
InChI
1S/C15H13NO2S/c1-19(17,18)14-8-6-13(7-9-14)16-11-10-12-4-2-3-5-15(12)16/h2-11H,1H3
InChIKey
XRGCFRFZQVGLLT-UHFFFAOYSA-N
PubChem CID
11958319
TTD Drug ID
D07AFA
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.
Prostaglandin G/H synthase 2 (COX-2)
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Prostaglandin G/H synthase 2 (COX-2) is a therapeutic target for 1-(4-(methylsulfonyl)phenyl)-1H-indole. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of 1-(4-(methylsulfonyl)phenyl)-1H-indole through regulating the expression of Prostaglandin G/H synthase 2 (COX-2). [1], [2]
References
Ref 1 METTL3 promotes experimental osteoarthritis development by regulating inflammatory response and apoptosis in chondrocyte. Biochem Biophys Res Commun. 2019 Aug 13;516(1):22-27. doi: 10.1016/j.bbrc.2019.05.168. Epub 2019 Jun 8.
Ref 2 Synthesis, anti-inflammatory activity, and in vitro antitumor effect of a novel class of cyclooxygenase inhibitors: 4-(aryloyl)phenyl methyl sulfones. J Med Chem. 2010 Sep 23;53(18):6560-71. doi: 10.1021/jm100398z.