General Information of the Drug (ID: M6APDG00176)
Name
5-(2-Imidazol-1-yl-ethyl)-7,8-dihydro-quinoline
Synonyms
CHEMBL293122; dihydroquinoline 31; BDBM10027; ZINC13808192; 5-[2-(Imidazol-1-yl)ethyl]-7,8-dihydroquinoline; 5-[2-(1H-imidazol-1-yl)ethyl]-7,8-dihydroquinoline
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Status
Investigative
Structure
Formula
C14H15N3
InChI
1S/C14H15N3/c1-3-12(6-9-17-10-8-15-11-17)13-4-2-7-16-14(13)5-1/h2-4,7-8,10-11H,1,5-6,9H2
InChIKey
DJMSMHXCSIBVSA-UHFFFAOYSA-N
PubChem CID
10561174
TTD Drug ID
D04ZGF
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
Response Summary Prostaglandin G/H synthase 2 (COX-2) is a therapeutic target for 5-(2-Imidazol-1-yl-ethyl)-7,8-dihydro-quinoline. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of 5-(2-Imidazol-1-yl-ethyl)-7,8-dihydro-quinoline 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 The cyclooxygenase inhibitor flurbiprofen reduces radiation-induced angiogenic growth factor secretion of squamous cell carcinoma cell lines. Ann N Y Acad Sci. 2004 Dec;1030:37-42. doi: 10.1196/annals.1329.005.