m6A-centered Drug Response Information

General Information of the Drug (ID: M6APDG02186)
Name
Rabeprazole
Synonyms
2-(((4-(3-Methoxypropoxy)-3-methyl-2-pyridinyl)methyl)sulfinyl)-1H-benzimidazole; 2-((4-(3-methoxypropoxy)-3-methylpyridin-2-yl)methylsulfinyl)-1H-benzimidazole; 2-({[4-(3-methoxypropoxy)-3-methylpyridin-2-yl]methyl}sulfinyl)-1H-benzimidazole; 2-[[4-(3-methoxypropoxy)-3-methylpyridin-2-yl]methylsulfinyl]-1H-benzimidazole; Aciphex (TN); CL23619; Dexrabeprazole; Eraloc; Eraloc (TN); LY307640; Pariet (TN); Rabeprazole (INN); Rabeprazole [BAN:INN]; Rabeprazole [INN:BAN]; Rablet (TN); Rebeprazole sodium
    Click to Show/Hide
Status
Approved
Structure
Formula
C18H21N3O3S
InChI
1S/C18H21N3O3S/c1-13-16(19-9-8-17(13)24-11-5-10-23-2)12-25(22)18-20-14-6-3-4-7-15(14)21-18/h3-4,6-9H,5,10-12H2,1-2H3,(H,20,21)
InChIKey
YREYEVIYCVEVJK-UHFFFAOYSA-N
PubChem CID
5029
VARIDT Drug ID
DR01195
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.
Breast cancer resistance protein (ABCG2)
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Breast cancer resistance protein (ABCG2) is a therapeutic target for Rabeprazole. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of Rabeprazole through regulating the expression of Breast cancer resistance protein (ABCG2). [1], [2]
References
Ref 1 METTL3 promotes adriamycin resistance in MCF-7 breast cancer cells by accelerating pri-microRNA-221-3p maturation in a m6A-dependent manner. Exp Mol Med. 2021 Jan;53(1):91-102. doi: 10.1038/s12276-020-00510-w. Epub 2021 Jan 8.
Ref 2 Co-administration of proton pump inhibitors delays elimination of plasma methotrexate in high-dose methotrexate therapy. Br J Clin Pharmacol. 2009 Jan;67(1):44-9. doi: 10.1111/j.1365-2125.2008.03303.x. Epub 2008 Nov 17.