m6A-centered Drug Response Information

General Information of the Drug (ID: M6APDG00628)
Name
Acyclovir
Synonyms
2-Amino-1,9-dihydro-9-((2-hydroxyethoxy)methyl)-6H-purin-6-one; 2-Amino-1,9-dihydro-9-[(2-hydroxyethoxy)methyl]-6H-purin-6-one; 2-Amino-9-(2-hydroxy-ethoxymethyl)-1,9-dihydro-purin-6-one; 2-Amino-9-[(2-hydroxyethoxy)methyl]-1,9-dihydro-6H-purin-6-one; 2-amino-9-(2-hydroxyethoxymethyl)-3H-purin-6-one; 2-amino-9-{[(2-hydroxyethyl)oxy]methyl}-1,9-dihydro-6H-purin-6-one; 6H-Purin-6-one,2-amino-1,9-dihydro-9-((2-hydroxyethoxy)mehtyl); 9-((2-Hydroxyethoxy)methyl)guanine; 9-(2-Hydroxyethoxy)methylguanine; 9-HYROXYETHOXYMETHYLGUANINE; 9-[(2-Hydroxyethoxy)-methyl]guanine; 9-[(2-Hydroxyethoxy)methyl]guanine; A 4669; ACV; ACV & Pluronic F-68; Aciclovier; Aciclovir (JAN/INN); Aciclovir, Acycloguanosine, Zovirax, Acyclovir; Aciclovirum; Aciclovirum [INN-Latin]; Aciclovirum [Latin]; Acivir (TN); Acivirax (TN); Activir; AcycloFoam; Acycloguanosine; Acyclovir; Acyclovir & Pluronic F-68; Acyclovir (USP); Acyclovir Lauriad; Acyclovir [USAN]; Acyclovir-side chain-2-3H; Alti-Acyclovir; Avirax; B-LF& ACV; BW-248-U; BW-248U; BW-248U74; Bovine lactoferrin & 2-Amino-1,9-dihydro-9-[(2-hydroxyethoxy)methyl]-6H-purin-6-one; Cyclovir (TN); DRG-0008; Genvir; Hascovir; Herpex (TN); Maynar; Vipral; Virolex; Viropump; Virorax; W-248-U; Wellcome-248U; Zovir; Zovir (TN); Zovirax; Zovirax (TN); Zovirax Oral Acyclovir (ACV) Suspension
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Status
Approved
Structure
Formula
C8H11N5O3
InChI
1S/C8H11N5O3/c9-8-11-6-5(7(15)12-8)10-3-13(6)4-16-2-1-14/h3,14H,1-2,4H2,(H3,9,11,12,15)
InChIKey
MKUXAQIIEYXACX-UHFFFAOYSA-N
PubChem CID
135398513
VARIDT Drug ID
DR00325
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.
Alanine/serine/cysteine/threonine transporter 2 (SLC1A5)
Fat mass and obesity-associated protein (FTO)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Alanine/serine/cysteine/threonine transporter 2 (SLC1A5) is a therapeutic target for Acyclovir. The Fat mass and obesity-associated protein (FTO) has potential in affecting the response of Acyclovir through regulating the expression of Alanine/serine/cysteine/threonine transporter 2 (SLC1A5). [1], [2]
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 Acyclovir. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of Acyclovir through regulating the expression of Breast cancer resistance protein (ABCG2). [3], [4]
References
Ref 1 The m(6)A RNA demethylase FTO is a HIF-independent synthetic lethal partner with the VHL tumor suppressor. Proc Natl Acad Sci U S A. 2020 Sep 1;117(35):21441-21449. doi: 10.1073/pnas.2000516117. Epub 2020 Aug 19.
Ref 2 Amino Acid Transporter ATB0,+ as a delivery system for drugs and prodrugs. Curr Drug Targets Immune Endocr Metabol Disord. 2005 Dec;5(4):357-64. doi: 10.2174/156800805774912953.
Ref 3 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 4 Acyclovir is a substrate for the human breast cancer resistance protein (BCRP/ABCG2): implications for renal tubular transport and acyclovir-induced nephrotoxicity. Can J Physiol Pharmacol. 2011 Sep;89(9):675-80.