m6A-centered Drug Response Information

General Information of the Drug (ID: M6APDG01145)
Name
TG-C
Synonyms
3-Thiaglutaryl-Coa; S-[[(2-Hydroxy-2-oxoethyl)thio]acetyl]coenzyme A; (3R,5S,9R)-1-[(2R,3S,4R,5R)-5-(6-amino-9H-purin-9-yl)-4-hydroxy-3-(phosphonooxy)tetrahydrofuran-2-yl]-3,5,9-trihydroxy-8,8-dimethyl-10,14,19-trioxo-2,4,6-trioxa-18,21-dithia-11,15-diaza-3,5-diphosphatricosan-23-oic acid 3,5-dioxide; TGC
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Status
Phase 3
Structure
3D MOL
2D MOL
Formula
C25H40N7O19P3S2
InChI
1S/C25H40N7O19P3S2/c1-25(2,20(38)23(39)28-4-3-14(33)27-5-6-56-16(36)9-55-8-15(34)35)10-48-54(45,46)51-53(43,44)47-7-13-19(50-52(40,41)42)18(37)24(49-13)32-12-31-17-21(26)29-11-30-22(17)32/h11-13,18-20,24,37-38H,3-10H2,1-2H3,(H,27,33)(H,28,39)(H,34,35)(H,43,44)(H,45,46)(H2,26,29,30)(H2,40,41,42)/t13-,18-,19-,20+,24-/m1/s1
InChIKey
GKSSRSUPHZUOQO-ITIYDSSPSA-N
PubChem CID
24768536
TTD Drug ID
D0DP3V
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.
Transforming growth factor beta 1 (TGFB1)
Eukaryotic initiation factor 3 (EIF3A)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Transforming growth factor beta 1 (TGFB1) is a therapeutic target for TG-C. The Eukaryotic initiation factor 3 (EIF3A) has potential in affecting the response of TG-C through regulating the expression of Transforming growth factor beta 1 (TGFB1). [1], [2]
Heterogeneous nuclear ribonucleoproteins A2/B1 (HNRNPA2B1)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Transforming growth factor beta 1 (TGFB1) is a therapeutic target for TG-C. The Heterogeneous nuclear ribonucleoproteins A2/B1 (HNRNPA2B1) has potential in affecting the response of TG-C through regulating the expression of Transforming growth factor beta 1 (TGFB1). [2], [3]
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Transforming growth factor beta 1 (TGFB1) is a therapeutic target for TG-C. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of TG-C through regulating the expression of Transforming growth factor beta 1 (TGFB1). [2], [4]
YTH domain-containing family protein 2 (YTHDF2)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Transforming growth factor beta 1 (TGFB1) is a therapeutic target for TG-C. The YTH domain-containing family protein 2 (YTHDF2) has potential in affecting the response of TG-C through regulating the expression of Transforming growth factor beta 1 (TGFB1). [2], [5]
References
Ref 1 Knockdown of elF3a inhibits TGF?Beta1?induced extracellular matrix protein expression in keloid fibroblasts. Mol Med Rep. 2018 Mar;17(3):4057-4061. doi: 10.3892/mmr.2017.8365. Epub 2017 Dec 29.
Ref 2 Drugs@FDA. U.S. Food and Drug Administration. U.S. Department of Health & Human Services.
Ref 3 HNRNPA2B1, as a m(6)A Reader, Promotes Tumorigenesis and Metastasis of Oral Squamous Cell Carcinoma. Front Oncol. 2021 Sep 23;11:716921. doi: 10.3389/fonc.2021.716921. eCollection 2021.
Ref 4 N6-Methyladenosine Regulates the Expression and Secretion of TGFBeta1 to Affect the Epithelial-Mesenchymal Transition of Cancer Cells. Cells. 2020 Jan 25;9(2):296. doi: 10.3390/cells9020296.
Ref 5 YTHDF2 Inhibits the Migration and Invasion of Lung Adenocarcinoma by Negatively Regulating the FAM83D-TGFBeta1-SMAD2/3 Pathway. Front Oncol. 2022 Feb 2;12:763341. doi: 10.3389/fonc.2022.763341. eCollection 2022.