m6A-centered Drug Response Information

General Information of the Drug (ID: M6APDG00950)
Name
(-)-hydroxycitrate
Synonyms
Garcinia acid; 3-c-carboxy-2-deoxy-d-erythro-pentaric acid; CHEMBL118715; UNII-8W94T9026R; (1S,2S)-1,2-dihydroxypropane-1,2,3-tricarboxylic acid; 8W94T9026R; Super CitriMax HCA 600SXS; 4373-35-7; (-)-Hydroxycitrate; 27750-10-3; 7A3; Citric acid, 2-hydroxy-, (-)-; AC1Q5QYE; AC1L4H7S; (2S,3S)-3-Carboxy-2,3-dihydroxy-pentanedioic acid; SCHEMBL6773065; DTXSID20276669; ZINC1656422; BDBM50036210; LMFA01050511; AJ-28889; D-erythro-Pentaric acid,
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Status
Investigative
Structure
Formula
C6H8O8
InChI
1S/C6H8O8/c7-2(8)1-6(14,5(12)13)3(9)4(10)11/h3,9,14H,1H2,(H,7,8)(H,10,11)(H,12,13)/t3-,6+/m1/s1
InChIKey
ZMJBYMUCKBYSCP-CVYQJGLWSA-N
PubChem CID
185620
TTD Drug ID
D0IC1N
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.
ATP-citrate synthase (ACLY)
Heterogeneous nuclear ribonucleoproteins A2/B1 (HNRNPA2B1)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary ATP-citrate synthase (ACLY) is a therapeutic target for (-)-hydroxycitrate. The Heterogeneous nuclear ribonucleoproteins A2/B1 (HNRNPA2B1) has potential in affecting the response of (-)-hydroxycitrate through regulating the expression of ATP-citrate synthase (ACLY). [1], [2]
Methyltransferase-like 14 (METTL14)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary ATP-citrate synthase (ACLY) is a therapeutic target for (-)-hydroxycitrate. The Methyltransferase-like 14 (METTL14) has potential in affecting the response of (-)-hydroxycitrate through regulating the expression of ATP-citrate synthase (ACLY). [2], [3]
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary ATP-citrate synthase (ACLY) is a therapeutic target for (-)-hydroxycitrate. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of (-)-hydroxycitrate through regulating the expression of ATP-citrate synthase (ACLY). [2], [4]
References
Ref 1 m(6)A Reader HNRNPA2B1 Promotes Esophageal Cancer Progression via Up-Regulation of ACLY and ACC1. Front Oncol. 2020 Sep 29;10:553045. doi: 10.3389/fonc.2020.553045. eCollection 2020.
Ref 2 Drugs@FDA. U.S. Food and Drug Administration. U.S. Department of Health Human Services. 2020
Ref 3 Dysregulated m6A modification promotes lipogenesis and development of non-alcoholic fatty liver disease and hepatocellular carcinoma. Mol Ther. 2022 Jun 1;30(6):2342-2353. doi: 10.1016/j.ymthe.2022.02.021. Epub 2022 Feb 19.
Ref 4 METTL3 inhibits hepatic insulin sensitivity via N6-methyladenosine modification of Fasn mRNA and promoting fatty acid metabolism. Biochem Biophys Res Commun. 2019 Oct 8;518(1):120-126. doi: 10.1016/j.bbrc.2019.08.018. Epub 2019 Aug 10.