m6A-centered Drug Response Information

General Information of the Drug (ID: M6APDG00315)
Name
4,5,6-trihydroxy-3-methylphthalide
Synonyms
CHEMBL486813; 4,5,6-trihydroxy-3-methylphthalide; AGUVVAYMPQDJDX-UHFFFAOYSA-; BDBM50242174; 3-methyl-4,5,6-trihydroxy-phthalide; 4,5,6-Trihydroxy-3-methylisobenzofuran-1(3H)-one
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Status
Investigative
Structure
Formula
C9H8O5
InChI
1S/C9H8O5/c1-3-6-4(9(13)14-3)2-5(10)7(11)8(6)12/h2-3,10-12H,1H3
InChIKey
AGUVVAYMPQDJDX-UHFFFAOYSA-N
PubChem CID
11424128
TTD Drug ID
D0RZ1H
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.
RAC-alpha serine/threonine-protein kinase (AKT1)
Heterogeneous nuclear ribonucleoproteins A2/B1 (HNRNPA2B1)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary RAC-alpha serine/threonine-protein kinase (AKT1) is a therapeutic target for 4,5,6-trihydroxy-3-methylphthalide. The Heterogeneous nuclear ribonucleoproteins A2/B1 (HNRNPA2B1) has potential in affecting the response of 4,5,6-trihydroxy-3-methylphthalide through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [1], [2]
Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary RAC-alpha serine/threonine-protein kinase (AKT1) is a therapeutic target for 4,5,6-trihydroxy-3-methylphthalide. The Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) has potential in affecting the response of 4,5,6-trihydroxy-3-methylphthalide through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [2], [3]
Methyltransferase-like 14 (METTL14)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary RAC-alpha serine/threonine-protein kinase (AKT1) is a therapeutic target for 4,5,6-trihydroxy-3-methylphthalide. The Methyltransferase-like 14 (METTL14) has potential in affecting the response of 4,5,6-trihydroxy-3-methylphthalide through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [2], [4]
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary RAC-alpha serine/threonine-protein kinase (AKT1) is a therapeutic target for 4,5,6-trihydroxy-3-methylphthalide. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of 4,5,6-trihydroxy-3-methylphthalide through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [2], [5]
RNA demethylase ALKBH5 (ALKBH5)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary RAC-alpha serine/threonine-protein kinase (AKT1) is a therapeutic target for 4,5,6-trihydroxy-3-methylphthalide. The RNA demethylase ALKBH5 (ALKBH5) has potential in affecting the response of 4,5,6-trihydroxy-3-methylphthalide through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [2], [6]
YTH domain-containing family protein 1 (YTHDF1)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary RAC-alpha serine/threonine-protein kinase (AKT1) is a therapeutic target for 4,5,6-trihydroxy-3-methylphthalide. The YTH domain-containing family protein 1 (YTHDF1) has potential in affecting the response of 4,5,6-trihydroxy-3-methylphthalide through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [2], [7]
YTH domain-containing family protein 2 (YTHDF2)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary RAC-alpha serine/threonine-protein kinase (AKT1) is a therapeutic target for 4,5,6-trihydroxy-3-methylphthalide. The YTH domain-containing family protein 2 (YTHDF2) has potential in affecting the response of 4,5,6-trihydroxy-3-methylphthalide through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [2], [8]
YTH domain-containing family protein 3 (YTHDF3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary RAC-alpha serine/threonine-protein kinase (AKT1) is a therapeutic target for 4,5,6-trihydroxy-3-methylphthalide. The YTH domain-containing family protein 3 (YTHDF3) has potential in affecting the response of 4,5,6-trihydroxy-3-methylphthalide through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [2], [3]
YTH domain-containing protein 2 (YTHDC2)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary RAC-alpha serine/threonine-protein kinase (AKT1) is a therapeutic target for 4,5,6-trihydroxy-3-methylphthalide. The YTH domain-containing protein 2 (YTHDC2) has potential in affecting the response of 4,5,6-trihydroxy-3-methylphthalide through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [2], [9]
References
Ref 1 HNRNPA2B1 regulates tamoxifen- and fulvestrant-sensitivity and hallmarks of endocrine resistance in breast cancer cells. Cancer Lett. 2021 Oct 10;518:152-168. doi: 10.1016/j.canlet.2021.07.015. Epub 2021 Jul 14.
Ref 2 Specificity and mechanism of action of some commonly used protein kinase inhibitors. Biochem J. 2000 Oct 1;351(Pt 1):95-105. doi: 10.1042/0264-6021:3510095.
Ref 3 N6-methyladenosine reader YTH N6-methyladenosine RNA binding protein 3 or insulin like growth factor 2 mRNA binding protein 2 knockdown protects human bronchial epithelial cells from hypoxia/reoxygenation injury by inactivating p38 MAPK, AKT, ERK1/2, and NF-KappaB pathways. Bioengineered. 2022 May;13(5):11973-11986. doi: 10.1080/21655979.2021.1999550.
Ref 4 METTL14 Inhibits Hepatocellular Carcinoma Metastasis Through Regulating EGFR/PI3K/AKT Signaling Pathway in an m6A-Dependent Manner. Cancer Manag Res. 2020 Dec 23;12:13173-13184. doi: 10.2147/CMAR.S286275. eCollection 2020.
Ref 5 Methyltransferase-like 3 promotes the progression of lung cancer via activating PI3K/AKT/mTOR pathway. Clin Exp Pharmacol Physiol. 2022 Jul;49(7):748-758. doi: 10.1111/1440-1681.13647. Epub 2022 May 23.
Ref 6 ALKBH5-mediated m(6)A demethylation of KCNK15-AS1 inhibits pancreatic cancer progression via regulating KCNK15 and PTEN/AKT signaling. Cell Death Dis. 2021 Dec 1;12(12):1121. doi: 10.1038/s41419-021-04401-4.
Ref 7 YTHDF1 promotes hepatocellular carcinoma progression via activating PI3K/AKT/mTOR signaling pathway and inducing epithelial-mesenchymal transition. Exp Hematol Oncol. 2021 Jun 4;10(1):35. doi: 10.1186/s40164-021-00227-0.
Ref 8 YTHDF2 mediates the mRNA degradation of the tumor suppressors to induce AKT phosphorylation in N6-methyladenosine-dependent way in prostate cancer. Mol Cancer. 2020 Oct 29;19(1):152. doi: 10.1186/s12943-020-01267-6.
Ref 9 m(6)A Reader YTHDC2 Promotes Radiotherapy Resistance of Nasopharyngeal Carcinoma via Activating IGF1R/AKT/S6 Signaling Axis. Front Oncol. 2020 Jul 31;10:1166. doi: 10.3389/fonc.2020.01166. eCollection 2020.