m6A-centered Drug Response Information

General Information of the Drug (ID: M6APDG02318)
Name
KN-62
Synonyms
KN-62 (non-isomeric); GTPL6001; HMS3229A04; CCG-206863
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Status
Investigative
Structure
3D MOL
2D MOL
Formula
C38H35N5O6S2
InChI
1S/C38H35N5O6S2/c1-41(50(45,46)36-11-5-7-29-26-39-19-17-33(29)36)35(38(44)43-23-21-42(22-24-43)31-9-3-2-4-10-31)25-28-13-15-32(16-14-28)49-51(47,48)37-12-6-8-30-27-40-20-18-34(30)37/h2-20,26-27,35H,21-25H2,1H3/t35-/m0/s1
InChIKey
RJVLFQBBRSMWHX-DHUJRADRSA-N
PubChem CID
5312126
TTD Drug ID
D0N6ES
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.
Extracellular signal-regulated kinase 2 (ERK2)
Heterogeneous nuclear ribonucleoproteins A2/B1 (HNRNPA2B1)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Extracellular signal-regulated kinase 2 (ERK2) is a therapeutic target for KN-62. The Heterogeneous nuclear ribonucleoproteins A2/B1 (HNRNPA2B1) has potential in affecting the response of KN-62 through regulating the expression of Extracellular signal-regulated kinase 2 (ERK2). [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 Extracellular signal-regulated kinase 2 (ERK2) is a therapeutic target for KN-62. The Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) has potential in affecting the response of KN-62 through regulating the expression of Extracellular signal-regulated kinase 2 (ERK2). [2], [3]
YTH domain-containing family protein 3 (YTHDF3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Extracellular signal-regulated kinase 2 (ERK2) is a therapeutic target for KN-62. The YTH domain-containing family protein 3 (YTHDF3) has potential in affecting the response of KN-62 through regulating the expression of Extracellular signal-regulated kinase 2 (ERK2). [2], [3]
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 KN-62. The Heterogeneous nuclear ribonucleoproteins A2/B1 (HNRNPA2B1) has potential in affecting the response of KN-62 through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [4], [5]
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 KN-62. The Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) has potential in affecting the response of KN-62 through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [3], [5]
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 KN-62. The Methyltransferase-like 14 (METTL14) has potential in affecting the response of KN-62 through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [5], [6]
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 KN-62. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of KN-62 through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [5], [7]
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 KN-62. The RNA demethylase ALKBH5 (ALKBH5) has potential in affecting the response of KN-62 through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [5], [8]
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 KN-62. The YTH domain-containing family protein 1 (YTHDF1) has potential in affecting the response of KN-62 through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [5], [9]
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 KN-62. The YTH domain-containing family protein 2 (YTHDF2) has potential in affecting the response of KN-62 through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [5], [10]
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 KN-62. The YTH domain-containing family protein 3 (YTHDF3) has potential in affecting the response of KN-62 through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [3], [5]
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 KN-62. The YTH domain-containing protein 2 (YTHDC2) has potential in affecting the response of KN-62 through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [5], [11]
Ribosomal protein S6 kinase beta-1 (S6K1)
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Ribosomal protein S6 kinase beta-1 (S6K1) is a therapeutic target for KN-62. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of KN-62 through regulating the expression of Ribosomal protein S6 kinase beta-1 (S6K1). [2], [12]
Stress-activated protein kinase 2a (p38 alpha)
Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Stress-activated protein kinase 2a (p38 alpha) is a therapeutic target for KN-62. The Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) has potential in affecting the response of KN-62 through regulating the expression of Stress-activated protein kinase 2a (p38 alpha). [3], [13]
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Stress-activated protein kinase 2a (p38 alpha) is a therapeutic target for KN-62. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of KN-62 through regulating the expression of Stress-activated protein kinase 2a (p38 alpha). [13], [14]
YTH domain-containing family protein 3 (YTHDF3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Stress-activated protein kinase 2a (p38 alpha) is a therapeutic target for KN-62. The YTH domain-containing family protein 3 (YTHDF3) has potential in affecting the response of KN-62 through regulating the expression of Stress-activated protein kinase 2a (p38 alpha). [3], [13]
Stress-activated protein kinase JNK1 (JNK1)
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Stress-activated protein kinase JNK1 (JNK1) is a therapeutic target for KN-62. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of KN-62 through regulating the expression of Stress-activated protein kinase JNK1 (JNK1). [2], [15]
RNA demethylase ALKBH5 (ALKBH5)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Stress-activated protein kinase JNK1 (JNK1) is a therapeutic target for KN-62. The RNA demethylase ALKBH5 (ALKBH5) has potential in affecting the response of KN-62 through regulating the expression of Stress-activated protein kinase JNK1 (JNK1). [2], [16]
References
Ref 1 hnRNPA2B1 Promotes Colon Cancer Progression via the MAPK Pathway. Front Genet. 2021 Sep 22;12:666451. doi: 10.3389/fgene.2021.666451. eCollection 2021.
Ref 2 Optimization of protein kinase CK2 inhibitors derived from 4,5,6,7-tetrabromobenzimidazole. J Med Chem. 2004 Dec 2;47(25):6239-47. doi: 10.1021/jm049854a.
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 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 5 Indolinone based phosphoinositide-dependent kinase-1 (PDK1) inhibitors. Part 1: design, synthesis and biological activity. Bioorg Med Chem Lett. 2007 Jul 15;17(14):3814-8. doi: 10.1016/j.bmcl.2007.04.071. Epub 2007 Apr 27.
Ref 6 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 7 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 8 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 9 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 10 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 11 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.
Ref 12 m(6)A methyltransferase METTL3 promotes retinoblastoma progression via PI3K/AKT/mTOR pathway. J Cell Mol Med. 2020 Oct 8;24(21):12368-78. doi: 10.1111/jcmm.15736. Online ahead of print.
Ref 13 Synthesis and biological evaluation of trisubstituted imidazole derivatives as inhibitors of p38alpha mitogen-activated protein kinase. Bioorg Med Chem Lett. 2008 Jul 15;18(14):4006-10. doi: 10.1016/j.bmcl.2008.06.007. Epub 2008 Jun 6.
Ref 14 m(6)A methyltransferase METTL3 suppresses colorectal cancer proliferation and migration through p38/ERK pathways. Onco Targets Ther. 2019 Jun 4;12:4391-4402. doi: 10.2147/OTT.S201052. eCollection 2019.
Ref 15 METTL3 regulates alternative splicing of MyD88 upon the lipopolysaccharide-induced inflammatory response in human dental pulp cells. J Cell Mol Med. 2018 May;22(5):2558-2568. doi: 10.1111/jcmm.13491. Epub 2018 Mar 4.
Ref 16 Post-translational modification of RNA m6A demethylase ALKBH5 regulates ROS-induced DNA damage response. Nucleic Acids Res. 2021 Jun 4;49(10):5779-5797. doi: 10.1093/nar/gkab415.