m6A-centered Drug Response Information

General Information of the Drug (ID: M6APDG01115)
Name
Bisindolylmaleimide-I
Synonyms
Bisindolylmaleimide i; bisindolylmaleimide i; 133052-90-1; GF 109203X; GF109203X; Go 6850; GF-109203X; RBT205 INHIBITOR; Go-6850; UNII-L79H6N0V6C; 6850; Bisindolylmaleimide I (GF 109203X); CHEMBL7463; 3-{1-[3-(DIMETHYLAMINO)PROPYL]-1H-INDOL-3-YL}-4-(1H-INDOL-3-YL)-1H-PYRROLE-2,5-DIONE; 3-(1-(3-(Dimethylamino)propyl)-1H-indol-3-yl)-4-(1H-indol-3-yl)-1H-pyrrole-2,5-dione; L79H6N0V6C; QMGUOJYZJKLOLH-UHFFFAOYSA-N; 2-[1-(3-dimethylaminopropyl)indol-3-yl]-3-(indol-3-yl)maleimide; GF-109203; Go6850
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Status
Investigative
Structure
Formula
C25H24N4O2
InChI
1S/C25H24N4O2/c1-28(2)12-7-13-29-15-19(17-9-4-6-11-21(17)29)23-22(24(30)27-25(23)31)18-14-26-20-10-5-3-8-16(18)20/h3-6,8-11,14-15,26H,7,12-13H2,1-2H3,(H,27,30,31)
InChIKey
QMGUOJYZJKLOLH-UHFFFAOYSA-N
PubChem CID
2396
TTD Drug ID
D0TO6S
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.
Cyclin-dependent kinase 1 (CDK1)
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Cyclin-dependent kinase 1 (CDK1) is a therapeutic target for Bisindolylmaleimide-I. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of Cyclin-dependent kinase 1 (CDK1). [1], [2]
Protein virilizer homolog (VIRMA)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Cyclin-dependent kinase 1 (CDK1) is a therapeutic target for Bisindolylmaleimide-I. The Protein virilizer homolog (VIRMA) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of Cyclin-dependent kinase 1 (CDK1). [2], [3]
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 Bisindolylmaleimide-I. The Heterogeneous nuclear ribonucleoproteins A2/B1 (HNRNPA2B1) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of Extracellular signal-regulated kinase 2 (ERK2). [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 Extracellular signal-regulated kinase 2 (ERK2) is a therapeutic target for Bisindolylmaleimide-I. The Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of Extracellular signal-regulated kinase 2 (ERK2). [5], [6]
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 Bisindolylmaleimide-I. The YTH domain-containing family protein 3 (YTHDF3) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of Extracellular signal-regulated kinase 2 (ERK2). [5], [6]
Glycogen synthase kinase-3 beta (GSK-3B)
Fat mass and obesity-associated protein (FTO)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Glycogen synthase kinase-3 beta (GSK-3B) is a therapeutic target for Bisindolylmaleimide-I. The Fat mass and obesity-associated protein (FTO) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of Glycogen synthase kinase-3 beta (GSK-3B). [2], [7]
Methyltransferase-like 14 (METTL14)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Glycogen synthase kinase-3 beta (GSK-3B) is a therapeutic target for Bisindolylmaleimide-I. The Methyltransferase-like 14 (METTL14) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of Glycogen synthase kinase-3 beta (GSK-3B). [2], [8]
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 Bisindolylmaleimide-I. The Heterogeneous nuclear ribonucleoproteins A2/B1 (HNRNPA2B1) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [9], [10]
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 Bisindolylmaleimide-I. The Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [6], [10]
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 Bisindolylmaleimide-I. The Methyltransferase-like 14 (METTL14) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [10], [11]
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 Bisindolylmaleimide-I. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [10], [12]
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 Bisindolylmaleimide-I. The RNA demethylase ALKBH5 (ALKBH5) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [10], [13]
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 Bisindolylmaleimide-I. The YTH domain-containing family protein 1 (YTHDF1) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [10], [14]
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 Bisindolylmaleimide-I. The YTH domain-containing family protein 2 (YTHDF2) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [10], [15]
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 Bisindolylmaleimide-I. The YTH domain-containing family protein 3 (YTHDF3) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [6], [10]
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 Bisindolylmaleimide-I. The YTH domain-containing protein 2 (YTHDC2) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of RAC-alpha serine/threonine-protein kinase (AKT1). [10], [16]
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 Bisindolylmaleimide-I. The Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of Stress-activated protein kinase 2a (p38 alpha). [6], [17]
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 Bisindolylmaleimide-I. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of Stress-activated protein kinase 2a (p38 alpha). [17], [18]
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 Bisindolylmaleimide-I. The YTH domain-containing family protein 3 (YTHDF3) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of Stress-activated protein kinase 2a (p38 alpha). [6], [17]
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 Bisindolylmaleimide-I. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of Stress-activated protein kinase JNK1 (JNK1). [19], [20]
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 Bisindolylmaleimide-I. The RNA demethylase ALKBH5 (ALKBH5) has potential in affecting the response of Bisindolylmaleimide-I through regulating the expression of Stress-activated protein kinase JNK1 (JNK1). [20], [21]
References
Ref 1 CircMETTL3, upregulated in a m6A-dependent manner, promotes breast cancer progression. Int J Biol Sci. 2021 Mar 15;17(5):1178-1190. doi: 10.7150/ijbs.57783. eCollection 2021.
Ref 2 1-Azakenpaullone is a selective inhibitor of glycogen synthase kinase-3 beta. Bioorg Med Chem Lett. 2004 Jan 19;14(2):413-6. doi: 10.1016/j.bmcl.2003.10.062.
Ref 3 KIAA1429 acts as an oncogenic factor in breast cancer by regulating CDK1 in an N6-methyladenosine-independent manner. Oncogene. 2019 Aug;38(33):6123-6141. doi: 10.1038/s41388-019-0861-z. Epub 2019 Jul 8.
Ref 4 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 5 Potent inhibition of checkpoint kinase activity by a hymenialdisine-derived indoloazepine. Bioorg Med Chem Lett. 2004 Aug 16;14(16):4319-21. doi: 10.1016/j.bmcl.2004.05.079.
Ref 6 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 7 Vascular Smooth Muscle FTO Promotes Aortic Dissecting Aneurysms via m6A Modification of Klf5. Front Cardiovasc Med. 2020 Nov 20;7:592550. doi: 10.3389/fcvm.2020.592550. eCollection 2020.
Ref 8 N6-methyladenosine regulated FGFR4 attenuates ferroptotic cell death in recalcitrant HER2-positive breast cancer. Nat Commun. 2022 May 13;13(1):2672. doi: 10.1038/s41467-022-30217-7.
Ref 9 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 10 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 11 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 12 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 13 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 14 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 15 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 16 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 17 Synthesis and biological testing of purine derivatives as potential ATP-competitive kinase inhibitors. J Med Chem. 2005 Feb 10;48(3):710-22. doi: 10.1021/jm0408767.
Ref 18 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 19 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 20 The selectivity of protein kinase inhibitors: a further update. Biochem J. 2007 Dec 15;408(3):297-315. doi: 10.1042/BJ20070797.
Ref 21 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.