m6A-centered Drug Response Information

General Information of the Drug (ID: M6APDG00834)
Name
6-o-tolylquinazolin-2-amine
Synonyms
6-o-tolylquinazolin-2-amine; CHEMBL215952; SCHEMBL5494575; RAWAQXBVMDKSIO-UHFFFAOYSA-N; ZINC35049815
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Status
Investigative
Structure
Formula
C15H13N3
InChI
1S/C15H13N3/c1-10-4-2-3-5-13(10)11-6-7-14-12(8-11)9-17-15(16)18-14/h2-9H,1H3,(H2,16,17,18)
InChIKey
RAWAQXBVMDKSIO-UHFFFAOYSA-N
PubChem CID
16086113
TTD Drug ID
D09HXU
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.
Janus kinase 3 (JAK-3)
Wilms tumor 1-associating protein (WTAP)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Janus kinase 3 (JAK-3) is a therapeutic target for 6-o-tolylquinazolin-2-amine. The Wilms tumor 1-associating protein (WTAP) has potential in affecting the response of 6-o-tolylquinazolin-2-amine through regulating the expression of Janus kinase 3 (JAK-3). [1], [2]
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 6-o-tolylquinazolin-2-amine. The Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) has potential in affecting the response of 6-o-tolylquinazolin-2-amine through regulating the expression of Stress-activated protein kinase 2a (p38 alpha). [3], [4]
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 6-o-tolylquinazolin-2-amine. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of 6-o-tolylquinazolin-2-amine through regulating the expression of Stress-activated protein kinase 2a (p38 alpha). [4], [5]
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 6-o-tolylquinazolin-2-amine. The YTH domain-containing family protein 3 (YTHDF3) has potential in affecting the response of 6-o-tolylquinazolin-2-amine through regulating the expression of Stress-activated protein kinase 2a (p38 alpha). [3], [4]
References
Ref 1 Transcriptome-Wide High-Throughput m6A Sequencing of Differential m6A Methylation Patterns in the Human Rheumatoid Arthritis Fibroblast-Like Synoviocytes Cell Line MH7A. J Inflamm Res. 2021 Feb 25;14:575-586. doi: 10.2147/JIR.S296006. eCollection 2021.
Ref 2 Janus kinase 2 inhibitors. Synthesis and characterization of a novel polycyclic azaindole. J Med Chem. 2009 Dec 24;52(24):7938-41. doi: 10.1021/jm901383u.
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 In silico search for multi-target anti-inflammatories in Chinese herbs and formulas. Bioorg Med Chem. 2010 Mar 15;18(6):2204-2218. doi: 10.1016/j.bmc.2010.01.070. Epub 2010 Feb 8.
Ref 5 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.