General Information of the Drug (ID: M6APDG03012)
Name
N-(6-ethoxypyridin-2-yl)acetamide
Synonyms
N-(6-ethoxypyridin-2-yl)acetamide; N-(6-ethoxy-pyridin-2-yl)-acetamide; 775-38-2; AC1LGO22; CHEMBL210256; BDBM15972; Aminopyridine-Based Inhibitor 46
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Status
Investigative
Structure
Formula
C9H12N2O2
InChI
1S/C9H12N2O2/c1-3-13-9-6-4-5-8(11-9)10-7(2)12/h4-6H,3H2,1-2H3,(H,10,11,12)
InChIKey
NSIROEGSOFOSDV-UHFFFAOYSA-N
PubChem CID
824661
TTD Drug ID
D0E8KF
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.
Stress-activated protein kinase JNK1 (JNK1)
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
Response Summary Stress-activated protein kinase JNK1 (JNK1) is a therapeutic target for N-(6-ethoxypyridin-2-yl)acetamide. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of N-(6-ethoxypyridin-2-yl)acetamide through regulating the expression of Stress-activated protein kinase JNK1 (JNK1). [1], [2]
RNA demethylase ALKBH5 (ALKBH5)
In total 1 mechanisms lead to this potential drug response
Response Summary Stress-activated protein kinase JNK1 (JNK1) is a therapeutic target for N-(6-ethoxypyridin-2-yl)acetamide. The RNA demethylase ALKBH5 (ALKBH5) has potential in affecting the response of N-(6-ethoxypyridin-2-yl)acetamide through regulating the expression of Stress-activated protein kinase JNK1 (JNK1). [2], [3]
References
Ref 1 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 2 Aminopyridine-based c-Jun N-terminal kinase inhibitors with cellular activity and minimal cross-kinase activity. J Med Chem. 2006 Jun 15;49(12):3563-80. doi: 10.1021/jm060199b.
Ref 3 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.