m6A-centered Drug Response Information

General Information of the Drug (ID: M6APDG03256)
Name
PKF-241-466
Synonyms
PKF-241-466; CHEMBL306090; BDBM50240611; N*4*-(2,2-Dimethyl-1-methylcarbamoyl-propyl)-N*1*-hydroxy-2-hydroxymethyl-3-p-tolyl-succinamide
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Status
Investigative
Structure
Formula
C19H29N3O5
InChI
1S/C19H29N3O5/c1-11-6-8-12(9-7-11)14(13(10-23)16(24)22-27)17(25)21-15(18(26)20-5)19(2,3)4/h6-9,13-15,23,27H,10H2,1-5H3,(H,20,26)(H,21,25)(H,22,24)/t13-,14+,15+/m0/s1
InChIKey
KNCYWVRUUBOHGE-RRFJBIMHSA-N
PubChem CID
9907830
TTD Drug ID
D02UYR
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.
Tumor necrosis factor (TNF)
Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Tumor necrosis factor (TNF) is a therapeutic target for PKF-241-466. The Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) has potential in affecting the response of PKF-241-466 through regulating the expression of Tumor necrosis factor (TNF). [1], [2]
Methyltransferase-like 14 (METTL14)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Tumor necrosis factor (TNF) is a therapeutic target for PKF-241-466. The Methyltransferase-like 14 (METTL14) has potential in affecting the response of PKF-241-466 through regulating the expression of Tumor necrosis factor (TNF). [2], [3]
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Tumor necrosis factor (TNF) is a therapeutic target for PKF-241-466. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of PKF-241-466 through regulating the expression of Tumor necrosis factor (TNF). [2], [4]
YTH domain-containing family protein 1 (YTHDF1)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Tumor necrosis factor (TNF) is a therapeutic target for PKF-241-466. The YTH domain-containing family protein 1 (YTHDF1) has potential in affecting the response of PKF-241-466 through regulating the expression of Tumor necrosis factor (TNF). [2], [4]
YTH domain-containing family protein 3 (YTHDF3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Tumor necrosis factor (TNF) is a therapeutic target for PKF-241-466. The YTH domain-containing family protein 3 (YTHDF3) has potential in affecting the response of PKF-241-466 through regulating the expression of Tumor necrosis factor (TNF). [1], [2]
References
Ref 1 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 2 Beta-aryl-succinic acid hydroxamates as dual inhibitors of matrix metalloproteinases and tumor necrosis factor alpha converting enzyme. J Med Chem. 2002 May 23;45(11):2289-93. doi: 10.1021/jm0110993.
Ref 3 METTL14 promotes glomerular endothelial cell injury and diabetic nephropathy via m6A modification of Alpha-klotho. Mol Med. 2021 Sep 9;27(1):106. doi: 10.1186/s10020-021-00365-5.
Ref 4 Mettl3 inhibits the apoptosis and autophagy of chondrocytes in inflammation through mediating Bcl2 stability via Ythdf1-mediated m(6)A modification. Bone. 2022 Jan;154:116182. doi: 10.1016/j.bone.2021.116182. Epub 2021 Sep 13.