General Information of the Drug (ID: M6APDG02214)
Name
Oxindole 94
Synonyms
SB 202190; 152121-30-7; SB202190; SB-202190; FHPI; SB202190 (FHPI); UNII-PVX798P8GI; 4-(4-Fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)-1H-imidazole; CHEBI:79090; 4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole; PVX798P8GI; SB 202190, Immobilized; C20H14FN3O; Phenol, 4-[4-(4-fluorophenyl)-5-(4-pyridinyl)-1H-imidazol-2-yl]-; 4-[4-(4-fluorophenyl)-5-(pyridin-4-yl)-1H-imidazol-2-yl]phenol; 4-[5-(4-fluorophenyl)-4-(pyridin-4-yl)-1H-imidazol-2-yl]phenol
    Click to Show/Hide
Status
Investigative
Structure
Formula
C20H14FN3O
InChI
1S/C20H14FN3O/c21-16-5-1-13(2-6-16)18-19(14-9-11-22-12-10-14)24-20(23-18)15-3-7-17(25)8-4-15/h1-12,25H,(H,23,24)
InChIKey
QHKYPYXTTXKZST-UHFFFAOYSA-N
PubChem CID
5169
TTD Drug ID
D0VC0I
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.
Prostaglandin G/H synthase 2 (COX-2)
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
Response Summary Prostaglandin G/H synthase 2 (COX-2) is a therapeutic target for Oxindole 94. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of Oxindole 94 through regulating the expression of Prostaglandin G/H synthase 2 (COX-2). [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
Response Summary Stress-activated protein kinase 2a (p38 alpha) is a therapeutic target for Oxindole 94. The Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) has potential in affecting the response of Oxindole 94 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
Response Summary Stress-activated protein kinase 2a (p38 alpha) is a therapeutic target for Oxindole 94. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of Oxindole 94 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
Response Summary Stress-activated protein kinase 2a (p38 alpha) is a therapeutic target for Oxindole 94. The YTH domain-containing family protein 3 (YTHDF3) has potential in affecting the response of Oxindole 94 through regulating the expression of Stress-activated protein kinase 2a (p38 alpha). [3], [4]
References
Ref 1 METTL3 promotes experimental osteoarthritis development by regulating inflammatory response and apoptosis in chondrocyte. Biochem Biophys Res Commun. 2019 Aug 13;516(1):22-27. doi: 10.1016/j.bbrc.2019.05.168. Epub 2019 Jun 8.
Ref 2 SB-239063, a potent and selective inhibitor of p38 map kinase: preclinical pharmacokinetics and species-specific reversible isomerization. Pharm Res. 2001 Sep;18(9):1336-44. doi: 10.1023/a:1013002414678.
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 Two classes of p38alpha MAP kinase inhibitors having a common diphenylether core but exhibiting divergent binding modes. Bioorg Med Chem Lett. 2005 Dec 1;15(23):5274-9. doi: 10.1016/j.bmcl.2005.08.038. Epub 2005 Sep 19.
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.