General Information of the Drug (ID: M6APDG03202)
Name
SB-242235
Synonyms
193746-75-7; SB-242235; SB242235; SB 242235; 4-(4-(4-fluorophenyl)-1-(piperidin-4-yl)-1H-imidazol-5-yl)-2-methoxypyrimidine; CHEMBL95692; 4-[5-(4-fluorophenyl)-3-piperidin-4-ylimidazol-4-yl]-2-methoxypyrimidine; 4-[4-(4-fluorophenyl)-1-(piperidin-4-yl)-1H-imidazol-5-yl]-2-methoxypyrimidine; Kinome_3169; SCHEMBL2267209; BDBM15458; SYN1076; PDTYLGXVBIWRIM-UHFFFAOYSA-N; MolPort-028-720-427; HMS3244I18; HMS3244J17; HMS3244I17; EX-A1881; BCP05992; ZINC1487129; 3254AH; RS0056; AKOS027323444; CS-2097; NCGC00345831-01; NCGC00345831-03
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Status
Discontinued in Phase 1
Structure
Formula
C19H20FN5O
InChI
1S/C19H20FN5O/c1-26-19-22-11-8-16(24-19)18-17(13-2-4-14(20)5-3-13)23-12-25(18)15-6-9-21-10-7-15/h2-5,8,11-12,15,21H,6-7,9-10H2,1H3
InChIKey
PDTYLGXVBIWRIM-UHFFFAOYSA-N
PubChem CID
9863367
TTD Drug ID
D0A9KI
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.
Heat shock protein beta-1 (HSPB1)
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
Response Summary Heat shock protein beta-1 (HSPB1) is a therapeutic target for SB-242235. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of SB-242235 through regulating the expression of Heat shock protein beta-1 (HSPB1). [1], [2]
YTH domain-containing family protein 2 (YTHDF2)
In total 1 mechanisms lead to this potential drug response
Response Summary Heat shock protein beta-1 (HSPB1) is a therapeutic target for SB-242235. The YTH domain-containing family protein 2 (YTHDF2) has potential in affecting the response of SB-242235 through regulating the expression of Heat shock protein beta-1 (HSPB1). [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 SB-242235. The Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) has potential in affecting the response of SB-242235 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 SB-242235. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of SB-242235 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 SB-242235. The YTH domain-containing family protein 3 (YTHDF3) has potential in affecting the response of SB-242235 through regulating the expression of Stress-activated protein kinase 2a (p38 alpha). [3], [4]
References
Ref 1 Modification of N6-methyladenosine RNA methylation on heat shock protein expression. PLoS One. 2018 Jun 14;13(6):e0198604. doi: 10.1371/journal.pone.0198604. eCollection 2018.
Ref 2 Therapy with the hsp60 peptide DiaPep277 in C-peptide positive type 1 diabetes patients. Diabetes Metab Res Rev. 2007 May;23(4):269-75. doi: 10.1002/dmrr.691.
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 Selective p38alpha inhibitors clinically evaluated for the treatment of chronic inflammatory disorders. J Med Chem. 2010 Mar 25;53(6):2345-53. doi: 10.1021/jm9012906.
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.