m6A-centered Drug Response Information

General Information of the Drug (ID: M6APDG00718)
Name
7-fluoroindirubin-3-acetoxime
Status
Investigative
Structure
Formula
C18H12FN3O3
InChI
1S/C18H12FN3O3/c1-9(23)25-22-16-10-5-2-3-8-13(10)20-17(16)14-11-6-4-7-12(19)15(11)21-18(14)24/h2-8,21,24H,1H3/b22-16-
InChIKey
NFIUKUJUBYCMTC-JWGURIENSA-N
PubChem CID
136104466
TTD Drug ID
D0I1IK
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.
Aurora kinase B (AURKB)
RNA demethylase ALKBH5 (ALKBH5)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Aurora kinase B (AURKB) is a therapeutic target for 7-fluoroindirubin-3-acetoxime. The RNA demethylase ALKBH5 (ALKBH5) has potential in affecting the response of 7-fluoroindirubin-3-acetoxime through regulating the expression of Aurora kinase B (AURKB). [1], [2]
References
Ref 1 ALKBH5 promotes the proliferation of renal cell carcinoma by regulating AURKB expression in an m(6)A-dependent manner. Ann Transl Med. 2020 May;8(10):646. doi: 10.21037/atm-20-3079.
Ref 2 An integrated computational approach to the phenomenon of potent and selective inhibition of aurora kinases B and C by a series of 7-substituted indirubins. J Med Chem. 2007 Aug 23;50(17):4027-37. doi: 10.1021/jm070077z. Epub 2007 Aug 1.