m6A-centered Drug Response Information

General Information of the Drug (ID: M6APDG03150)
Name
NVP-ADW742
Synonyms
NVP-ADW742; 475488-23-4; ADW-742; 475489-15-7; UNII-MXS2N5862L; ADW742; MXS2N5862L; CHEMBL399021; 5-(3-(Benzyloxy)phenyl)-7-((1r,3r)-3-(pyrrolidin-1-ylmethyl)-cyclobutyl)-7H-pyrrolo[2,3-d]pyrimidin-4-amine; 5-(3-(Benzyloxy)phenyl)-7-(cis-3-(pyrrolidin-1-ylmethyl)cyclobutyl)-7H-pyrrolo[2,3-d]pyrimidin-4-amine; C28H31N5O; 5-(3-Benzyloxyphenyl)-7-[trans-3-[(pyrrolidin-1-yl)methyl]cyclobutyl]-7H-pyrrolo[2,3-d]pyrimidin-4-amine
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Status
Investigative
Structure
Formula
C28H31N5O
InChI
1S/C28H31N5O/c29-27-26-25(22-9-6-10-24(15-22)34-18-20-7-2-1-3-8-20)17-33(28(26)31-19-30-27)23-13-21(14-23)16-32-11-4-5-12-32/h1-3,6-10,15,17,19,21,23H,4-5,11-14,16,18H2,(H2,29,30,31)
InChIKey
LSFLAQVDISHMNB-UHFFFAOYSA-N
PubChem CID
9825149
TTD Drug ID
D06NMZ
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.
Insulin-like growth factor I receptor (IGF1R)
Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Insulin-like growth factor I receptor (IGF1R) is a therapeutic target for NVP-ADW742. The Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) has potential in affecting the response of NVP-ADW742 through regulating the expression of Insulin-like growth factor I receptor (IGF1R). [1], [2]
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Insulin-like growth factor I receptor (IGF1R) is a therapeutic target for NVP-ADW742. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of NVP-ADW742 through regulating the expression of Insulin-like growth factor I receptor (IGF1R). [2], [3]
RNA demethylase ALKBH5 (ALKBH5)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Insulin-like growth factor I receptor (IGF1R) is a therapeutic target for NVP-ADW742. The RNA demethylase ALKBH5 (ALKBH5) has potential in affecting the response of NVP-ADW742 through regulating the expression of Insulin-like growth factor I receptor (IGF1R). [2], [4]
YTH domain-containing protein 2 (YTHDC2)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Insulin-like growth factor I receptor (IGF1R) is a therapeutic target for NVP-ADW742. The YTH domain-containing protein 2 (YTHDC2) has potential in affecting the response of NVP-ADW742 through regulating the expression of Insulin-like growth factor I receptor (IGF1R). [2], [5]
References
Ref 1 IGF2BP2 promotes gastric cancer progression by regulating the IGF1R-RhoA-ROCK signaling pathway. Cell Signal. 2022 Jun;94:110313. doi: 10.1016/j.cellsig.2022.110313. Epub 2022 Mar 16.
Ref 2 Emerging therapies for multiple myeloma. Expert Opin Emerg Drugs. 2009 Mar;14(1):99-127. doi: 10.1517/14728210802676278.
Ref 3 m(6) A modification of lncRNA PCAT6 promotes bone metastasis in prostate cancer through IGF2BP2-mediated IGF1R mRNA stabilization. Clin Transl Med. 2021 Jun;11(6):e426. doi: 10.1002/ctm2.426.
Ref 4 ALKBH5 regulates IGF1R expression to promote the Proliferation and Tumorigenicity of Endometrial Cancer. J Cancer. 2020 Jul 25;11(19):5612-5622. doi: 10.7150/jca.46097. eCollection 2020.
Ref 5 m(6)A Reader YTHDC2 Promotes Radiotherapy Resistance of Nasopharyngeal Carcinoma via Activating IGF1R/AKT/S6 Signaling Axis. Front Oncol. 2020 Jul 31;10:1166. doi: 10.3389/fonc.2020.01166. eCollection 2020.