General Information of the Drug (ID: M6APDG03057)
Name
KML110
Synonyms
KML110
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Status
Investigative
Structure
Formula
C22H23N3O3
InChI
1S/C22H23N3O3/c1-15-18-9-8-17(25(27)28)14-19(18)21(16-6-4-3-5-7-16)20(15)22(26)24-12-10-23(2)11-13-24/h3-9,14-15H,10-13H2,1-2H3
InChIKey
BBPOBHFPZPRPGB-UHFFFAOYSA-N
PubChem CID
91827387
TTD Drug ID
D0S9AT
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.
Nucleobindin-1 (NUCB1)
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
Response Summary Nucleobindin-1 (NUCB1) is a therapeutic target for KML110. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of KML110 through regulating the expression of Nucleobindin-1 (NUCB1). [1], [2]
YTH domain-containing family protein 2 (YTHDF2)
In total 1 mechanisms lead to this potential drug response
Response Summary Nucleobindin-1 (NUCB1) is a therapeutic target for KML110. The YTH domain-containing family protein 2 (YTHDF2) has potential in affecting the response of KML110 through regulating the expression of Nucleobindin-1 (NUCB1). [1], [2]
References
Ref 1 NUCB1 Suppresses Growth and Shows Additive Effects With Gemcitabine in Pancreatic Ductal Adenocarcinoma via the Unfolded Protein Response. Front Cell Dev Biol. 2021 Mar 29;9:641836. doi: 10.3389/fcell.2021.641836. eCollection 2021.
Ref 2 A Global Map of Lipid-Binding Proteins and Their Ligandability in Cells. Cell. 2015 Jun 18;161(7):1668-80. doi: 10.1016/j.cell.2015.05.045.