General Information of the Drug (ID: M6APDG01151)
Name
AP-Cav
Synonyms
AP-Cav
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Status
Investigative
Structure
3D MOL
Formula
C33H51ClN2O6
InChI
1S/C20H30NO3.C13H21NO3.ClH/c1-14(2)21(3)16-9-10-17(21)12-18(11-16)24-20(23)19(13-22)15-7-5-4-6-8-15;1-13(2,3)14-7-12(17)9-4-5-11(16)10(6-9)8-15;/h4-8,14,16-19,22H,9-13H2,1-3H3;4-6,12,14-17H,7-8H2,1-3H3;1H/q+1;;/p-1/t16-,17+,18?,19?,21?;12-;/m.0./s1
InChIKey
ABSQYTODNZGQMD-ORLLXICISA-M
PubChem CID
24779772
TTD Drug ID
D01FMS
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.
Nitric oxide synthase endothelial (NOS3)
Fat mass and obesity-associated protein (FTO)
In total 1 mechanisms lead to this potential drug response
Response Summary Nitric oxide synthase endothelial (NOS3) is a therapeutic target for AP-Cav. The Fat mass and obesity-associated protein (FTO) has potential in affecting the response of AP-Cav through regulating the expression of Nitric oxide synthase endothelial (NOS3). [1], [2]
References
Ref 1 N6-Methyladenosine Demethylase FTO (Fat Mass and Obesity-Associated Protein) as a Novel Mediator of Statin Effects in Human Endothelial Cells. Arterioscler Thromb Vasc Biol. 2022 May;42(5):644-658. doi: 10.1161/ATVBAHA.121.317295. Epub 2022 Mar 17.
Ref 2 Bicyclic amidine inhibitors of nitric oxide synthase: discovery of perhydro-iminopyrindine and perhydro-iminoquinoline as potent, orally active inhibitors of inducible nitric oxide synthase. Bioorg Med Chem Lett. 2005 Apr 15;15(8):1997-2001. doi: 10.1016/j.bmcl.2005.02.067.