General Information of the Drug (ID: M6APDG00410)
Name
PTosyl-Glu(OtBu)-Ala-LeuVSMe
Synonyms
CHEMBL207016; pTosyl-Glu(OtBu)-Ala-LeuVSMe
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Status
Investigative
Structure
3D MOL
Formula
C27H43N3O8S2
InChI
1S/C27H43N3O8S2/c1-18(2)17-21(15-16-39(8,34)35)29-25(32)20(4)28-26(33)23(13-14-24(31)38-27(5,6)7)30-40(36,37)22-11-9-19(3)10-12-22/h9-12,15-16,18,20-21,23,30H,13-14,17H2,1-8H3,(H,28,33)(H,29,32)/b16-15+/t20-,21+,23-/m0/s1
InChIKey
RSODQDWVGCCUGL-HSNUOWKJSA-N
PubChem CID
11621347
TTD Drug ID
D0A5WN
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.
Cathepsin B (CTSB)
Fat mass and obesity-associated protein (FTO)
In total 1 mechanisms lead to this potential drug response
Response Summary Cathepsin B (CTSB) is a therapeutic target for PTosyl-Glu(OtBu)-Ala-LeuVSMe. The Fat mass and obesity-associated protein (FTO) has potential in affecting the response of PTosyl-Glu(OtBu)-Ala-LeuVSMe through regulating the expression of Cathepsin B (CTSB). [1], [2]
References
Ref 1 A dynamic N(6)-methyladenosine methylome regulates intrinsic and acquired resistance to tyrosine kinase inhibitors. Cell Res. 2018 Nov;28(11):1062-1076. doi: 10.1038/s41422-018-0097-4. Epub 2018 Oct 8.
Ref 2 Optimization of subsite binding to the beta5 subunit of the human 20S proteasome using vinyl sulfones and 2-keto-1,3,4-oxadiazoles: syntheses and cellular properties of potent, selective proteasome inhibitors. J Med Chem. 2006 May 18;49(10):2953-68. doi: 10.1021/jm058289o.