General Information of the Drug (ID: M6APDG04330)
Name
VCB101
Status
Preclinical
TTD Drug ID
D46EBX
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.
Cysteines of Keap1 (KEAP1 Cysteines)
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
Response Summary Cysteines of Keap1 (KEAP1 Cysteines) is a therapeutic target for VCB101. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of VCB101 through regulating the expression of Cysteines of Keap1 (KEAP1 Cysteines). [1], [2]
YTH domain-containing family protein 1 (YTHDF1)
In total 1 mechanisms lead to this potential drug response
Response Summary Cysteines of Keap1 (KEAP1 Cysteines) is a therapeutic target for VCB101. The YTH domain-containing family protein 1 (YTHDF1) has potential in affecting the response of VCB101 through regulating the expression of Cysteines of Keap1 (KEAP1 Cysteines). [2], [3]
References
Ref 1 METTL3-mediated M6A methylation modification is involved in colistin-induced nephrotoxicity through apoptosis mediated by Keap1/Nrf2 signaling pathway. Toxicology. 2021 Oct;462:152961. doi: 10.1016/j.tox.2021.152961. Epub 2021 Sep 21.
Ref 2 NRF2 Regulation Processes as a Source of Potential Drug Targets against Neurodegenerative Diseases. Biomolecules. 2020 Jun 14;10(6):904. doi: 10.3390/biom10060904.
Ref 3 YTHDF1 links hypoxia adaptation and non-small cell lung cancer progression. Nat Commun. 2019 Oct 25;10(1):4892. doi: 10.1038/s41467-019-12801-6.