m6A-centered Drug Response Information

General Information of the Drug (ID: M6APDG03941)
Name
VOB560
Synonyms
S 65487
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Status
Phase 1
TTD Drug ID
DP63FS
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.
Apoptosis regulator Bcl-2 (BCL-2)
Fat mass and obesity-associated protein (FTO)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Apoptosis regulator Bcl-2 (BCL-2) is a therapeutic target for VOB560. The Fat mass and obesity-associated protein (FTO) has potential in affecting the response of VOB560 through regulating the expression of Apoptosis regulator Bcl-2 (BCL-2). [1], [2]
Methyltransferase-like 14 (METTL14)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Apoptosis regulator Bcl-2 (BCL-2) is a therapeutic target for VOB560. The Methyltransferase-like 14 (METTL14) has potential in affecting the response of VOB560 through regulating the expression of Apoptosis regulator Bcl-2 (BCL-2). [2], [3]
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Apoptosis regulator Bcl-2 (BCL-2) is a therapeutic target for VOB560. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of VOB560 through regulating the expression of Apoptosis regulator Bcl-2 (BCL-2). [2], [4]
RNA demethylase ALKBH5 (ALKBH5)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Apoptosis regulator Bcl-2 (BCL-2) is a therapeutic target for VOB560. The RNA demethylase ALKBH5 (ALKBH5) has potential in affecting the response of VOB560 through regulating the expression of Apoptosis regulator Bcl-2 (BCL-2). [2], [5]
YTH domain-containing family protein 1 (YTHDF1)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Apoptosis regulator Bcl-2 (BCL-2) is a therapeutic target for VOB560. The YTH domain-containing family protein 1 (YTHDF1) has potential in affecting the response of VOB560 through regulating the expression of Apoptosis regulator Bcl-2 (BCL-2). [2], [4]
YTH domain-containing family protein 2 (YTHDF2)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Apoptosis regulator Bcl-2 (BCL-2) is a therapeutic target for VOB560. The YTH domain-containing family protein 2 (YTHDF2) has potential in affecting the response of VOB560 through regulating the expression of Apoptosis regulator Bcl-2 (BCL-2). [2], [6]
References
Ref 1 The Complex Roles and Therapeutic Implications of m(6)A Modifications in Breast Cancer. Front Cell Dev Biol. 2021 Jan 11;8:615071. doi: 10.3389/fcell.2020.615071. eCollection 2020.
Ref 2 Clinical pipeline report, company report or official report of BeiGene.
Ref 3 Methyltransferase-like 14 silencing relieves the development of atherosclerosis via m(6)A modification of p65 mRNA. Bioengineered. 2022 May;13(5):11832-11843. doi: 10.1080/21655979.2022.2031409.
Ref 4 Mettl3 inhibits the apoptosis and autophagy of chondrocytes in inflammation through mediating Bcl2 stability via Ythdf1-mediated m(6)A modification. Bone. 2022 Jan;154:116182. doi: 10.1016/j.bone.2021.116182. Epub 2021 Sep 13.
Ref 5 ALKBH5 inhibited autophagy of epithelial ovarian cancer through miR-7 and BCL-2. J Exp Clin Cancer Res. 2019 Apr 15;38(1):163. doi: 10.1186/s13046-019-1159-2.
Ref 6 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.