m6A-centered Drug Response Information

General Information of the Drug (ID: M6APDG03707)
Name
AHL
Synonyms
AHLi-11; SiRNA therapeutics (hearing loss), Quark; P53 gene-silencing siRNA (hearing loss), Quark
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Status
Investigative
TTD Drug ID
D0T8EL
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.
Cellular tumor antigen p53 (TP53)
Fat mass and obesity-associated protein (FTO)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Cellular tumor antigen p53 (TP53) is a therapeutic target for AHL. The Fat mass and obesity-associated protein (FTO) has potential in affecting the response of AHL through regulating the expression of Cellular tumor antigen p53 (TP53). [1], [2]
Methyltransferase-like 14 (METTL14)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Cellular tumor antigen p53 (TP53) is a therapeutic target for AHL. The Methyltransferase-like 14 (METTL14) has potential in affecting the response of AHL through regulating the expression of Cellular tumor antigen p53 (TP53). [2], [3]
Methyltransferase-like 16 (METTL16)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Cellular tumor antigen p53 (TP53) is a therapeutic target for AHL. The Methyltransferase-like 16 (METTL16) has potential in affecting the response of AHL through regulating the expression of Cellular tumor antigen p53 (TP53). [2], [4]
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Cellular tumor antigen p53 (TP53) is a therapeutic target for AHL. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of AHL through regulating the expression of Cellular tumor antigen p53 (TP53). [2], [5]
RNA demethylase ALKBH5 (ALKBH5)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Cellular tumor antigen p53 (TP53) is a therapeutic target for AHL. The RNA demethylase ALKBH5 (ALKBH5) has potential in affecting the response of AHL through regulating the expression of Cellular tumor antigen p53 (TP53). [2], [6]
YTH domain-containing family protein 1 (YTHDF1)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Cellular tumor antigen p53 (TP53) is a therapeutic target for AHL. The YTH domain-containing family protein 1 (YTHDF1) has potential in affecting the response of AHL through regulating the expression of Cellular tumor antigen p53 (TP53). [2], [7]
References
Ref 1 Meclofenamic acid promotes cisplatin-induced acute kidney injury by inhibiting fat mass and obesity-associated protein-mediated m(6)A abrogation in RNA. J Biol Chem. 2019 Nov 8;294(45):16908-16917. doi: 10.1074/jbc.RA119.011009. Epub 2019 Oct 2.
Ref 2 2011 Pipeline of Quark Pharm.
Ref 3 The m(6)A RNA methyltransferase METTL3/METTL14 promotes leukemogenesis through the mdm2/p53 pathway in acute myeloid leukemia. J Cancer. 2022 Jan 4;13(3):1019-1030. doi: 10.7150/jca.60381. eCollection 2022.
Ref 4 Gene Signatures and Prognostic Values of m6A Regulators in Hepatocellular Carcinoma. Front Genet. 2020 Oct 2;11:540186. doi: 10.3389/fgene.2020.540186. eCollection 2020.
Ref 5 p53 m(6)A modulation sensitizes hepatocellular carcinoma to apatinib through apoptosis. Apoptosis. 2022 Jun;27(5-6):426-440. doi: 10.1007/s10495-022-01728-x. Epub 2022 May 3.
Ref 6 RNA Demethylase ALKBH5 Prevents Lung Cancer Progression by Regulating EMT and Stemness via Regulating p53. Front Oncol. 2022 Apr 22;12:858694. doi: 10.3389/fonc.2022.858694. eCollection 2022.
Ref 7 N(6)-methyladenosine mediates arsenite-induced human keratinocyte transformation by suppressing p53 activation. Environ Pollut. 2020 Apr;259:113908. doi: 10.1016/j.envpol.2019.113908. Epub 2020 Jan 7.