General Information of the Drug (ID: M6APDG02175)
Name
torin 1
Synonyms
Torin-1
    Click to Show/Hide
Status
Investigative
Structure
Formula
C35H28F3N5O2
InChI
1S/C35H28F3N5O2/c1-2-32(44)42-15-13-41(14-16-42)31-11-9-26(19-28(31)35(36,37)38)43-33(45)12-8-24-20-40-30-10-7-22(18-27(30)34(24)43)25-17-23-5-3-4-6-29(23)39-21-25/h3-12,17-21H,2,13-16H2,1H3
InChIKey
AKCRNFFTGXBONI-UHFFFAOYSA-N
PubChem CID
49836027
TTD Drug ID
D0H0HR
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.
Serine/threonine-protein kinase mTOR (mTOR)
Fat mass and obesity-associated protein (FTO)
In total 1 mechanisms lead to this potential drug response
Response Summary Serine/threonine-protein kinase mTOR (mTOR) is a therapeutic target for torin 1. The Fat mass and obesity-associated protein (FTO) has potential in affecting the response of torin 1 through regulating the expression of Serine/threonine-protein kinase mTOR (mTOR). [1], [2]
Methyltransferase-like 14 (METTL14)
In total 1 mechanisms lead to this potential drug response
Response Summary Serine/threonine-protein kinase mTOR (mTOR) is a therapeutic target for torin 1. The Methyltransferase-like 14 (METTL14) has potential in affecting the response of torin 1 through regulating the expression of Serine/threonine-protein kinase mTOR (mTOR). [2], [3]
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
Response Summary Serine/threonine-protein kinase mTOR (mTOR) is a therapeutic target for torin 1. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of torin 1 through regulating the expression of Serine/threonine-protein kinase mTOR (mTOR). [2], [4]
YTH domain-containing family protein 1 (YTHDF1)
In total 1 mechanisms lead to this potential drug response
Response Summary Serine/threonine-protein kinase mTOR (mTOR) is a therapeutic target for torin 1. The YTH domain-containing family protein 1 (YTHDF1) has potential in affecting the response of torin 1 through regulating the expression of Serine/threonine-protein kinase mTOR (mTOR). [2], [5]
YTH domain-containing family protein 2 (YTHDF2)
In total 1 mechanisms lead to this potential drug response
Response Summary Serine/threonine-protein kinase mTOR (mTOR) is a therapeutic target for torin 1. The YTH domain-containing family protein 2 (YTHDF2) has potential in affecting the response of torin 1 through regulating the expression of Serine/threonine-protein kinase mTOR (mTOR). [1], [2]
References
Ref 1 Targeting ATF4-dependent pro-survival autophagy to synergize glutaminolysis inhibition. Theranostics. 2021 Jul 25;11(17):8464-8479. doi: 10.7150/thno.60028. eCollection 2021.
Ref 2 Targeted polypharmacology: discovery of dual inhibitors of tyrosine and phosphoinositide kinases. Nat Chem Biol. 2008 Nov;4(11):691-9. doi: 10.1038/nchembio.117. Epub 2008 Oct 12.
Ref 3 The m6A methyltransferase METTL14 inhibits the proliferation, migration, and invasion of gastric cancer by regulating the PI3K/AKT/mTOR signaling pathway. J Clin Lab Anal. 2021 Mar;35(3):e23655. doi: 10.1002/jcla.23655. Epub 2020 Dec 12.
Ref 4 Methyltransferase-like 3 promotes the progression of lung cancer via activating PI3K/AKT/mTOR pathway. Clin Exp Pharmacol Physiol. 2022 Jul;49(7):748-758. doi: 10.1111/1440-1681.13647. Epub 2022 May 23.
Ref 5 YTHDF1 promotes hepatocellular carcinoma progression via activating PI3K/AKT/mTOR signaling pathway and inducing epithelial-mesenchymal transition. Exp Hematol Oncol. 2021 Jun 4;10(1):35. doi: 10.1186/s40164-021-00227-0.