Ferroptosis-centered Drug Response Information

General Information of the Drug (ID: ferrodrug0320)
Name
SRT1720
Synonyms
1001645-58-4; SRT1720; SRT 1720 Hydrochloride; SRT1720 HCl; SRT 1720 (Hydrochloride); SRT1720 xHydrochloride; N-(2-(3-(piperazin-1-ylmethyl)imidazo[2,1-b]thiazol-6-yl)phenyl)quinoxaline-2-carboxamide hydrochloride; N-[2-[3-(1-Piperazinylmethyl)imidazo[2,1-b]thiazol-6-yl]phenyl]-2-quinoxalinecarboxamide hydrochloride; N-[2-[3-(piperazin-1-ylmethyl)imidazo[2,1-b][1,3]thiazol-6-yl]phenyl]quinoxaline-2-carboxamide;hydrochloride; SRT1720 Hydrochloride; SRT1720xHydrochloride; SRT1720 xHCl; MLS006011149; CHEMBL4639328; SCHEMBL16372055; DTXSID80649411; SRT-1720, SRT 1720, 1001645-58-4; BCP01774; s1129; AKOS025401934; SRT-1720, SRT1720; CCG-264830; CS-0509; AC-27409; AS-35151; HY-15145; N-[2-[3-(piperazin-1-ylmethyl)imidazo[2,1-b][1,3]thiazol-6-yl]phenyl]quinoxaline-2-carboxamide,hydrochloride; SMR004702924; FT-0761472; SW218151-2; A24478; J-000057; J-523315; N-(2-(3-(Piperazin-1-ylmethyl)imidazo[2,1-b]thiazol-6-yl)phenyl)quinoxaline-2-carboxamide xhydrochloride; N-(2-{3-[(Piperazin-1-yl)methyl]imidazo[2,1-b][1,3]thiazol-6-yl}phenyl)quinoxaline-2-carboxamide--hydrogen chloride (1/1)

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Status
Investigative
Drug Type
Small molecular drug
Structure
3D MOL
2D MOL
Formula
C25H24ClN7OS
IUPAC Name
N-[2-[3-(piperazin-1-ylmethyl)imidazo[2,1-b][1,3]thiazol-6-yl]phenyl]quinoxaline-2-carboxamide;hydrochloride
Canonical SMILES
C1CN(CCN1)CC2=CSC3=NC(=CN23)C4=CC=CC=C4NC(=O)C5=NC6=CC=CC=C6N=C5.Cl
InChI
InChI=1S/C25H23N7OS.ClH/c33-24(22-13-27-20-7-3-4-8-21(20)28-22)29-19-6-2-1-5-18(19)23-15-32-17(16-34-25(32)30-23)14-31-11-9-26-10-12-31;/h1-8,13,15-16,26H,9-12,14H2,(H,29,33);1H
InChIKey
DTGRRMPPXCRRIM-UHFFFAOYSA-N
PubChem CID
25232708
TTD Drug ID
D03EGA
Full List of Ferroptosis Target Related to This Drug
Unspecific Target
In total 1 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Responsed Disease Head neck squamous cell carcinoma ICD-11: 2D60
 Disease Info 
Responsed Regulator NAD-dependent protein deacetylase sirtuin-1 (SIRT1) Driver
 Regulator Info 
Pathway Response Ferroptosis hsa04216
Cell adhesion molecules hsa04514
Cell Process Cell ferroptosis
In Vitro Model AMC-HN-3 cells Laryngeal squamous cell carcinoma Homo sapiens CVCL_5961
HN4 cells Clear cell renal cell carcinoma Homo sapiens CVCL_IS30
HN5 cells Squamous cell carcinoma Homo sapiens CVCL_8128
HN6 cells Tongue squamous cell carcinoma Homo sapiens CVCL_8129
NH-9 cells Tongue squamous cell carcinoma Homo sapiens CVCL_8132
HN-10 cells Laryngeal squamous cell carcinoma Homo sapiens CVCL_8124
In Vivo Model
Six-week-old athymic BALB/c male nude mice (nu/nu) were purchased from OrientBio (Seoul, Republic of Korea). HN9 cells with transfection of CDH1 or control vector or HN4 cells with ZEB1 or control vector were subcutaneously injected into the bilateral flank of nude mice. From the day when gross nodules were detected in tumor implants, mice were subjected to different treatments: vehicle or sulfasalazine (250 mg/kg daily per intraperitoneal route). Each group included six mice.

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Response regulation Histone deacetylase SIRT1 gene silencing or pharmacological inhibition by EX-527 suppressed EMT and consequently decreased ferroptosis, whereas SIRT inducers, resveratrol and SRT1720, increased ferroptosis. In head and neck cancer (HNC) cells with low expression of E-cadherin, the treatment of 5-azacitidine diminished the hypermethylation of CDH1, resulting in increased E-cadherin expression and decreased ferroptosis susceptibility.
References
Ref 1 Epigenetic reprogramming of epithelial-mesenchymal transition promotes ferroptosis of head and neck cancer. Redox Biol. 2020 Oct;37:101697. doi: 10.1016/j.redox.2020.101697. Epub 2020 Aug 28.