Ferroptosis-centered Drug Response Information

General Information of the Drug (ID: ferrodrug0040)
Name
5-Azacitidine
Synonyms
5-azacytidine; Azacitidine; 320-67-2; Ladakamycin; Azacytidine; Vidaza; Mylosar; 5-azacitidine; Azacitidinum; Azacitidina; Azacitidinum [INN-Latin]; 5-AZAC; Azacitidina [INN-Spanish]; C8H12N4O5; NSC-102816; U-18496; Onureg; 4-Amino-1-beta-D-ribofuranosyl-s-triazin-2(1H)-one; NSC102816; 5AzaC; 4-Amino-1-beta-d-ribofuranosyl-1,3,5-triazin-2(1H)-one; Antibiotic U 18496; 5-AZCR; 4-amino-1-((2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)tetrahydrofuran-2-yl)-1,3,5-triazin-2(1H)-one; 5 AZC; 5-AC; NSC 102816; CHEBI:2038; M801H13NRU; DTXSID9020116; 4-Amino-1-(beta-D-ribofuranosyl)-1,3,5-triazin-2(1H)-one; U-18,496; 4-amino-1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]-1,2-dihydro-1,3,5-triazin-2-one; WR-183027; NCGC00090851-04; 4-Amino-1-beta-D-ribofuranosyl-1,3,5-triazine-2(1H)-one; U 18496; 4-amino-1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]-1,3,5-triazin-2-one; DTXCID10116; 1,3,5-Triazin-2(1H)-one, 4-amino-1-.beta.-D-ribofuranosyl-; MFCD00006539; CCRIS 60; SMR000857239; Vidaza (TN); HSDB 6879; 5-aza-CR; SR-01000075662; EINECS 206-280-2; Azacitidine;5-AzaC;Ladakamycin; BRN 0620461; UNII-M801H13NRU; Azacitidine (JAN/USAN/INN); Azacitidine [USAN:INN:BAN]; 4-Amino-1-beta-D-ribofuranosyl-1,3,5-traizin-2(1H)-one; NS-17; 4-amino-1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)tetrahydrofuran-2-yl]-1,3,5-triazin-2-one; CAS-320-67-2; Azacitidine (Vidaza); 2-(beta-D-Ribofuranosyl)-4-amino-1,3,5-triazin-2-one; Antibiotic U18496; U18496; Spectrum_001262; AZACITIDINE [MI]; Spectrum2_000786; Spectrum3_001509; Spectrum4_000922; Spectrum5_001166; AZACITIDINE [INN]; AZACITIDINE [JAN]; AZACITIDINE [HSDB]; AZACITIDINE [IARC]; AZACITIDINE [USAN]; MolMap_000062; 4-Amino-1-.beta.-D-ribofuranosyl-s-triazin-2(1H)-one; A 2385; AZACITIDINE [VANDF]; SCHEMBL3741; AZACITIDINE [MART.]; CHEMBL1489; Azacitidine (5-Azacytidine); Lopac0_000035; AZACITIDINE [USP-RS]; AZACITIDINE [WHO-DD]; BSPBio_003157; KBioGR_001444; KBioGR_002556; KBioSS_001742; KBioSS_002565; MLS001333121; MLS001333122; MLS002153249; MLS002548894; DivK1c_000125; SPECTRUM1502111; SPBio_000892; AZACITIDINE [EMA EPAR]; GTPL6796; s-Triazin-2(1H)-one, 4-amino-1-beta-D-ribofuranosyl-; BCBcMAP01_000083; HMS500G07; KBio1_000125; KBio2_001742; KBio2_002556; KBio2_004310; KBio2_005124; KBio2_006878; KBio2_007692; KBio3_002657; KBio3_003034; NMUSYJAQQFHJEW-KVTDHHQDSA-; AZACITIDINE [ORANGE BOOK]; pyrimidine antimetabolite: inhibits nucleic acid replication; cMAP_000082; NINDS_000125; NMUSYJAQQFHJEW-KVTDHHQDSA-N; HMS1921J22; HMS2092D08; HMS2231F15; HMS3259D19; HMS3260G11; Pharmakon1600-01502111; 5-Azacytidine, >=98% (HPLC); Tox21_111032; Tox21_302985; Tox21_500035; BDBM50424715; CCG-39046; HB1374; NSC758186; s1782; Onureg (CC-486; oral azacitidine); AKOS015896938; Tox21_111032_1; AM83944; CS-1287; DB00928; LP00035; NC00672; NSC-758186; NSC103-627; 4-amino-1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]-1,3,5-triaz; IDI1_000125; NCGC00090851-01; NCGC00090851-02; NCGC00090851-03; NCGC00090851-05; NCGC00090851-06; NCGC00090851-07; NCGC00090851-08; NCGC00090851-10; NCGC00090851-14; NCGC00090851-22; NCGC00178234-01; NCGC00256541-01; NCGC00260720-01; AS-13697; HY-10586; SRI-10756_10; SRI-10756_12; WR183027; SL-000003; EU-0100035; D03021; EN300-118700; F10504; A821115; Q416451; J-700085; SR-01000075662-1; SR-01000075662-3; SR-01000075662-7; BRD-K03406345-001-02-1; BRD-K03406345-001-27-8; 4-Amino-1-?-D-ribofuranosyl-1,3,5-triazin-2(1H)-one; Z1515383340; 4-Amino-1-(bet.-D-ribofuranosyl)-1,3,5-triazin-2(1H)-one; 4-Amino-1-beta-D-ribofuranosyl-1,3,5-tr iazin-2(1H)-one; Azacitidine, United States Pharmacopeia (USP) Reference Standard; 4-Amino-1-(beta-D-ribofuranosyl)-1,3,5-triazin-2(1H)-one; Ladakamycin; Azacitidine, Pharmaceutical Secondary Standard; Certified Reference Material; 1401238-97-8; 5-Azacytidine, Hybri-Max(TM), gamma-irradiated, lyophilized powder, BioXtra, suitable for hybridoma; 5AE; 6-amino-3-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)tetrahydrofuran-2-yl]-1H-1,3,5-triazin-3-ium-2-one; InChI=1/C8H12N4O5/c9-7-10-2-12(8(16)11-7)6-5(15)4(14)3(1-13)17-6/h2-6,13-15H,1H2,(H2,9,11,16)/t3-,4-,5-,6-/m1/s1

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Structure
Formula
C8H12N4O5
IUPAC Name
4-amino-1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]-1,3,5-triazin-2-one
Canonical SMILES
C1=NC(=NC(=O)N1C2C(C(C(O2)CO)O)O)N
InChI
InChI=1S/C8H12N4O5/c9-7-10-2-12(8(16)11-7)6-5(15)4(14)3(1-13)17-6/h2-6,13-15H,1H2,(H2,9,11,16)/t3-,4-,5-,6-/m1/s1
InChIKey
NMUSYJAQQFHJEW-KVTDHHQDSA-N
PubChem CID
9444
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 Cadherin-1 (CDH1) Suppressor
 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.