Ferroptosis-centered Drug Response Information
General Information of the Drug (ID: ferrodrug0004)
| Name |
Hydrogen Peroxide
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| Synonyms |
hydrogen peroxide; 7722-84-1; perhydrol; oxydol; Superoxol; Interox; Hydrogen dioxide; Inhibine; Peroxaan; Albone; Hioxyl; Kastone; Albone 35; Albone DS; Dihydrogen dioxide; hydroperoxide; T-Stuff; Elawox; Lensept; Perone; Albone 35CG; Albone 50; Albone 50CG; Albone 70; Albone 70CG; Perone 50; Peroxan; Peroxide; H2O2; Hydrogen peroxide, 30%; Hydrogen peroxide, 90%; Perone 30; Perone 35; Waterstofperoxyde; Hydrogen peroxide (H2O2); Wasserstoffperoxid; Hydrogen peroxide, 3%; Caswell No. 486AAA; dioxidane; Peroxyde d'hydrogene; Oxyfull; Perossido di idrogeno; Eskata; Hyrogen peroxide; CCRIS 1060; HSDB 547; Astri-UC; High Test Peroxide; Teat dip HP 5; Asepticper; Baquashock; Crystacide; Peroxclean; Pre milk HP 0.5; Pre milk HP 1.0; Dentasept; Hybrite; Metrokur; Mirasept; Oxigenal; Oxysept; Pegasyl; EPA Pesticide Chemical Code 000595; Hipox; Hydrogen peroxide, 8% to 20%; Select Bleach; Xtra White; Hydrogen peroxide (conc > 52%); Hydrogen peroxide, 20% to 60%; Oxysept I; Lensan A; Odosat D; UNII-BBX060AN9V; Adeka Super EL; dihydrogen peroxide; EINECS 231-765-0; BBX060AN9V; HTP [peroxide]; Crestal Whitestrips; NSC 19892; NSC-19892; Pre milk HP 0.5 10; UN2014; UN2015; UN2984; dihydrogen(peroxide); Anti-Keim 50; HOOH; UN 2015 (>52%); CHEBI:16240; UN 2984 (8%-20%); UN 2014 (20%-52%); Hydrogen peroxide (> 52% conc.); Hydrogen peroxide [USP]; MFCD00011333; bis(hydridooxygen)(O--O); DTXSID2020715; EC 231-765-0; HTP (peroxide); NSC19892; Hydrogen peroxide (USP); PEO; HYDROGEN PEROXIDE (II); HYDROGEN PEROXIDE [II]; (OH(OH)); [OH(OH)]; HYDROGEN PEROXIDE (IARC); HYDROGEN PEROXIDE [IARC]; HYDROGEN PEROXIDE (MART.); HYDROGEN PEROXIDE [MART.]; Puresept; hydrogenperoxide; Waterstofperoxyde [Dutch]; Wasserstoffperoxid [German]; HYDROGEN PEROXIDE (USP IMPURITY); HYDROGEN PEROXIDE [USP IMPURITY]; Peroxide, Hydrogen; CIX; Peroxyde d'hydrogene [French]; Perossido di idrogeno [Italian]; Hydrogen peroxide 35%; Whitespeed; a peroxide; Magic Bleaching; Clarigel Gold; Lase Peroxide; Quasar Brite; Opalescence Xtra; Whiteness HP; Deslime LP; Hydrogen peroxide (conc >52%); hydrogen per oxide; Oxyfull (TN); hydrogen hydroperoxide; Nite White Excel 2; Oxydol (JP17); Hydrogen peroxide 50%; HYDROGEN-PEROXIDE; OXYDOL [JAN]; Hydrogen peroxide (8CI); MolMap_000025; 8007-30-5; CHEMBL71595; DTXCID40715; Hydrogen peroxide 32 wt. %; HYDROGEN PEROXIDE [MI]; HYDROGEN PEROXIDE [FCC]; HYDROGEN PEROXIDE [HSDB]; HYDROGEN PEROXIDE [INCI]; CHEBI:25940; HYDROGEN PEROXIDE [VANDF]; MHAJPDPJQMAIIY-UHFFFAOYSA-N; HYDROGEN PEROXIDE [WHO-DD]; Hydrogen peroxide (H2O2) (9CI); OXTERIL? 350 SPRAY (Evonik); WLN: H2 O2 90%; AKOS015856794; HYDROGEN PEROXIDE [GREEN BOOK]; DB11091; HYDROGEN PEROXIDE [ORANGE BOOK]; QTL1_000041; FT-0627133; H1222; C00027; D00008; Q171877; Q1088474; Hydrogen peroxide 30%, meets the analytical specifications of Ph. Eur., stabilized
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| Structure |
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| Formula |
H2O2
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| IUPAC Name |
hydrogen peroxide
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| Canonical SMILES |
OO
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| InChI |
InChI=1S/H2O2/c1-2/h1-2H
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| InChIKey |
MHAJPDPJQMAIIY-UHFFFAOYSA-N
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| PubChem CID | |||||
Full List of Ferroptosis Target Related to This Drug
Cytochrome b-245 heavy chain (CYBB)
| In total 5 item(s) under this Target | ||||
| Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target | [1] | |||
| Target for Ferroptosis | Driver | |||
| Responsed Disease | Cervical cancer | ICD-11: 2C77 | ||
| Responsed Regulator | Aquaporin-3 (AQP3) | Driver | ||
| Pathway Response | Fatty acid metabolism | hsa01212 | ||
| Ferroptosis | hsa04216 | |||
| Cell Process | Cell ferroptosis | |||
| In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
| SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
| Response regulation | Mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQPs( AQP3, AQP5,AQP8) expression. H2O2 treatment enhances AQPs expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2 in endocervical adenocarcinoma, and thus, is a promising modality for effective cancer treatment. Moreover, NOX2 expression is upregulated in 0 cells, and that NOX2 binds to AQP3, 5, and 8 in both HeLa and SAS cells. | |||
| Experiment 2 Reporting the Ferroptosis-centered Drug Act on This Target | [1] | |||
| Target for Ferroptosis | Driver | |||
| Responsed Disease | Cervical cancer | ICD-11: 2C77 | ||
| Responsed Regulator | Aquaporin-5 (AQP5) | Driver | ||
| Pathway Response | Fatty acid metabolism | hsa01212 | ||
| Ferroptosis | hsa04216 | |||
| Cell Process | Cell ferroptosis | |||
| In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
| SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
| Response regulation | Mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQPs(AQP3, AQP5,AQP8) expression. H2O2 treatment enhances AQPs expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2 in endocervical adenocarcinoma, and thus, is a promising modality for effective cancer treatment. Moreover, NOX2 expression is upregulated in 0 cells, and that NOX2 binds to AQP3, 5, and 8 in both HeLa and SAS cells. | |||
| Experiment 3 Reporting the Ferroptosis-centered Drug Act on This Target | [1] | |||
| Target for Ferroptosis | Driver | |||
| Responsed Disease | Cervical cancer | ICD-11: 2C77 | ||
| Responsed Regulator | Aquaporin-8 (AQP8) | Driver | ||
| Pathway Response | Fatty acid metabolism | hsa01212 | ||
| Ferroptosis | hsa04216 | |||
| Cell Process | Cell ferroptosis | |||
| In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
| SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
| Response regulation | Mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQPs(AQP3, AQP5, AQP8) expression. H2O2 treatment enhances AQPs expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2 in endocervical adenocarcinoma, and thus, is a promising modality for effective cancer treatment. Moreover, NOX2 expression is upregulated in 0 cells, and that NOX2 binds to AQP3, 5, and 8 in both HeLa and SAS cells. | |||
| Experiment 4 Reporting the Ferroptosis-centered Drug Act on This Target | [1] | |||
| Target for Ferroptosis | Driver | |||
| Responsed Disease | Cervical cancer | ICD-11: 2C77 | ||
| Responsed Regulator | Aquaporin-8 (AQP8) | Driver | ||
| Pathway Response | Fatty acid metabolism | hsa01212 | ||
| Ferroptosis | hsa04216 | |||
| Cell Process | Cell ferroptosis | |||
| In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
| SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
| Response regulation | Mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQPs(AQP3, AQP5,AQP8) expression. H2O2 treatment enhances AQPs expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2 in endocervical adenocarcinoma, and thus, is a promising modality for effective cancer treatment. Moreover, NOX2 expression is upregulated in 0 cells, and that NOX2 binds to AQP3, 5, and 8 in both HeLa and SAS cells. | |||
| Experiment 5 Reporting the Ferroptosis-centered Drug Act on This Target | [1] | |||
| Target for Ferroptosis | Driver | |||
| Responsed Disease | Cervical cancer | ICD-11: 2C77 | ||
| Responsed Regulator | Aquaporin-3 (AQP3) | Driver | ||
| Pathway Response | Fatty acid metabolism | hsa01212 | ||
| Ferroptosis | hsa04216 | |||
| Cell Process | Cell ferroptosis | |||
| In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
| SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
| Response regulation | Mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQPs(AQP3, AQP5,AQP8) expression. H2O2 treatment enhances AQPs expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2 in endocervical adenocarcinoma, and thus, is a promising modality for effective cancer treatment. Moreover, NOX2 expression is upregulated in 0 cells, and that NOX2 binds to AQP3, 5, and 8 in both HeLa and SAS cells. | |||