General Information of the Drug (ID: ferrodrug0200)
Name
Alumina
Synonyms
Alumina; Emery; Corundum; 1302-74-5; oxo(oxoalumanyloxy)alumane; Corundum (Al2O3); Sapphire (Al2O3); 12415-34-8; Aluminum oxide, alpha-phase; Electrocorundum; Aluminum oxide, alpha; Aluminum oxide, gamma; Korund; alpha-Corundum; Aluminum oxide, gamma-alpha; Abramant F 36; Abramax F 46; Abramax F 54; Aluminum oxide, catalyst support; MP 1 (Refractory); Dural F 30; MFCD00003424; Aluminum oxide, fused, insulating powder; KO 7; Aluminum oxide, neutral, HPLC Flash Grade; EKF 100; KER 710; KU 10; NK 63; FN 237; KU 5-3; Aluminum oxide, Drysphere desiccant, without indicator; Aluminumoxide; Aluminum oxide, CP; Anti-bumping granules; Aluminum oxide, cement; Aluminum oxide, puriss.; gamma-Alumina, low soda; Aluminum oxide 90 acidic; Aluminum oxide, Type A-5; Aluminum oxide, Puratronic?; Aluminum oxide, 1-5 micron; Aluminum oxide, Type CG-20; Aluminum oxide, pellets, 3 mm; Aluminum oxide 90 active basic; CHEMBL4594252; gamma-Alumina, 1/16' spheres; Aluminum Oxide Powder, 99.5%; Aluminum oxide desiccant, regular; TWNQGVIAIRXVLR-UHFFFAOYSA-N; Aluminum oxide, for chromatography; Aluminum oxide, powder, ultra dry; Aluminum oxide, Type WA-4: Acid; Aluminum oxide, Type WA-7: Acid; Aluminum oxide, Type WB-5: Basic; MFCD00211795; MFCD07370730; Aluminum oxide, Type WN-9: Neutral; AKOS015903822; Aluminum oxide, -100, +325 mesh; Aluminum oxide, 5 mum mean particle size; Aluminum oxide, basic, HPLC Flash Grade; BP-31011; Aluminum oxide, acidic, HPLC Flash Grade; Aluminum oxide, Grade H-152, 1/8 in.; Aluminum oxide, calcined, insulating powder; Aluminum oxide, catalyst support, low silica; Aluminum oxide (alpha) powder, 99.97% Nano; Aluminum oxide Corundum, a-phase, -100 mesh; Aluminum Oxide Powder (alpha), 99.9% Nano; Aluminum oxide, 99.997% trace metals basis; Aluminum oxide (gamma) Powder, 99.97% Nano; Aluminum oxide, polishing compound, 2oz (57g); Aluminum oxide, puriss., >=98% Al2O3 basis; Aluminum oxide, SAJ special grade, >=98.0%; Aluminum oxide, pore size 58 ??, ~150 mesh; Alumina, NIST(R) SRM(R) 699, reduction grade; Alumina, NIST(R) SRM(R) 742, reference point; Aluminum oxide, 20% in H2O, colloidal dispersion; Aluminum oxide, Aerosol Refractory Brushable Paint; Aluminum oxide, catalyst support, low surface area; Aluminum oxide, Corundum, alpha-phase, -100 mesh; Aluminum oxide, powder, 99.99% trace metals basis; Aluminum oxide, Drysphere desiccant, with 20% indicator; Aluminum oxide, nanopowder, <50 nm particle size (TEM); Aluminum oxide, basic, for TLC, 5-15 Micron APS Powder; Aluminum oxide, nanofiber, diam. x L <20 nm x 100 mum; Aluminum oxide, nanofiber, diam. x L <20 nm x 500 mum; Aluminum oxide, 99.3%, < 325 mesh, d 50 5 - 7 micron; Aluminum oxide, nanowires, diam. x L 2-6 nm x 200-400 nm; Aluminum oxide, single crystal substrate, <0001>; Aluminum oxide, Type WN-6, Neutral, Activity Grade Super I; Aluminum oxide substrate, 10x10x0.5mm, polished one side, A plane; Aluminum oxide substrate, 10x10x1mm, polished one side, C plane; Aluminum oxide, alpha, catalyst support, low surface area, trimodal; Aluminum oxide, fused, powder, primarily alpha-phase, -325 mesh; Aluminum oxide, fused, powder, primarily alpha-phase, 100-200 mesh; Aluminum oxide, gamma, catalyst support, high surface area, bimodal; Inhibitor removers, Prepacked column, for removing tert-butylcatechol; Aluminum oxide, calcined, powder, primarily alpha-phase, 100-325 mesh; Aluminum oxide, catalyst support, intermediate surface area (low SiO2); Aluminum oxide, mesoporous, MSU-X (wormhole), average pore size 3.8 nm; Aluminum oxide, primarily alpha-phase, fused, 200-325 mesh, >=99%; Inhibitor removers, replacement packing, for removing tert-butylcatechol; Aluminum oxide, nanopowder, 13 nm primary particle size (TEM), 99.8% trace metals basis; Sapphire substrate, 10x10x0.432mm, EPI polished two sides, C-axis, LED grade; 12174-49-1; Aluminum oxide 90 active neutral, (activity stage I) for column chromatography 0.063-0.200 mm (70 - 230 mesh ASTM); Aluminum oxide, powder, primarily alpha phase, <=10 mum avg. part. size, 99.5% trace metals basis; Inhibitor removers, Prepacked column for removing hydroquinone and monomethyl ether hydroquinone; Inhibitor removers, replacement packing for removing hydroquinone and monomethyl ether hydroquinone; Sapphire substrate, 50.8mm dia x 0.332mm thick, EPI polished one side, C-axis, HEMCOR single crystal; Sapphire substrate, 50.8mm dia x 0.332mm thick, EPI polished two sides, C-axis, HEMCOR single crystal; Sapphire substrate, 50.8mm dia x 0.432mm thick, EPI polished one side, C-axis, HEMCOR single crystal

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Structure
3D MOL
Formula
Al2O3
IUPAC Name
oxo(oxoalumanyloxy)alumane
Canonical SMILES
O=[Al]O[Al]=O
InChI
InChI=1S/2Al.3O
InChIKey
TWNQGVIAIRXVLR-UHFFFAOYSA-N
PubChem CID
14769
Full List of Ferroptosis Target Related to This Drug
Unspecific Target
In total 2 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Responsed Disease Health ICD-11: N.A.
Responsed Regulator Mitogen-activated protein kinase 8 (MAPK8) Driver
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model hHCs (Hippocampal cells)
In Vivo Model
Male healthy Wistar rats (six-week-old, provided by Experimental Animal Centre of Harbin Medical University, China) were used in this study. All rats (3-4 rats per cage) access to standard diet anddeionized waterad libitum and were placed in standard laboratory conditions. Seventy-two rats (weighing 200-220 g) were randomly divided into 4 groups (n = 18): AlNPs group was exposed to 50 mg/kg AlNPs (< 50nm, Sigma-Aldrich, USA) by gavage once a day for 90 days. CRS + AlNPs group was received CRS for 21 days and was exposed to 50 mg/kg AlNPs daily by gavage for 90 days. CRS + H2O group was subjected to CRS for 21 days and was given the same volume of deionized water daily by gavage for 90 days. The control (CON) group was given the same volume of deionized water daily and not affected by restraint stress for 90 days.

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Response regulation Alumina nanoparticles (AlNPs) and CRS activated IFN-/ASK1/JNK ( MAPK8) signaling pathway. Furthermore, IFN- neutralizing antibody R4-6A2 effectively inhibited the activation of IFN-/ASK1/JNK signaling pathway, alleviated hippocampal neuronal ferroptosis and improved cognition ability. ASK1 inhibitor GS-4997 also improved hippocampal neuronal ferroptosis and cognitive dysfunction by inhibiting ASK1/JNK signaling pathway. JNK inhibits ubiquitin-mediated p53 degradation by increasing phosphorylation of p53 at Ser6, which helps mediate oxidative stress to trigger ferroptosis.
Experiment 2 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Responsed Disease Health ICD-11: N.A.
Responsed Regulator Cellular tumor antigen p53 (TP53) Driver
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model hHCs (Hippocampal cells)
In Vivo Model
Male healthy Wistar rats (six-week-old, provided by Experimental Animal Centre of Harbin Medical University, China) were used in this study. All rats (3-4 rats per cage) access to standard diet anddeionized waterad libitum and were placed in standard laboratory conditions. Seventy-two rats (weighing 200-220 g) were randomly divided into 4 groups (n = 18): AlNPs group was exposed to 50 mg/kg AlNPs (< 50nm, Sigma-Aldrich, USA) by gavage once a day for 90 days. CRS + AlNPs group was received CRS for 21 days and was exposed to 50 mg/kg AlNPs daily by gavage for 90 days. CRS + H2O group was subjected to CRS for 21 days and was given the same volume of deionized water daily by gavage for 90 days. The control (CON) group was given the same volume of deionized water daily and not affected by restraint stress for 90 days.

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Response regulation Alumina nanoparticles (AlNPs) and CRS activated IFN-/ASK1/JNK (MAPK8) signaling pathway. Furthermore, IFN- neutralizing antibody R4-6A2 effectively inhibited the activation of IFN-/ASK1/JNK signaling pathway, alleviated hippocampal neuronal ferroptosis and improved cognition ability. ASK1 inhibitor GS-4997 also improved hippocampal neuronal ferroptosis and cognitive dysfunction by inhibiting ASK1/JNK signaling pathway. JNK inhibits ubiquitin-mediated p53 degradation by increasing phosphorylation of p53 at Ser6, which helps mediate oxidative stress to trigger ferroptosis.
References
Ref 1 Combined exposure of alumina nanoparticles and chronic stress exacerbates hippocampal neuronal ferroptosis via activating IFN-/ASK1/JNK signaling pathway in rats. J Hazard Mater. 2021 Jun 5;411:125179. doi: 10.1016/j.jhazmat.2021.125179. Epub 2021 Jan 19.