Ferroptosis-centered Drug Response Information

General Information of the Drug (ID: ferrodrug0249)
Name
Atranorin
Synonyms
Atranorin; 479-20-9; Atranoric acid; Atranorine; Parmelin; Usnarin; Antranoric acid; Parmelin acid; Usnarin acid; 3-Hydroxy-4-(methoxycarbonyl)-2,5-dimethylphenyl 3-formyl-2,4-dihydroxy-6-methylbenzoate; NSC 249980; NSC 685591; NSC-685591; 450U2VJ2VG; CHEMBL173395; Benzoic acid,3-formyl-2,4-dihydroxy-6-methyl-,3-hydroxy-4-(methoxycarbonyl)-2,5-dimethylphenyl ester; NSC685591; NSC-249980; 3-formyl-2,4-dihydroxy-6-methylbenzoic acid 3-hydroxy-4-(methoxycarbonyl)-2,5-dimethylphenyl ester; Benzoic acid, 3-formyl-2,4-dihydroxy-6-methyl-, 3-hydroxy-4-(methoxycarbonyl)-2,5-dimethylphenyl ester; EINECS 207-527-7; UNII-450U2VJ2VG; Benzoic acid,4-dihydroxy-6-methyl-, 3-hydroxy-4-(methoxycarbonyl)-2,5-dimethylphenyl ester; Isophthalaldehydic acid,4-dihydroxy-6-methyl-, 4-ester with methyl 3,6-dimethyl-.beta.-resorcylate; Spectrum_000143; SpecPlus_000239; ATRANORIN [MI]; Spectrum2_001749; Spectrum3_001716; Spectrum4_001700; Spectrum5_000380; (3-hydroxy-4-methoxycarbonyl-2,5-dimethylphenyl) 3-formyl-2,4-dihydroxy-6-methylbenzoate; BSPBio_003332; KBioGR_002000; KBioSS_000623; SPECTRUM200034; DivK1c_006335; SPBio_001858; SCHEMBL1370191; KBio1_001279; KBio2_000623; KBio2_003191; KBio2_005759; KBio3_002552; DTXSID10197319; CHEBI:144119; YLOYKYXNDHOHHT-UHFFFAOYSA-N; HY-N2907; NSC87512; BDBM50056919; CCG-38801; MFCD00016597; NSC-87512; NSC249980; AKOS024319117; SDCCGMLS-0066426.P001; NCGC00095465-01; NCGC00095465-02; Isophthalaldehydic acid, 2,4-dihydroxy-6-methyl-, 4-ester with methyl 3,6-dimethyl-beta-resorcylate; MS-26044; CS-0023502; FT-0769622; SR-05000002629; SR-05000002629-1; Q27258788; (3-hydroxy-4-methoxycarbonyl-2,5-dimethyl-phenyl) 3-formyl-2,4-dihydroxy-6-methyl-benzoate; 3-Hydroxy-4-(methoxycarbonyl)-2,5-dimethylphenyl 3-formyl-2,4-dihydroxy-6-methylbenzoate #; Methyl 4-(3-formyl-2,4-dihydroxy-6-methyl-benzoyloxy)-2-hydroxy- 3,6-dimethyl-benzoate; Isophthalaldehydic acid, 2,4-dihydroxy-6-methyl-, 4-ester with methyl 3,6-dimethyl-.beta.-resorcylate; methyl 1-(3-formyl-2,4-dihydroxy-6-methylphenylcarbonyloxy)-3-hydroxy-2,5-dimethyl-4-benzenecarboxylate

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Structure
Formula
C19H18O8
IUPAC Name
(3-hydroxy-4-methoxycarbonyl-2,5-dimethylphenyl) 3-formyl-2,4-dihydroxy-6-methylbenzoate
Canonical SMILES
CC1=CC(=C(C(=C1C(=O)OC2=C(C(=C(C(=C2)C)C(=O)OC)O)C)O)C=O)O
InChI
InChI=1S/C19H18O8/c1-8-5-12(21)11(7-20)17(23)15(8)19(25)27-13-6-9(2)14(18(24)26-4)16(22)10(13)3/h5-7,21-23H,1-4H3
InChIKey
YLOYKYXNDHOHHT-UHFFFAOYSA-N
PubChem CID
68066
Full List of Ferroptosis Target Related to This Drug
Phospholipid hydroperoxide glutathione peroxidase (GPX4)
 Target Info 
In total 1 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Target for Ferroptosis Suppressor
Responsed Disease Gastric cancer ICD-11: 2B72
 Disease Info 
Pathway Response Ferroptosis hsa04216
Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
In Vitro Model hGCCs (Gastric cancer cells)
In Vivo Model
NOD-scid mice (NOD.CB17-Prkdcscid/NcrCrl) aged 6-7 weeks and weighing 20-22 g were used in the experiment. The animal study was performed at the Shanghai University of Traditional Chinese Medicine with approval from the Institutional Animal Care and Use Committee in accordance with the institutional guidelines. All mice were randomly divided into two groups, and each group consisted of four mice. In experimental group, approximately 1 x 105 GCSCs in logarithmic growth phase were harvested and inoculated subcutaneously into NOD-scid mice, and intraperitoneal injection of 100 ul Atranorin@SPION (10 mg/kg) every 2 days. In control group, approximately 1 x 105 GCSCs in logarithmic growth phase were harvested and inoculated subcutaneously into NOD-scid mice, and intraperitoneal injection of 100 ul SPION (10 mg/kg) alone every 2 days. After 2 months, the mice were sacrificed, and their tumors were excised.

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Response regulation Atranorin@SPIONs significantly reduced the 5-hydroxymethylcytidine modification level of GPX4 and SLC7A11 mRNA 3' untranslated region in gastric cancer cells. This study revealed the molecular biological mechanism by which Atranorin@SPION inhibit the in vitro and in vivo activity of GCSCs, that is, Atranorin@SPION reduced the expression of members of the Xc-/GPX4 axis and reduced their mRNA 5-hydroxymethylcytidine modification, finally induced ferroptosis of GCSCs.
Cystine/glutamate transporter (SLC7A11)
 Target Info 
In total 1 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Target for Ferroptosis Suppressor
Responsed Disease Gastric cancer ICD-11: 2B72
 Disease Info 
Pathway Response Ferroptosis hsa04216
Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
In Vitro Model hGCCs (Gastric cancer cells)
In Vivo Model
NOD-scid mice (NOD.CB17-Prkdcscid/NcrCrl) aged 6-7 weeks and weighing 20-22 g were used in the experiment. The animal study was performed at the Shanghai University of Traditional Chinese Medicine with approval from the Institutional Animal Care and Use Committee in accordance with the institutional guidelines. All mice were randomly divided into two groups, and each group consisted of four mice. In experimental group, approximately 1 x 105 GCSCs in logarithmic growth phase were harvested and inoculated subcutaneously into NOD-scid mice, and intraperitoneal injection of 100 ul Atranorin@SPION (10 mg/kg) every 2 days. In control group, approximately 1 x 105 GCSCs in logarithmic growth phase were harvested and inoculated subcutaneously into NOD-scid mice, and intraperitoneal injection of 100 ul SPION (10 mg/kg) alone every 2 days. After 2 months, the mice were sacrificed, and their tumors were excised.

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Response regulation Atranorin@SPIONs significantly reduced the 5-hydroxymethylcytidine modification level of GPX4 and SLC7A11 mRNA 3' untranslated region in gastric cancer cells. This study revealed the molecular biological mechanism by which Atranorin@SPION inhibit the in vitro and in vivo activity of GCSCs, that is, Atranorin@SPION reduced the expression of members of the Xc-/GPX4 axis and reduced their mRNA 5-hydroxymethylcytidine modification, finally induced ferroptosis of GCSCs.
References
Ref 1 Atranorin driven by nano materials SPION lead to ferroptosis of gastric cancer stem cells by weakening the mRNA 5-hydroxymethylcytidine modification of the Xc-/GPX4 axis and its expression. Int J Med Sci. 2022 Sep 25;19(11):1680-1694. doi: 10.7150/ijms.73701. eCollection 2022.