Ferroptosis-centered Drug Response Information
General Information of the Drug (ID: ferrodrug0221)
| Name |
SP600125
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| Synonyms |
129-56-6; 1,9-Pyrazoloanthrone; SP600125; Pyrazolanthrone; Dibenzo[cd,g]indazol-6(2H)-one; Pyrazoleanthrone; SP 600125; Anthra[1,9-cd]pyrazol-6(2H)-one; SP-600125; JNK Inhibitor II; Anthra-1,9-pyrazol-6-none; ANTHRA(1,9-cd)PYRAZOL-6(2H)-ONE; C.I. 70300; 2H-Dibenzo[cd,g]indazol-6-one; NSC 75890; 1pmv; NSC75890; NSC-75890; 2h-dibenzo(cd,g)indazol-6-one; CHEMBL7064; MLS002693964; DTXSID2040525; CHEBI:90695; 2,6-DIHYDROANTHRA/1,9-CD/PYRAZOL-6-ONE; Anthra[1-9-cd]pyrazol-6(2H)-one; 1TW30Y2766; NCGC00015958-03; 14,15-diazatetracyclo[7.6.1.02,7.013,16]hexadeca-1(15),2,4,6,9(16),10,12-heptaen-8-one; SMR000015440; SR-01000075840; EINECS 204-955-6; BRN 0746890; UNII-1TW30Y2766; 2zmd; Kinome_3844; Tocris-1496; CI 70300; BiomolKI_000068; Lopac-S-5567; BiomolKI2_000072; cid_8515; CBiol_002049; Lopac0_000473; BMK1-G8; BSPBio_001066; ChemBiol10705 Compound 4; KBioGR_000406; KBioSS_000406; JMC517015 Compound 2; MLS002153267; MLS006011577; SCHEMBL170980; anthra[1,9-cd]pyrazol-6-one; GTPL5273; Pyrazolanthrone (SP600125); CHEMBL1725279; DTXCID0020525; SCHEMBL15583517; BCBcMAP01_000053; BDBM16018; KBio2_000406; KBio2_002974; KBio2_005542; KBio3_000771; KBio3_000772; Bio1_000335; Bio1_000824; Bio1_001313; Bio2_000373; Bio2_000853; HMS1362F07; HMS1667K13; HMS1792F07; HMS1990F07; HMS2250C03; HMS3229I16; HMS3261O08; HMS3267P06; HMS3295M01; HMS3403F07; HMS3412F05; HMS3654P10; HMS3676F05; HMS3747M19; AMY31086; Anthra[1,9cd]pyrazol-6(2H)-one; BCP05457; EX-A1998; Tox21_110267; Tox21_500473; BDBM50024294; BDBM50433916; CCG-47500; Dibenzo[cd,g]indazol-6(2H)-one #; HB2234; HSCI1_000136; MFCD00022289; NSC755773; s1460; AKOS000115584; AKOS040751313; Anthrapyrazolone; 1,9-Pyrazoloanthrone; CCG-100672; CS-0196; DB01782; LP00473; NSC-755773; SDCCGSBI-0050458.P003; WLN: T C66651A P IV OMNJ; 1,6-dihydrodibenzo[cd,g]indazol-6-one; 2,6-dihydrodibenzo[cd,g]indazol-6-one; IDI1_002128; QTL1_000077; s10332; SMP2_000240; NCGC00015958-01; NCGC00015958-02; NCGC00015958-04; NCGC00015958-05; NCGC00015958-06; NCGC00015958-07; NCGC00015958-08; NCGC00015958-22; NCGC00025186-01; NCGC00025186-02; NCGC00025186-03; NCGC00025186-04; NCGC00025186-05; NCGC00261158-01; WLN: T C6665 1A P IV OMNJ; AC-32051; AS-14374; CAS-129-56-6; HY-12041; JNK Inhibitor II - CAS 129-56-6; SMR002530644; EU-0100473; FT-0607068; SW218106-2; EN300-02083; Anthra[1,9-cd]pyrazol-6(2H)-one & Z-100; K00068; S 5567; SP600125, >=98% (HPLC); AB00075935-01; SP 600125 & Z-100; A888840; Anthra[1,9-cd]pyrazol-6(2H)-one;SP-600125; Q4545713; SR-01000075840-1; SR-01000075840-2; SR-01000075840-4; SR-01000075840-6; SR-01000637108-1; W-108360; BRD-K01567962-001-04-0; BRD-K01567962-001-06-5; BRD-K01567962-001-08-1; BRD-K01567962-001-22-2; Z56785477; F1414-1245; 14,15-diazatetracyclo[7.6.1.0;{2,7}.0;{13,16}]hexadeca-1(15),2(7),3,5,9(16),10,12-heptaen-8-one; 14,15-diazatetracyclo[7.6.1.0^{2,7}.0^{13,16}]hexadeca-1(15),2,4,6,9(16),10,12-heptaen-8-one
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| Structure |
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| Formula |
C14H8N2O
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| IUPAC Name |
14,15-diazatetracyclo[7.6.1.02,7.013,16]hexadeca-1(15),2,4,6,9(16),10,12-heptaen-8-one
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| Canonical SMILES |
C1=CC=C2C(=C1)C3=NNC4=CC=CC(=C43)C2=O
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| InChI |
InChI=1S/C14H8N2O/c17-14-9-5-2-1-4-8(9)13-12-10(14)6-3-7-11(12)15-16-13/h1-7H,(H,15,16)
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| InChIKey |
ACPOUJIDANTYHO-UHFFFAOYSA-N
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| PubChem CID | |||||
Full List of Ferroptosis Target Related to This Drug
Heme oxygenase 1 (HMOX1)
| In total 1 item(s) under this Target | ||||
| Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target | [1] | |||
| Target for Ferroptosis | Driver/Suppressor | |||
| 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 | BV-2 cells | Normal | Mus musculus | CVCL_0182 |
| Response regulation | Following addition of the JNK (MAPK8) inhibitor SP600125, the expression of HO-1 decreased, expression of FTH1 was increased and iron accumulation was decreased. Therefore, it was hypothesized that NPs induced ferroptosis in BV2 cells via the JNK/HO-1/FTH1 pathway. | |||