Evidence & regulatory context
- Mechanism
- Thioredoxin reductase 1 inhibitor (INHIBITOR; direct interaction; IC50 = 65 nM)
- Target
- CHEMBL1927 (thioredoxin reductase 1)
- Injury models
- Endotoxin/LPS
- Reported indication
- Not recorded
- First approval
- 1940
- Development stage
- Not recorded
- ChEMBL max phase
- 4 / 4 (development scale, not regulatory approval)
- Synonyms
- (1-thio-d-glucopyranosato)gold; Aureotan; Aurothioglucose; Aurumine; Authron; Brenol; Glysanol B; NSC-759601; Oronol; Solganal B
- Note
- Not recorded
Clinical trials 0
0 linked trials carry an injury-indication flag. These flags support record-level exploration and sit alongside the stringent aggregate counts described in Methods.
No linked human trial in this dataset.
Preclinical evidence 1
1 studies reported at therapy level; 1 evidence entries itemised.
MouseEndotoxin/LPSintraperitoneal25 mg/kg12 h after intratracheal LPS, before hyperoxia exposure
Model: Acute respiratory distress syndrome induced by a single intratracheal dose of lipopolysaccharide (0.375 microg/g) followed by exposure to hyperoxia (>95% O2)
Aurothioglucose significantly attenuated LPS plus hyperoxia induced lung injury, increased lung GCLM expression and glutathione levels, and decreased mortality. Glutathione depletion completely prevented the protective effects, indicating the benefit is glutathione dependent.
Extraction: extract · Supplied extraction confidence: 0.8. Machine-extracted fields require source verification.