THERAPY DOSSIER · th-17eb2b6857c3

Anti-miR-382 locked nucleic acid inhibitor, plus genetic miR-382 knockout

Other · Locked-nucleic-acid inhibitor of miR-382 (plus genetic knockout); antisense oligonucleotide.

Evidence & regulatory context

Mechanism: Locked-nucleic-acid inhibitor of miR-382 (plus genetic knockout); antisense oligonucleotide.
Target: Not recorded
Injury models: Chemical/toxin
Reported indication: Not recorded
First approval: Not recorded
Development stage: Not recorded
ChEMBL record: Not recorded
ChEMBL max phase: Not recorded
Synonyms: Not recorded
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.

PMID 32796834 ↗2020Reported benefit

Upregulation of miR-382 contributes to renal fibrosis secondary to aristolochic acid-induced kidney injury via PTEN signaling pathway.

MouseChemical/toxinC57BL/6J, including miR-382 knockout miceMalen = n = 6 per group at days 1, 3, 7, 14 and 28Intraperitoneal10 mg/kg anti-miR-382First dose within 30 minutes before aristolochic acid injection

Model: Aristolochic acid I nephropathy, single intraperitoneal dose of 10 or 20 mg/kg

Aristolochic acid caused dose- and time-dependent renal fibrosis through NF-kappaB-driven miR-382 upregulation, and miR-382 knockdown or knockout partially reversed tubulointerstitial fibrosis and inflammation.

Extraction: extract · Supplied extraction confidence: 0.85. Machine-extracted fields require source verification.

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