THERAPY DOSSIER · th-7d9290feff6e

LincRNA-p21 inhibition (loss-of-function)

Other

Evidence & regulatory context

Mechanism: Not recorded
Target: Not recorded
Injury models: Endotoxin/LPS
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 32362153 ↗2020Reported benefit

LincRNA-p21 promotes classical macrophage activation in acute respiratory distress syndrome by activating NF-κB.

MouseEndotoxin/LPSC57BL/6Male

Model: Intratracheal instillation of lipopolysaccharide to induce acute respiratory distress syndrome, with parallel LPS-treated alveolar macrophage cultures

LincRNA-p21 was elevated in LPS-induced acute respiratory distress syndrome and in LPS-treated alveolar macrophages. Inhibition of lincRNA-p21 counteracted M1 activation and p65 nuclear translocation and attenuated LPS-induced lung injury.

Extraction: extract · Supplied extraction confidence: 0.62. Machine-extracted fields require source verification.

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