THERAPY DOSSIER · th-2aae8d20b8a4

Hepatocyte-specific tamoxifen-inducible p38alpha (MAPK14) genetic ablation; anti-Ccl2 and anti-Ccl5 blocking antibodies used mechanistically

Other

Evidence & regulatory context

Mechanism: Not recorded
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 31601995 ↗2019Reported benefit

Hepatospecific ablation of p38alpha MAPK governs liver regeneration through modulation of inflammatory response to CCl4-induced acute injury.

MouseChemical/toxinMalen = 3 to 10 animals per genotypeIntraperitoneal for carbon tetrachloride, antibodies and BrdU; tamoxifen given in the dietCarbon tetrachloride 0.56 g/kg; tamoxifen diet 1000 mg/kg;…Genetic ablation induced weeks before injury; antibody cocktail given 5 hours b…

Model: Acute liver injury by a single intraperitoneal injection of carbon tetrachloride in sunflower oil (1:9)

Hepatocyte-specific p38alpha deletion protected against carbon tetrachloride-induced acute liver injury by limiting reactive oxygen species and shaping a Ccl2/Ccl5-dependent inflammatory response, and antibody blockade of Ccl2 and Ccl5 abrogated this protection.

Extraction: extract · Supplied extraction confidence: 0.8. Machine-extracted fields require source verification.

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