THERAPY DOSSIER · th-f09453429fee

E-prostanoid 3 (Ep3, PTGER3) receptor manipulation: macrophage-targeted Ep3alpha overexpression, myeloid-specific Ep3 deletion, wild-type bone marrow transplantation; Ep3 antagonist L-798,106 used pharmacologically

Other

Evidence & regulatory context

Mechanism: Not recorded
Target: Not recorded
Injury models: Ischaemia-reperfusion
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 28256515 ↗2017Reported benefit

Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction

MouseIschaemia-reperfusionCardiacC57BL/6 background; Ep3 floxed, myeloid-specific Ep3 knockout (LysM-Cre), global Ep3 knockout and CD68 promoter-driven macrophage-specific Ep3alpha transgenic linesmale and female

Model: Permanent left anterior descending coronary artery ligation to induce myocardial infarction; zymosan-induced peritonitis used as a companion sterile inflammation model

Ep3 deficiency in monocytes and macrophages reduced Ly6C-low cell accumulation in infarcted hearts from day 4, lowered CX3CR1 and VEGF expression by roughly half, reduced peri-infarct neovascularisation at day 14, expanded infarct area and impaired recovery of cardiac function. Wild-type bone marro…

Extraction: extract · Subtype source: rule · Supplied extraction confidence: 0.75. Machine-extracted fields require source verification.

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