THERAPY DOSSIER · th-db78e62571cf

Apremilast

Drug · Selective PDE4 inhibitor.

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This record is classified as “NO TRAUMA TRANSLATION”. Read the indication and notes below for the specific context.

Evidence & regulatory context

Mechanism: Selective PDE4 inhibitor.
Target: CHEMBL2093863 (PDE4)
Injury models: Chemical/toxin
Reported indication: Not recorded
First approval: 2014
Development stage: Not recorded
ChEMBL record: CHEMBL514800 ↗
ChEMBL max phase: 4 / 4 (development scale, not regulatory approval)
Synonyms: Otezla; CC-10004
Note: Not recorded

Clinical trials 3

0 linked trials carry an injury-indication flag. These flags support record-level exploration and sit alongside the stringent aggregate counts described in Methods.

NCT03082729 ↗PHASE4completed

Apremilast on Vascular Inflammation and Cardiometabolic Function in Psoriasis

Psoriasis

Enrolment: 70 · Results not recorded

NCT03777436 ↗PHASE3completed

Apremilast in Moderate to Severe Genital Psoriasis (Phase 3)

Psoriasis

Enrolment: 289 · Results not recorded

NCT04804553 ↗PHASE3recruiting

Apremilast in Juvenile Psoriatic Arthritis (PEAPOD)

Juvenile Psoriatic Arthritis

Enrolment: 60 · Results not recorded

Preclinical evidence 1

1 studies reported at therapy level; 1 evidence entries itemised.

PMID 30500623 ↗2018Reported benefit

Apremilast ameliorates carfilzomib-induced pulmonary inflammation and vascular injuries.

RatChemical/toxinMale

Model: Carfilzomib-induced acute lung injury and pulmonary vascular injury

Apremilast reduced myeloperoxidase activity, tumour necrosis factor alpha levels and alveolar infiltrating cells and reversed the observed toxic effects of carfilzomib, preventing acute lung injury in rats.

Extraction: extract · Supplied extraction confidence: 0.5. Machine-extracted fields require source verification.

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