THERAPY DOSSIER · th-fd05f50c2280

TWEAK (tumour necrosis factor-like weak inducer of apoptosis)

Biologic

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 2

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

NCT01943513 ↗PHASE1completed

A Study to Evaluate the Effect of Intravenous BIIB023 (Anti-TWEAK) on Lower Limb Muscle Mass and Strength During and After Knee-Joint Immobilization

Healthy

Enrolment: 34 · Results not recorded

NCT03974997 ↗NAunknown

TNF-related Weak Inducer of Apoptosis (TWEAK), a New Biomarker Predicting Inflammatory Thrust in Multiple Sclerosis

Multiple Sclerosis

Enrolment: 50 · Results not recorded

Preclinical evidence 1

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

PMID 27725864 ↗2016Reported benefit

TWEAK protects cardiomyocyte against apoptosis in a PI3K/AKT pathway dependent manner.

RatIschaemia-reperfusionCardiacInjection into the infarct scar and border zoneIn vitro, dose-dependent protection at 50 ng/mL and above.…Immediately after induction of ischaemia (preconditioning)

Model: Myocardial ischaemia and reperfusion by ligation of the left anterior descending coronary artery for 50 minutes followed by reperfusion; hypoxia and reoxygenation in H9C2 cells

TWEAK reduced cardiomyocyte apoptosis in a dose-dependent manner in vitro. In rats, TWEAK preconditioning significantly improved cardiac function and reduced infarct size 21 days after reperfusion, with activation of PI3K/AKT signalling.

Extraction: extract · Subtype source: rule · Supplied extraction confidence: 0.6. Machine-extracted fields require source verification.

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