Evidence & regulatory context
- Mechanism
- Biologic (CX3CL1/fractalkine chemokine); no confident ChEMBL drug match, preclinical
- 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.
MixedIschaemia-reperfusionCerebral (MCAO/stroke)C57BL/6 wild type, cx3cl1 knockout, cx3cr1(GFP/GFP) and adenosine A1 receptor knockout miceMaleAcute administration at the time of permanent middle cerebral artery occlusion
Model: Permanent middle cerebral artery occlusion, with in vitro oxygen-glucose deprivation
Exogenous CX3CL1 reduced infarct size, neurological deficits and caspase-3 activation with effects lasting up to 50 days, dependent on adenosine A1 receptor signalling, yet cx3cl1 and cx3cr1 deficient mice sustained less injury and CX3CL1 increased damage in cx3cl1 knockout mice.
Extraction: extract · Subtype source: rule · Supplied extraction confidence: 0.6. Machine-extracted fields require source verification.