THERAPY DOSSIER · th-6a5796c02bab

EphA4 antagonist peptides VTM-EEKK and KYL (plus genetic deletion of EphA4)

Drug

Evidence & regulatory context

Mechanism: Not recorded
Target: Not recorded
Injury models: TBI
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 31711546 ↗2019Reported benefit

Peripheral loss of EphA4 ameliorates TBI-induced neuroinflammation and tissue damage.

MouseTBIControlled cortical impactCD1 background; EphA4 floxed, Rosa, Cx3cr1-Cre and Tie2-Cre lines on C57BL/6 background bred onto CD1Malen = Seven mice pooled per group for CD45+ immune cell isolation…Subcutaneous Alzet mini-osmotic pump (Model 1007D), continuous infusion at 0.5 microlitre/h10 mg/kg/day of each peptidePumps implanted immediately following injury

Model: Controlled cortical impact, 4 mm craniotomy over right parietal-temporal cortex, 3 mm bevelled tip, 5.0 m/s, 2.0 mm depth, 100 ms dwell

Continuous infusion of VTM-EEKK or KYL at 10 mg/kg/day for 4 days after controlled cortical impact significantly reduced cortical lesion volume (2.00 +/- 0.26 mm and 1.97 +/- 0.43 mm versus 3.58 +/- 0.36 mm for vehicle), whereas the scrambled control peptide did not. Treatment lowered pro-inflammat…

Extraction: extract · Subtype source: rule · Supplied extraction confidence: 0.9. Machine-extracted fields require source verification.

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