THERAPY DOSSIER · th-40c4bc66b858

MP201, a prodrug of 2,4-dinitrophenol

Drug · Mitochondrial oxidative phosphorylation uncoupler; 2,4-dinitrophenol is the active core of the prodrug MP201 (ChEMBL has no explicit mechanism record). MP201 itself not found in ClinicalTrials.gov.

Not approved Suggest a correction

Evidence & regulatory context

Mechanism: Mitochondrial oxidative phosphorylation uncoupler; 2,4-dinitrophenol is the active core of the prodrug MP201 (ChEMBL has no explicit mechanism record). MP201 itself not found in ClinicalTrials.gov.
Target: Not recorded
Injury models: TBI
Reported indication: Not recorded
First approval: Not recorded
Development stage: Preclinical/no trial
ChEMBL record: CHEMBL273386 ↗
ChEMBL max phase: 2 / 4 (development scale, not regulatory approval)
Synonyms: Dinitrophenol; Aldifen; MP-101
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 30063076 ↗2018Reported benefit

Mitochondrial uncoupling prodrug improves tissue sparing, cognitive outcome, and mitochondrial bioenergetics after traumatic brain injury in male mice.

MouseTBIControlled cortical impactC57BL/6MaleOral gavage80 mg/kgFirst dose 2 h after injury

Model: Controlled cortical impact traumatic brain injury

MP201 improved mitochondrial bioenergetics in the ipsilateral cortex and hippocampus at 25 h and reduced oxidative damage markers. At 2 weeks it increased cortical tissue sparing (p = 0.0059, 38% of lesion spared) and improved novel object recognition (p = 0.0133) versus vehicle, and preserved CA3…

Extraction: extract · Subtype source: rule · Supplied extraction confidence: 0.88. Machine-extracted fields require source verification.

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