Landmark 171 · Trial in people

MitoQ (PROTECT)

No difference from placebo in 128 newly diagnosed people over 12 months. It did not slow Parkinson's.

In short

A pill designed to sit inside mitochondria and mop up damaging oxygen molecules did nothing to slow progression in 128 newly diagnosed people over 12 months.

What it is
Trial in people
Outcome
Did not work
When
2010
Size
128 people · Phase 2
Approach
Help cells clean up
Research lane
Mitochondria & energy
Trial registry
NCT00329056
Last checked
19 Oct 2026

The research record

This is the project's file for this landmark, as written and checked. Sources are listed at the end; anything not yet confirmed is marked "Not yet verified".

Who

B. J. Snow and colleagues (the Otago repository holds the record, so the work is linked to New Zealand). Sponsor: Antipodean Pharmaceuticals. The drug, mitoquinone (MitoQ), is a form of coenzyme Q10 chemically tied to a carrier that makes it collect inside mitochondria. Published in Movement Disorders 2010;25:1670–1674. The registry gives May 2006 to November 2007 for the trial itself.

What happened

Mitochondria are the cell's power plants, and they make harmful oxygen by-products. Parkinson's brains show a fault in the first step of the energy chain (landmark 11). MitoQ was meant to protect mitochondria from that damage better than ordinary antioxidants.

  • Design. Double-blind, placebo-controlled. 128 newly diagnosed, untreated people took one of two MitoQ doses (40 mg or 80 mg once daily, per the registry) or placebo for 12 months. Main measure: change in the total UPDRS score (a standard symptom rating scale).
  • Result. No difference between MitoQ and placebo on any measure of progression. The authors concluded that MitoQ does not slow Parkinson's and that this should be weighed against the oxidative-stress idea of the disease.

Why it moved us toward a cure

It was a direct test of a specific version of the mitochondrial idea: that mopping up oxygen damage inside mitochondria would slow the disease. The answer was no. It sits beside the energy-supplement failures, and pushed the field toward fixing mitochondrial quality control instead (see landmark 11 for the starting observation).

Outcome

Dead end for mitochondria-targeted antioxidants as a slowing treatment. The mitochondria branch continues through other approaches.

Sources

How it connects

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Led to

None recorded.

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