Creatine phosphate (also known as phosphocreatine) has been investigated for its potential neuroprotective effects in the context of acute ischemic stroke. The rationale is based on its role in cellular energy metabolism: during ischemia, ATP depletion occurs rapidly, contributing to cell injury and death. By providing a phosphate reservoir for the rapid regeneration of ATP, exogenous creatine phosphate might help sustain neuronal viability during periods of oxygen and glucose deprivation.

Several clinical studies, mostly from China and Eastern Europe, have tested intravenous creatine phosphate as an adjunct to standard stroke care. Some small trials have reported improvements in neurological outcomes and reduction in infarct size when creatine phosphate was administered acutely after stroke onset. However, these studies often have methodological limitations, such as small sample sizes, lack of blinding, and inconsistent outcome measures. A few meta-analyses suggest a possible benefit, but emphasize the low quality of the evidence and the need for larger, well-designed randomized controlled trials.

International guidelines do not currently recommend creatine phosphate for stroke treatment due to insufficient high-quality evidence. Thus, while there is scientific rationale and some clinical investigation, the evidence remains limited and inconclusive.