Clemastine fumarate, a common over-the-counter antihistamine, successfully triggered myelin repair in nonhuman primates with experimentally induced brain damage that mimics multiple sclerosis. The primate model showed no natural recovery, making the drug's regenerative effects particularly striking and clinically relevant. This represents a crucial validation step between promising rodent studies and human clinical applications. The finding strengthens the case for repurposing existing antihistamines as neurological therapeutics, offering hope for millions with demyelinating diseases where current treatments primarily slow progression rather than restore function. Primate physiology more closely resembles human neural architecture than rodent models, making these results more predictive of human outcomes. The study addresses a critical gap in translational research, where many promising rodent findings fail to translate to humans. While clemastine has already shown modest benefits in human MS trials, this primate validation suggests the therapeutic potential may be greater than initially recognized. The research also opens questions about optimal dosing and treatment timing, as the controlled primate model allows for more precise intervention than human studies. For patients with progressive MS or other demyelinating conditions, this represents movement toward actual repair rather than just damage limitation.