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Current clinical advancement strategies include structural engineering of vitamin K analogs (e.g., C11-alkyl chain-modified MK4-C11) to enhance brain bioavailability and adeno-associated virus (AAV)-mediated FSP1 gene delivery (NCT05543659) to restore vitamin K reduction capacity, driving the transformation of vitamin K from a fundamental nutrient into a clinically viable targeted ferroptosis therapeutic

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In animal experiments, increases in VEGF were observed at both 2 h and 1 month following TBI, indicating impaired vascularity in both the short and long term (120, 121)