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It inhibits GPX4, leading to tumor-specific ferroptosis, and TA is used to chemically reduce Fe 3+ to Fe 2+ and continuously supply Fe 2+ to maintain the iron redox cycle and maintain the Fenton reaction [201]

there is the potential for: Ischemic injury due to potent vasoconstrictor action and tissue hypoxia Mild bradycardia, probably as a reflex result of a rise in blood pressure Arrhythmias Anxiety Transient headache Respiratory difficulty Pharmacokinetics: When released from nerve terminals, its actions are primarily (75%) terminated by neuronal reuptake Diffusion and degredation by extracellualr COMT contribute to a lesser extent