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Chelators form coordinate complexes with metals, reducing free metal ion activity and limiting interactions with enzymes and proteins as well as metal-catalyzed oxidative damage. Complexes are generally eliminated through the kidneys, the biliary tract, or both. Pharmacokinetic profiles vary: for example, BAL can enter the brain, whereas EDTA does not; deferoxamine binds iron and is poorly absorbed orally; and oral deferasirox is eliminated largely through the fecal route. Selectivity reflects features such as donor-atom arrangement, ring size, and metal affinity. The full lesson compares these mechanisms and pathways across major agents, including their routes of administration, distribution, elimination, and the relevance of renal impairment.