Target intelligence / Profile preview

Molybdenum (Mo)

Target
Mo
Molecular classification
Trace element, Essential mineral, Transition metal, Enzyme cofactor
01

Overview

Molybdenum is an essential trace element that functions as a fundamental component of the molybdenum cofactor (Moco), which is indispensable for the catalytic activity of specific human enzymes: sulfite oxidase, xanthine oxidase, aldehyde oxidase, and the mitochondrial amidoxime-reducing component [2, 11, 21]. These enzymes facilitate vital metabolic processes, including the detoxifying conversion of sulfite to sulfate and the final steps of purine catabolism to uric acid [9, 15, 17]. While molybdenum itself is not a traditional therapeutic target such as a receptor or enzyme, its metabolic pathways are critical; genetic defects in Moco biosynthesis result in Molybdenum Cofactor Deficiency (MoCD), a severe neonatal disorder characterized by rapid neurodegeneration and early mortality [4, 6, 18]. Therapeutic strategies for MoCD Type A involve replacement of the missing Moco precursor using drugs like fosdenopterin (Nulibry) [1, 7]. Additionally, molybdenum-containing compounds like ammonium tetrathiomolybdate are utilized clinically as copper chelators to manage Wilson's disease or investigated for anti-angiogenic properties in oncology [13]. High dietary or industrial exposure to molybdenum can disrupt mineral balance, potentially leading to secondary copper deficiency or gout-like symptoms due to excessive uric acid production [2, 14, 16].

Other names
Molybdenum elementMoMolybdenum cofactor (Moco)Molybdopterin
02

Mechanism of action

Molybdenum serves as a catalytic metal center within the molybdenum cofactor (Moco), facilitating oxygen atom transfer and redox cycling between Mo(IV) and Mo(VI) states in specific metabolic enzymes [11, 18, 22].

03

Biological functions

Cofactor for redox enzymesSulfur amino acid metabolismPurine catabolismDrug and toxin detoxificationRedox homeostasis
04

Disease associations

Molybdenum cofactor deficiency (MoCD)Isolated sulfite oxidase deficiencyWilson's diseaseHyperuricemiaGout
05

Safety considerations

Phototoxicity (associated with fosdenopterin therapy) [5, 7]Secondary copper deficiency (induced by thiomolybdates) [13]Gout-like symptoms (from hyperuricemia) [2, 14]Renal and hepatic toxicity at high concentrations [8, 10]Respiratory irritation from metal dust inhalation [3, 14]
06

Interacting drugs

Fosdenopterin

4 more in the full profile.

07

Biomarkers

Urinary sulfitePlasma S-sulfocysteine (SSC)Serum uric acidUrinary xanthineUrinary hypoxanthine

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