https://www.selleckchem.com/products/Perifosine.html Severe hypomagnesemia post-cetuximab or panitumumab treatment was significantly associated with low baseline magnesium concentrations (< 1.8mg/dL; odds ratio 18.100, 95% confidence interval 1.570-210.000; p = 0.020) and low serum magnesium concentrations during treatment (< 1.1mg/dL; odds ratio 93.800, 95% confidence interval 3.510-2510.000; p = 0.007). To minimize the risk of severe hypomagnesemia during anti-EGFR treatment, magnesium replenishment should be initiated in patients with pre-replenishment concentrations of < 1.8mg/dL, preferably before reaching intra-treatment concentrations of < 1.1mg/dL. To minimize the risk of severe hypomagnesemia during anti-EGFR treatment, magnesium replenishment should be initiated in patients with pre-replenishment concentrations of  less then  1.8 mg/dL, preferably before reaching intra-treatment concentrations of  less then  1.1 mg/dL.Xanthine oxidase inhibitors are primarily used in the clinical prevention and treatment of gout associated with hyperuricemia. The archetypal xanthine oxidase inhibitor, Allopurinol has been shown to have other beneficial effects such as a reduction in vascular reactive oxygen species and mechano-energetic uncoupling. This chapter discusses these properties and their relevance to human pathophysiology with a focus on Allopurinol as well as newer xanthine oxidase inhibitors such as Febuxostat and Topiroxostat. Xanthine oxidase (XO) and xanthine dehydrogenase (XDH) are collectively referred to as xanthine oxidoreductase (XOR). XDH is initially synthesised as a 150-kDa protein from which XO is derived, e.g. under conditions of ischemia/hypoxia either reversibly by conformational changes (calcium or SH oxidation) or irreversibly by proteolysis, the latter leading to formation of a 130-kDa form of XO. Both, XO and XDH, catalyse the conversion of hypoxanthine via xanthine to uric acid, the former by using oxygen forming superoxide and hydrogen pero