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This extension not only increased the molecular weight (from 7.6 kDa to 9.1 kDa), but also reduced the affinity for IGF binding proteins (IGFBPs) through steric hindrance effect
The proposed mechanisms involve enhanced perfusion to injured tissues, modulation of inflammatory responses, and promotion of satellite cell activation and myogenesis
The reaction is catalyzed by a family of enzymes called Glutathione S-transferases (GSTs), which facilitate a nucleophilic attack, covalently binding the sulfur atom of glutathione directly to the toxic Phase I metabolite
Minoxidil clearance depends on UGT1A-mediated glucuronidation and SULT1A1-mediated sulfation [1][2]
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