脱氧野霉素（AMP-dNM）是dNM的疏水衍生物，可有效抑制β-葡萄糖苷酶2（BGD，IC | 50 | = 0.3 nM），对葡萄糖苷神经酰胺合酶的拮抗作用较小（GCS，IC | 50 | = 25 nM），并且几乎不能抑制其他GCase亚型。脂质信使神经酰胺通过GCS转化为葡萄糖基神经酰胺。在相反的方向上，BGD从葡糖神经酰胺中切割出葡糖基部分，释放出神经酰胺，后者可以转化为鞘磷脂。AMP-dNM已显示可诱导Hep-G2细胞中固醇调节元件结合蛋白调节的基因表达和胆固醇合成，在半抗原诱导的结肠炎的鼠模型 AMP-Deoxynojirimycin (AMP-dNM) is a hydrophobic derivative of dNM that potently inhibits β-glucosidase 2 (BGD, IC|50|= 0.3 nM), less potently antagonizes glucosylceramide synthase (GCS, IC|50|= 25 nM), and only poorly inhibits other GCase isoforms. The lipid messenger ceramide is converted to glucosylceramide by GCS. In the reverse direction, BGD cleaves the glucosyl moiety from glucosylceramide, liberating ceramide, which can be converted into sphingomyelin. AMP-dNM has been shown to induce sterol regulatory element-binding protein-regulated gene expression and cholesterol synthesis in Hep-G2 cells, strongly suppress inflammation in a murine model of hapten-induced colitis, and enhance insulin sensitivity in murine and rat models of insulin resistance.