Allele variants at two regulatory SNPs namely rs1611115  and rs1989787  were shown to affect transcription of this gene. Mutations identified in Dopamine beta hydroxylase deficiency  and non-synonymous SNPs such as rs6271 in this gene were found to cause defective secretion of the protein from the endoplasmic reticulum. DBH primarily contributes to catecholamine and trace amine biosynthesis. It also participates in the metabolism of xenobiotics related to these substances; for example, the human DBH enzyme catalyzes the beta-hydroxylation of amphetamine and para-hydroxyamphetamine, producing norephedrine and para-hydroxynorephedrine respectively. DBH has been implicated as correlating factor in conditions associated with decision making and addictive drugs, e.g., alcoholism and smoking, attention deficit hyperactivity disorder, schizophrenia, and Alzheimer's disease. Inadequate DBH is called dopamine beta hydroxylase deficiency. The proximal promoter(genetics) SNPs rs1989787 and rs1611115 were found to be associated with cognition in Schizophrenia subjects. Further these SNPs and a distal promoter variant 19bp Ins/Del(rs141116007) were important in Tardive dyskinesia and Positive and Negative Syndrome Scale(PANSS) scores in schizophrenia subjects. It was difficult to obtain a stable crystal of dopamine beta-hydroxylase. Hence an homology model based on the primary sequence and comparison to PHM is available. However, a crystal structure was also put forward in 2016. This protein may use the morpheein model of allosteric regulation. DBH is inhibited by disulfiram, tropolone, and, most selectively, by nepicastat. DBH is reversibly inhibited by l-2H-Phthalazine hydrazone (hydralazine; HYD), 2-1H-pyridinone hydrazone (2-hydrazinopyridine; HP), 2-quinoline-carboxylic acid (QCA), l-isoquinolinecarboxylic acid (IQCA), 2,2'-bi-lH-imidazole (2,2'-biimidazole; BI), and IH-imidazole-4-acetic acid (imidazole-4-acetic acid; IAA). HYD, QCA, and IAA are allosteric competitive.