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N,N-Dimethyldopamine
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N,N-Dimethyldopamine
N,N-Dimethyldopamine (DMDA) is an organic compound belonging to the phenethylamine family. It is related structurally to the alkaloid epinine (N-methyldopamine) and to the major neurotransmitter dopamine (of which it is the N,N-dimethylated analog). Because of its structural relationship to dopamine, DMDA has been the subject of a number of pharmacological investigations. DMDA has been detected in Acacia rigidula.
DMDA has been reported from the plant Acacia rigidula Benth. (Fabaceae), in which it has been detected at levels of ~ 11-45 ppm.
Since N,N-dimethyldopamine is chemically an amine, it is basic (a weak base, technically), but it is also a catechol (a 1,2-dihydroxybenzene), which gives it weakly acidic properties, so that the compound is amphoteric.
Several different methods have been reported for the preparation of DMDA. An early synthesis by Buck and co-workers began with 3,4-dimethoxybenzaldehyde (veratraldehyde), which was condensed with hippuric acid to give the azlactone; this was hydrolyzed with NaOH to the corresponding pyruvic acid, which was then converted to its oxime; treatment of the oxime with acetic anhydride gave 3,4-dimethoxyphenylacetonitrile, which was catalytically reduced (H2/Pd) in the presence of excess dimethylamine to N,N-dimethyl-3,4-dimethoxyphenethylamine; finally, the methoxy-groups were cleaved with HCl to give DMDA as its hydrochloride salt.
A more recent method starts with 3,4-dimethoxyphenylacetic acid, which is converted to its acid chloride with thionyl chloride; this is reacted with dimethylamine to give the dimethylamide, which is then reduced using diborane to N,N-dimethyl 3,4-dimethoxyphenethylamine; the methoxy- groups are finally cleaved with hydriodic acid to give DMDA.
The shortest method is that of Borgman et al., who converted 3,4-dimethoxyphenethylamine into N,N-dimethyl 3,4-dimethoxyphenethylamine by catalytic reduction (H2/Pd) in the presence of formaldehyde; the methoxy-groups were then cleaved with hydrobromic acid.
One of the earliest pharmacological studies of DMDA was that of Daly and his co-workers, who studied the ability of a large number of substituted phenethylamines to release norepinephrine (NE) from the mouse heart. In this assay, a subcutaneous dose of 10 mg/kg of DMDA hydrochloride (referred to as "3,4-dihydroxy-N,N-dimethylphenethylamine HCl") failed to produce a significant change in the NE content of the heart. In comparison, a dose of 5 mg/kg, s.c., of N-methyldopamine ("3,4-dihydroxy-N-methylphenethylamine HCl") caused a 45% reduction in the NE content, while dopamine HCl itself caused a 50% decrease at a dose of 5 mg/kg, s.c.
Another early pharmacological investigation of DMDA was carried out by Goldberg and co-workers, who examined the effects of a range of phenethylamine analogs in an assay based on the vasodilation produced by injection of the test drug into the renal artery of the dog. In this assay, a drug was classed as "dopamine-like" if the vasoldilation it produced was not prevented by β-blocking drugs, and did not occur if the drug was injected into the femoral artery. Although DMDA, at a dose of 0.5 mg, caused a marked bradycardia, a dose of ~ 0.75 mg did not increase renal blood flow (i.e. cause vasodilation) after administration of atropine to abolish the bradycardia.
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N,N-Dimethyldopamine
N,N-Dimethyldopamine (DMDA) is an organic compound belonging to the phenethylamine family. It is related structurally to the alkaloid epinine (N-methyldopamine) and to the major neurotransmitter dopamine (of which it is the N,N-dimethylated analog). Because of its structural relationship to dopamine, DMDA has been the subject of a number of pharmacological investigations. DMDA has been detected in Acacia rigidula.
DMDA has been reported from the plant Acacia rigidula Benth. (Fabaceae), in which it has been detected at levels of ~ 11-45 ppm.
Since N,N-dimethyldopamine is chemically an amine, it is basic (a weak base, technically), but it is also a catechol (a 1,2-dihydroxybenzene), which gives it weakly acidic properties, so that the compound is amphoteric.
Several different methods have been reported for the preparation of DMDA. An early synthesis by Buck and co-workers began with 3,4-dimethoxybenzaldehyde (veratraldehyde), which was condensed with hippuric acid to give the azlactone; this was hydrolyzed with NaOH to the corresponding pyruvic acid, which was then converted to its oxime; treatment of the oxime with acetic anhydride gave 3,4-dimethoxyphenylacetonitrile, which was catalytically reduced (H2/Pd) in the presence of excess dimethylamine to N,N-dimethyl-3,4-dimethoxyphenethylamine; finally, the methoxy-groups were cleaved with HCl to give DMDA as its hydrochloride salt.
A more recent method starts with 3,4-dimethoxyphenylacetic acid, which is converted to its acid chloride with thionyl chloride; this is reacted with dimethylamine to give the dimethylamide, which is then reduced using diborane to N,N-dimethyl 3,4-dimethoxyphenethylamine; the methoxy- groups are finally cleaved with hydriodic acid to give DMDA.
The shortest method is that of Borgman et al., who converted 3,4-dimethoxyphenethylamine into N,N-dimethyl 3,4-dimethoxyphenethylamine by catalytic reduction (H2/Pd) in the presence of formaldehyde; the methoxy-groups were then cleaved with hydrobromic acid.
One of the earliest pharmacological studies of DMDA was that of Daly and his co-workers, who studied the ability of a large number of substituted phenethylamines to release norepinephrine (NE) from the mouse heart. In this assay, a subcutaneous dose of 10 mg/kg of DMDA hydrochloride (referred to as "3,4-dihydroxy-N,N-dimethylphenethylamine HCl") failed to produce a significant change in the NE content of the heart. In comparison, a dose of 5 mg/kg, s.c., of N-methyldopamine ("3,4-dihydroxy-N-methylphenethylamine HCl") caused a 45% reduction in the NE content, while dopamine HCl itself caused a 50% decrease at a dose of 5 mg/kg, s.c.
Another early pharmacological investigation of DMDA was carried out by Goldberg and co-workers, who examined the effects of a range of phenethylamine analogs in an assay based on the vasodilation produced by injection of the test drug into the renal artery of the dog. In this assay, a drug was classed as "dopamine-like" if the vasoldilation it produced was not prevented by β-blocking drugs, and did not occur if the drug was injected into the femoral artery. Although DMDA, at a dose of 0.5 mg, caused a marked bradycardia, a dose of ~ 0.75 mg did not increase renal blood flow (i.e. cause vasodilation) after administration of atropine to abolish the bradycardia.
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