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| Other names | DPDA; N,N-Di-n-propyldopamine; N,N-Dipropyldopamine; N,N-Di-n-propyl-DA; N,N-Dipropyl-DA |
| Drug class | Dopamine receptor agonist; Dopamine D1 and D2-like receptor agonist |
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| Formula | C14H23NO2 |
| Molar mass | 237.343 g·mol−1 |
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Dipropyldopamine (DPDA), also known as N,N-di-n-propyldopamine, is a synthetic dopamine receptor agonist related to the catecholamine neurotransmitter dopamine which has been used in scientific research.[1][2] It is a dual agonist of both dopamine D1-like and D2-like receptors, with much greater potency at dopamine D2 receptors than dopamine itself.[2][3] Unlike dopamine, the drug lacks β-adrenergic receptor activity and also has weaker vasoconstrictor effects.[1]
DPDA produces hypolocomotion across a wide range of doses in rodents.[4][5] It modestly reduces climbing behavior at low doses and markedly enhances it at much high doses.[6] The drug is thought to be resistant to metabolism by monoamine oxidase (MAO) but to still be susceptible to metabolism by catechol O-methyltransferase (COMT).[7] It was virtually inactive orally in rodents.[8] In contrast to dopamine, which is peripherally selective, DPDA can cross the blood–brain barrier and produce effects in the central nervous system.[8]
DPDA was first described in the scientific literature by 1977.[9] Other N,N-dialkyl derivatives of dopamine besides DPDA have been studied.[4] In addition, esters of DPDA have been developed and studied.[8]
See also
[edit]References
[edit]- ^ a b Kohli JD, Goldberg LI, Volkman PH, Cannon JG (October 1978). "N,N-Di-n-propyl dopamine: a qualitatively different dopamine vascular agonist". The Journal of Pharmacology and Experimental Therapeutics. 207 (1): 16–22. doi:10.1016/S0022-3565(25)31387-X. PMID 702336.
- ^ a b Kohli JD (June 1990). "Peripheral dopamine receptors". American Journal of Hypertension. 3 (6 Pt 2): 25S–28S. doi:10.1093/ajh/3.6.25s. PMID 2143385.
- ^ Mailman RB, Nichols DE, Tropsha A (1997). "Molecular Drug Design and Dopamine Receptors". The Dopamine Receptors. Totowa, NJ: Humana Press. pp. 105–133. doi:10.1007/978-1-4757-2635-0_4. ISBN 978-1-4757-2637-4. Retrieved 9 February 2026.
- ^ a b Costall B, Lim SK, Naylor RJ (July 1981). "Characterisation of the mechanisms by which purported dopamine agonists reduce spontaneous locomotor activity of mice". European Journal of Pharmacology. 73 (2–3): 175–188. doi:10.1016/0014-2999(81)90089-3. PMID 6118281.
- ^ Bradbury A, Costall B, Lim S, Naylor R (1982). "Reduction in Spontaneous Locomotor Activity by Purported Dopamine Agonists: an Analysis of the Site and Mechanism of Action". Advances in Dopamine Research. Elsevier. pp. 413–424. doi:10.1016/b978-0-08-027391-4.50046-0. ISBN 978-0-08-027391-4. Retrieved 9 February 2026.
- ^ Costall B, Eniojukan JF, Naylor RJ (November 1982). "Spontaneous climbing behaviour of mice, its measurement and dopaminergic involvement". European Journal of Pharmacology. 85 (2): 125–132. doi:10.1016/0014-2999(82)90457-5. PMID 7151866.
- ^ Sumners C, Dijkstra D, de Vries JB, Horn AS (July 1981). "Neurochemical and behavioural profiles of five dopamine analogues". Naunyn-schmiedeberg's Archives of Pharmacology. 316 (4): 304–310. doi:10.1007/BF00501362. PMID 7196506.
- ^ a b c Wikström H, Lindberg P, Martinson P, Hjorth S, Carlsson A (September 1978). "Pivaloyl esters of N,N-dialkylated dopamine congeners. Central dopamine-receptor stimulating activity". Journal of Medicinal Chemistry. 21 (9): 864–867. doi:10.1021/jm00207a005. PMID 722753.
- ^ Volkman PH, Kohli JD, Goldberg LI, Cannon JG (January 1977). "Dipropyldopamine, a qualitatively different dopamine (DA) agonist". Federation Proceedings. 36 (3): 1049.
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