Ensaculin
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Elimination half-life | 13.7 hours |
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Formula | C26H32N2O5 |
Molar mass | 452.543 g·mol−1 |
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Ensaculin (KA-672) is a drug from the coumarin family, which has been researched as a potential treatment for dementia. It acts on a number of receptor systems, being both a weak NMDA antagonist and a 5HT1A agonist.[1][2] Animal studies have shown promising nootropic effects,[3][4] although efficacy in humans has yet to be proven. It was well tolerated in human trials, with the main side effect being orthostatic hypotension (low blood pressure).[5]
References
- ^ Lishko, PV; Maximyuk, OP; Chatterjee, SS; Nöldner, M; Krishtal, OA (1998). "The putative cognitive enhancer KA-672.HCl is an uncompetitive voltage-dependent NMDA receptor antagonist". NeuroReport. 9 (18): 4193–7. doi:10.1097/00001756-199812210-00035. PMID 9926872.
- ^ Winter, JC; Helsley, SE; Rabin, RA (1998). "The discriminative stimulus effects of KA 672, a putative cognitive enhancer: evidence for a 5-HT1A component". Pharmacology Biochemistry and Behavior. 60 (3): 703–7. doi:10.1016/S0091-3057(98)00043-4. PMID 9678654.
- ^ Hoerr, R; Noeldner, M (2002). "Ensaculin (KA-672 HCl): a multitransmitter approach to dementia treatment". CNS Drug Reviews. 8 (2): 143–58. doi:10.1111/j.1527-3458.2002.tb00220.x. PMID 12177685.
- ^ Knauber, J; Müller, WE (2003). "Anseculin improves passive avoidance learning of aged mice". Pharmacological research : the official journal of the Italian Pharmacological Society. 47 (3): 225–33. doi:10.1016/S1043-6618(02)00311-0. PMID 12591018.
- ^ Sourgens, H; Hoerr, R; Biber, A; Steinbrede, H; Derendorf, H (1998). "KA 672-HCl, a neuronal activator against dementia: tolerability, safety, and preliminary pharmacokinetics after single and multiple oral doses in healthy male and female volunteers". Journal of clinical pharmacology. 38 (4): 373–81. doi:10.1002/j.1552-4604.1998.tb04438.x. PMID 9590466.