Ensaculin
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| Elimination half-life | 13.7 hours |
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| Formula | C26H32N2O5 |
| Molar mass | 452.551 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 upon standing).[5]
See also
References
- ^ Lishko PV, Maximyuk OP, Chatterjee SS, Nöldner M, Krishtal OA (December 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. S2CID 29960822.
- ^ Winter JC, Helsley SE, Rabin RA (July 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. S2CID 6493994.
- ^ 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. PMC 6741668. PMID 12177685.
- ^ Knauber J, Müller WE (March 2003). "Anseculin improves passive avoidance learning of aged mice". Pharmacological Research. 47 (3): 225–33. doi:10.1016/S1043-6618(02)00311-0. PMID 12591018.
- ^ Sourgens H, Hoerr R, Biber A, Steinbrede H, Derendorf H (April 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. S2CID 32558296.