321-64-2
Chemical Structure
Tacrine
- CAS No.: 321-64-2
- Formula:C13H14N2
- Molecular Weight:198.27
IUPAC Name: 1,2,3,4-tetrahydroacridin-9-amine
InChIKey: YLJREFDVOIBQDA-UHFFFAOYSA-N
SMILES: NC1=C2CCCCC2=NC3=CC=CC=C31
Biological Activity: Tacrine is an effective oral acetylcholine (AChE) inhibitor (IC50 = 109 nM) and also acts as an active substrate for CYP1A2. Tacrine can restore cognitive dysfunction in elderly rats. Tacrine can cause liver toxicity and is used in research related to Alzheimer's disease[1][2][3][4].
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Tacrine | 99.10% | Tacrine is an effective oral acetylcholine (AChE) inhibitor (IC50 = 109 nM) and also acts as an active substrate for CYP1A2. Tacrine can restore cognitive dysfunction in elderly rats. Tacrine can cause liver toxicity and is used in research related to Alzheimer's disease. | ||||||||||||||||||||
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Tacrine (Standard) | ≥98% | Tacrine (Standard) is the analytical standard of Tacrine. This product is intended for research and analytical applications. Tacrine is an effective oral acetylcholine (AChE) inhibitor (IC50 = 109 nM) and also acts as an active substrate for CYP1A2. Tacrine can restore cognitive dysfunction in elderly rats. Tacrine can cause liver toxicity and is used in research related to Alzheimer's disease. | ||||||||||||||||||||
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- [1]. C Scali, et al. Tacrine administration enhances extracellular acetylcholine in vivo and restores the cognitive impairment in aged rats. Pharmacol Res. 1997 Dec;36(6):463-9. [Content Brief]
- [2]. Patocka J, et al. Possible role of hydroxylated metabolites of tacrine in drug toxicity and therapy of Alzheimer's disease. Curr Drug Metab. 2008;9(4):332-335. [Content Brief]
- [3]. Bhatt S, et al. Assessment of the CYP1A2 Inhibition-Mediated Drug Interaction Potential for Pinocembrin Using In Silico, In Vitro, and In Vivo Approaches. ACS Omega. 2022;7(23):20321-20331. Published 2022 Jun 2. [Content Brief]
- [4]. Romero A, et al. Novel tacrine-related drugs as potential candidates for the treatment of Alzheimer's disease. Bioorg Med Chem Lett. 2013;23(7):1916-1922. [Content Brief]
Keywords