3471-05-4
3471-05-4
Chemical Structure
Anabaseine
- CAS No.: 3471-05-4
- Formula:C10H12N2
- Molecular Weight:160.22
IUPAC Name: 3,4,5,6-tetrahydro-2,3'-bipyridine
InChIKey: AUBPMADJYNSPOA-UHFFFAOYSA-N
SMILES: C1(C2=CC=CN=C2)=NCCCC1
Biological Activity: Anabaseine, a brain-penetrant occurring alkaloid toxin, is potent agonist of multiple nicotinic acetylcholine receptors (AChRs). Anabaseine stimulates the neuromuscular α12β1γδ or α12β1γɛ and α7 AChRs. Anabaseine is also a weak partial agonist at α4β2 nAChRs[1][2][3].
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Anabaseine | 97.77% | Anabaseine, a brain-penetrant occurring alkaloid toxin, is potent agonist of multiple nicotinic acetylcholine receptors (AChRs). Anabaseine stimulates the neuromuscular α12β1γδ or α12β1γɛ and α7 AChRs. Anabaseine is also a weak partial agonist at α4β2 nAChRs. | ||||||||||||||||||||
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Anabaseine (Standard) | ≥98% | Anabaseine (Standard) is the analytical standard of Anabaseine. This product is intended for research and analytical applications. Anabaseine is a non-selective nicotinic agonist. Anabaseine stimulates all AChRs, preferentially stimulates skeletal muscle and brain α7 subtypes. Anabaseine is also a weak partial agonist at α4β2 nAChRs. | ||||||||||||||||||||
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Anabaseine-d4 | Anabaseine-d4 is the deuterium labeled Anabaseine (HY-115766). Anabaseine is a non-selective nicotinic agonist. Anabaseine stimulates all AChRs, preferentially stimulates skeletal muscle and brain α7 subtypes. Anabaseine is also a weak partial agonist at α4β2 nAChRs. | |||||||||||||||||||||
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References
- [1]. Kem W, et al. The Nemertine Toxin Anabaseine and Its Derivative DMXBA (GTS-21): Chemical and Pharmacological Properties. Mar Drugs. 2006;4(3):255-273.
- [2]. Summers KL et al. Nicotinic agonist modulation of neurotransmitter levels in the rat frontoparietal cortex. Jpn J Pharmacol. 1997 Jun;74(2):139-46. [Content Brief]
- [3]. Andrud K, et al. Investigation of the Possible Pharmacologically Active Forms of the Nicotinic Acetylcholine Receptor Agonist Anabaseine. Mar Drugs. 2019;17(11):614. Published 2019 Oct 29. [Content Brief]
