Discontinued Productα-Conotoxin ImI (Cat. No. 3119) has been withdrawn from sale for commercial reasons.
Nicotinic receptor antagonist that displays selectivity for homomeric α7 and α9 receptors (IC50 values are 220 and 1800 nM respectively). Displays no effect on α2β2, α3β2, α4β2, α2β4, α3β3 and α4β4 subunit combinations.
Sold under license from University of Utah
(Modifications: Cys-12 = C-terminal amide, Disulfide bridge between 2 - 8, 3 - 12)
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
References are publications that support the biological activity of the product.
McIntosh et al (1994) A nicotinic acetylcholine receptor ligand of unique specificity, α-conotoxin ImI. J.Biol.Chem. 269 16733 PMID: 8206995
Johnson et al (1995) α-Conotoxin ImI exhibits subtype-specific nicotinic acetylcholine receptor blockade: preferential inhibition of homomeric α7 and α9 receptors. Mol.Pharmacol. 48 194 PMID: 7651351
Pereira et al (1996) α-Conotoxin-ImI: a competitive antagonist at α-Bungarotoxin-sensitive neuronal nicotinic receptors in hippocampal neurons. J.Pharmacol.Exp.Ther. 278 1472 PMID: 8819535
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Keywords: alpha-conotoxin ImI, alpha-conotoxin ImI supplier, α7, alpha7, a7, α9, alpha9, a9, selective, nAChR, antagonists, Nicotinic, Receptors, Acetylcholine, Non-Selective, α-conotoxin, alpha-conotoxin, ImI, a-conotoxinImI, conotoxins, venoms, (a7), (Other, Subtypes), 3119, Tocris Bioscience
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Literature in this Area
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Alzheimer's disease (AD) is a degenerative brain disease and the most common cause of dementia, affecting approximately 47 million people worldwide. Updated in 2015, this poster summarizes the structural and functional changes observed in the progression of this neurodegenerative disease, as well as classic AD drug targets.
Learning & Memory Poster
Recognition memory enables us to make judgements about whether or not we have encountered a particular stimulus before. This poster outlines the cellular mechanisms underlying recognition memory and its links to long-term depression, as well as the use of pharmacological intervention to assess the role of neurotransmitters in recognition memory.
Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.