M2 ion channel blocker

M2 ion channel blocker CAS# 1190215-03-2

M2 ion channel blocker

Catalog No. BCC1726----Order now to get a substantial discount!

Product Name & Size Price Stock
M2 ion channel blocker:100mg $184.00 In stock
M2 ion channel blocker:200mg $313.00 In stock
M2 ion channel blocker:500mg $736.00 In stock
M2 ion channel blocker:1000mg $1288.00 In stock
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Chemical structure

M2 ion channel blocker

3D structure

Chemical Properties of M2 ion channel blocker

Cas No. 1190215-03-2 SDF Download SDF
PubChem ID 46933130 Appearance Powder
Formula C19H29N3O2 M.Wt 331.45
Type of Compound N/A Storage Desiccate at -20°C
Synonyms L-Histidine, N-(tricyclo[3.3.1.13,7]dec-1-ylmethyl)-, methyl ester
Solubility H2O : < 0.1 mg/mL (insoluble)
Chemical Name methyl (2S)-2-(1-adamantylmethylamino)-3-(1H-imidazol-5-yl)propanoate
SMILES COC(=O)C(CC1=CN=CN1)NCC23CC4CC(C2)CC(C4)C3
Standard InChIKey GCZFPPAFJOOMRO-IEKYFPHUSA-N
Standard InChI InChI=1S/C18H27N3O2/c1-23-17(22)16(5-15-9-19-11-21-15)20-10-18-6-12-2-13(7-18)4-14(3-12)8-18/h9,11-14,16,20H,2-8,10H2,1H3,(H,19,21)/t12?,13?,14?,16-,18?/m0/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of M2 ion channel blocker

DescriptionM2 ion channel blocker is capable of inhibiting and blocking the activity of M2 ion channel;Antiviral agent.

References:
[1]. Zhang, Wenjuan; Xu, Jing; Liu, Fang. Heterodimers of histidine and amantadine as inhibitors for wild type and mutant M2 channels of influenza A. Chinese Journal of Chemistry (2010), 28(8), 1417-1423.

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Background on M2 ion channel blocker

This compound is capable of inhibiting and blocking the activity of M2 ion channel. Antiviral agents.

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References on M2 ion channel blocker

Side Fenestrations Provide an "Anchor" for a Stable Binding of A1899 to the Pore of TASK-1 Potassium Channels.[Pubmed:28494157]

Mol Pharm. 2017 Jul 3;14(7):2197-2208.

A1899 is a potent and selective inhibitor of the two-pore domain potassium (K2P) channel TASK-1. It was previously reported that A1899 acts as an open-channel blocker and binds to residues of the P1 and P2 regions, the M2 and M4 segments, and the halothane response element. The recently described crystal structures of K2P channels together with the newly identified side fenestrations indicate that residues relevant for TASK-1 inhibition are not purely facing the central cavity as initially proposed. Accordingly, the TASK-1 binding site and the mechanism of inhibition might need a re-evaluation. We have used TASK-1 homology models based on recently crystallized K2P channels and molecular dynamics simulation to demonstrate that the highly potent TASK-1 blocker A1899 requires binding to residues located in the side fenestrations. Unexpectedly, most of the previously described residues that interfere with TASK-1 blockade by A1899 project their side chains toward the fenestration lumina, underlining the relevance of these structures for drug binding in K2P channels. Despite its hydrophobicity, A1899 does not seem to use the fenestrations to gain access to the central cavity from the lipid bilayer. In contrast, binding of A1899 to residues of the side fenestrations might provide a physical "anchor", reflecting an energetically favorable binding mode that after pore occlusion stabilizes the closed state of the channels.

M3 cholinoreceptors alter electrical activity of rat left atrium via suppression of L-type Ca(2+) current without affecting K(+) conductance.[Pubmed:27858307]

J Physiol Biochem. 2017 May;73(2):167-174.

Electrophysiological effects produced by selective activation of M3 cholinoreceptors were studied in isolated left atrium preparations from rat using the standard sharp glass microelectrode technique. The stimulation of M3 receptors was obtained by application of muscarinic agonist pilocarpine (10(-5) M) in the presence of selective M2 antagonist methoctramine (10(-7) M). Stimulation of M3 receptors induced marked reduction of action potential duration by 14.4 +/- 2.4% and 16.1 +/- 2.5% of control duration measured at 50 and 90% of repolarization, respectively. This effect was completely abolished by selective M3 blocker 4-DAMP (10(-8) M). In isolated myocytes obtained from the rat left atrium, similar pharmacological stimulation of M3 receptors led to suppression of peak L-type calcium current by 13.9 +/- 2.6% of control amplitude (measured at +10 mV), but failed to affect K(+) currents I to, I Kur, and I Kir. In the absence of M2 blocker methoctramine, pilocarpine (10(-5) M) produced stronger attenuation of I CaL and induced an increase in I Kir. This additive inward rectifier current could be abolished by highly selective blocker of Kir3.1/3.4 channels tertiapin-Q (10(-6) M) and therefore was identified as I KACh. Thus, in the rat atrial myocardium activation of M3 receptors leads to shortening of action potentials via suppression of I CaL, but does not enhance the major potassium currents involved in repolarization. Joint stimulation of M2 and M3 receptors produces stronger action potential shortening due to M2-mediated activation of I KACh.

GABAA receptor cysteinyl mutants and the ginkgo terpenoid lactones bilobalide and ginkgolides.[Pubmed:26953225]

Eur J Pharmacol. 2016 Apr 15;777:136-46.

The terpenoid lactones from Ginkgo biloba, bilobalide and ginkgolides, have been shown to act as negative modulators at alpha1beta2gamma2L GABAA receptors. They have structural features similar to those of the chloride channel blocker picrotoxinin. Unlike picrotoxinin, however they are not known to produce convulsant effects. Using two-electrode voltage clamp electrophysiology, this study compared the effect of mutation of 2', 6' and 15' pore facing M2 domain residues to cysteine on the action of picrotoxinin, bilobalide and ginkgolides at alpha1beta2gamma2L GABAA receptors expressed in Xenopus oocytes. Picrotoxinin was affected by mutation differently from the ginkgo terpenoid lactones. Although some of these compounds were affected by the mutation at same position and/or subunit, the changes in their potency were found to be dissimilar. The results suggest that the intracellular pore binding site for picrotoxinin, bilobalide, ginkgolide A, ginkgolide B and ginkgolide C is comprised of 2'beta-6'beta6'gamma, 2'alpha2'beta-6'alpha6'beta, 2'alpha2'beta2'gamma-6'beta6'gamma, 2'alpha, 2'beta2'gamma-6'beta and 2'alpha2'beta, respectively. Unlike bilobalide and ginkgolides, the inhibitory action of picrotoxinin was not affected by mutations at 15' position. It is proposed that 15'alpha15'beta, 15'beta, 15'alpha15'beta and 15'alpha15'beta15'gamma forms an extracellular pore binding site for bilobalide, ginkgolide A, ginkgolide B and ginkgolide C, respectively. The lack of convulsant effects of bilobalide, and ginkgolide A and B may be associated in part with their different binding locations within the chloride channel.

Expression and purification of native and functional influenza A virus matrix 2 proton selective ion channel.[Pubmed:27825980]

Protein Expr Purif. 2017 Mar;131:42-50.

Influenza A virus displays one of the highest infection rates of all human viruses and therefore represents a severe human health threat associated with an important economical challenge. Influenza matrix protein 2 (M2) is a membrane protein of the viral envelope that forms a proton selective ion channel. Here we report the expression and native isolation of full length active M2 without mutations or fusions. The ability of the influenza virus to efficiently infect MDCK cells was used to express native M2 protein. Using a Calixarene detergents/surfactants based approach; we were able to solubilize most of M2 from the plasma membrane and purify it. The tetrameric form of native M2 was maintained during the protein preparation. Mass spectrometry shows that M2 was phosphorylated in its cytoplasmic tail (serine 64) and newly identifies an acetylation of the highly conserved Lysine 60. ELISA shows that solubilized and purified M2 was specifically recognized by M2 antibody MAB65 and was able to displace the antibody from M2 MDCK membranes. Using a bilayer voltage clamp measurement assay, we demonstrate a pH dependent proton selective ion channel activity. The addition of the M2 ion channel blocker amantadine allows a total inhibition of the channel activity, illustrating therefore the specificity of purified M2 activity. Taken together, this work shows the production and isolation of a tetrameric and functional native M2 ion channel that will pave the way to structural and functional characterization of native M2, conformational antibody development, small molecules compounds screening towards vaccine treatment.

Bioelectric modulation of macrophage polarization.[Pubmed:26869018]

Sci Rep. 2016 Feb 12;6:21044.

Macrophages play a critical role in regulating wound healing and tissue regeneration by changing their polarization state in response to local microenvironmental stimuli. The native roles of polarized macrophages encompass biomaterials and tissue remodeling needs, yet harnessing or directing the polarization response has been largely absent as a potential strategy to exploit in regenerative medicine to date. Recent data have revealed that specific alteration of cells' resting potential (Vmem) is a powerful tool to direct proliferation and differentiation in a number of complex tissues, such as limb regeneration, craniofacial patterning and tumorigenesis. In this study, we explored the bioelectric modulation of macrophage polarization by targeting ATP sensitive potassium channels (KATP). Glibenclamide (KATP blocker) and pinacidil (KATP opener) treatment not only affect macrophage polarization, but also influence the phenotype of prepolarized macrophages. Furthermore, modulation of cell membrane electrical properties can fine-tune macrophage plasticity. Glibenclamide decreased the secretion and gene expression of selected M1 markers, while pinacidil augmented M1 markers. More interestingly, glibencalmide promoted macrophage alternative activation by enhancing certain M2 markers during M2 polarization. These findings suggest that control of bioelectric properties of macrophages could offer a promising approach to regulate macrophage phenotype as a useful tool in regenerative medicine.

Description

M2 ion channel blocker is capable of inhibiting and blocking the activity of M2 ion channel;Antiviral agent.

Keywords:

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