Cyclothiazide

CAS# 2259-96-3

Cyclothiazide

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Product Name & Size Price Stock
Cyclothiazide:10mg $85.00 In stock
Cyclothiazide:20mg $145.00 In stock
Cyclothiazide:50mg $340.00 In stock
Cyclothiazide:100mg $595.00 In stock
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Chemical structure

Cyclothiazide

3D structure

Chemical Properties of Cyclothiazide

Cas No. 2259-96-3 SDF Download SDF
PubChem ID 2910 Appearance Powder
Formula C14H16ClN3O4S2 M.Wt 389.87
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 100 mM in DMSO and to 25 mM in ethanol
Chemical Name 3-(5-bicyclo[2.2.1]hept-2-enyl)-6-chloro-1,1-dioxo-3,4-dihydro-2H-1$l^{6},2,4-benzothiadiazine-7-sulfonamide
SMILES C1C2CC(C1C=C2)C3NC4=CC(=C(C=C4S(=O)(=O)N3)S(=O)(=O)N)Cl
Standard InChIKey BOCUKUHCLICSIY-UHFFFAOYSA-N
Standard InChI InChI=1S/C14H16ClN3O4S2/c15-10-5-11-13(6-12(10)23(16,19)20)24(21,22)18-14(17-11)9-4-7-1-2-8(9)3-7/h1-2,5-9,14,17-18H,3-4H2,(H2,16,19,20)
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 Cyclothiazide

DescriptionPositive allosteric modulator of AMPA receptors that potently inhibits AMPA receptor desensitization. Selective for the flip variant of each of the four receptor subunits. Also available as part of the AMPA Receptor.

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Preparing Stock Solutions of Cyclothiazide

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.565 mL 12.8248 mL 25.6496 mL 51.2992 mL 64.1239 mL
5 mM 0.513 mL 2.565 mL 5.1299 mL 10.2598 mL 12.8248 mL
10 mM 0.2565 mL 1.2825 mL 2.565 mL 5.1299 mL 6.4124 mL
50 mM 0.0513 mL 0.2565 mL 0.513 mL 1.026 mL 1.2825 mL
100 mM 0.0256 mL 0.1282 mL 0.2565 mL 0.513 mL 0.6412 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on Cyclothiazide

Cyclothiazide-induced persistent increase in respiratory-related activity in vitro.[Pubmed:22753547]

J Physiol. 2012 Oct 1;590(19):4897-915.

Hypoglossal (XII) motoneurons (MNs) innervate the genioglossus muscle of the tongue, which plays an important role in maintaining upper airway patency, particularly during sleep, and modulating upper airway resistance. Discovering methods for inducing long-term increases in genioglossal motoneuronal excitability to AMPA-mediated drive may help in the development of therapeutics for upper airway motor disorders such as obstructive sleep apnoea. We show that the diuretic, anti-hypertensive, AMPA receptor modulator Cyclothiazide (CTZ) induces a profound and long-lasting increase in the amplitude of respiratory-related XII nerve activity in rhythmically active neonatal rat medullary slices. Treatment of the slice with CTZ (90 muM) for 1 h increased the integrated XII ( XII) nerve burst amplitude to 262 +/- 23% of pre-treatment control at 1 h post-treatment;much of this increase lasted at least 12 h. The amount of CTZ-induced facilitation (CIF) was dependent upon both CTZ dose and exposure time and was accompanied by a long-lasting increase in endogenous AMPA-mediated drive currents to XII MNs. CIF, however, is not a form of plasticity and does not depend on AMPA or NMDA receptor activation for its induction. Nor does it depend on coincident protein kinase A or C activity. Rather, measurement of mEPSCs along with mass spectrometric analysis of CTZ-treated slices indicates that the cause is prolonged bioavailability of CTZ. These results illustrate a latent residual capacity for potentiating AMPA-mediated inspiratory drive to XII MNs that might be applied to the treatment of upper airway motor deficits.

Epileptiform response of CA1 neurones to convulsant stimulation by cyclothiazide, kainic acid and pentylenetetrazol in anaesthetized rats.[Pubmed:21269843]

Seizure. 2011 May;20(4):312-9.

We have previously reported that Cyclothiazide (CTZ) evokes epileptiform activities in hippocampal neurons and induces seizure behavior. Here we further studied in vivo the sensitivity of the hippocampal CA1 neurons in response to CTZ in epileptogenesis in comparison with two other classic convulsants of kainic acid (KA) and pentylenetetrazol (PTZ). CTZ administered intracerebral ventricle (i.c.v.) induced epileptiform activities from an initial of multiple evoked population spikes, progressed to spontaneous spikes and finally to highly synchronized burst activities in hippocampal CA1 neurons. PTZ, when given by subcutaneously, but not by intracerebral ventricle injection, evoked similar progressive epileptiform activities. In contrast, KA given by i.c.v. induced a quick development of epileptiform burst activities and then shortly switched to continuous high frequency firing as acute status epilepticus (ASE). Pharmacologically, alprazolam, a high-potency benzodiazepine ligand, inhibited CTZ and PTZ, but not KA, induced epileptiform burst activities while GYKI 53784, an AMPA receptor antagonist, suppressed CTZ and KA but not PTZ evoked epileptiform activities. In conclusion, CTZ and PTZ induced epileptiform activities are most likely to share a similar progressive pattern in hippocampus with GABAergic mechanism dominant in epileptogenesis, while CTZ model involves additional glutamate receptor activation. KA induced seizure in hippocampus is different to that of both CTA and PTZ. The results from this study indicate that hippocampal neurons respond to various convulsant stimulation differently which may reflect the complicated causes of the seizure in clinics.

Activation of extrasynaptic GABA(A) receptors inhibits cyclothiazide-induced epileptiform activity in hippocampal CA1 neurons.[Pubmed:25260800]

Neurosci Bull. 2014 Oct;30(5):866-76.

Extrasynaptic GABA(A) receptors (GABA(A)Rs)-mediated tonic inhibition is reported to involve in the pathogenesis of epilepsy. In this study, we used Cyclothiazide (CTZ)-induced in vitro brain slice seizure model to explore the effect of selective activation of extrasynaptic GABA(A)Rs by 4,5,6,7-tetrahydroisoxazolo[5,4-c] pyridine-3-ol (THIP) on the CTZ-induced epileptiform activity in hippocampal neurons. Perfusion with CTZ dose-dependently induced multiple epileptiform peaks of evoked population spikes (PSs) in CA1 pyramidal neurons, and treatment with THIP (5 mumol/L) significantly reduced the multiple PS peaks induced by CTZ stimulation. Western blot showed that the delta-subunit of the GABA(A)R, an extrasynaptic specific GABA(A)R subunit, was also significantly down-regulated in the cell membrane 2 h after CTZ treatment. Our results suggest that the CTZ-induced epileptiform activity in hippocampal CA1 neurons is suppressed by the activation of extrasynaptic GABA(A)Rs, and further support the hypothesis that tonic inhibition mediated by extrasynaptic GABA(A)Rs plays a prominent role in seizure generation.

Downregulated GABA and BDNF-TrkB pathway in chronic cyclothiazide seizure model.[Pubmed:24757570]

Neural Plast. 2014;2014:310146.

Cyclothiazide (CTZ) has been reported to simultaneously enhance glutamate receptor excitation and inhibit GABAA receptor inhibition, and in turn it evokes epileptiform activities in hippocampal neurons. It has also been shown to acutely induce epileptic seizure behavior in freely moving rats. However, whether CTZ induced seizure rats could develop to have recurrent seizure still remains unknown. In the current study, we demonstrated that 46% of the CTZ induced seizure rats developed to have recurrent seizure behavior as well as epileptic EEG with a starting latency between 2 weeks and several months. In those chronic seizure rats 6 months after the seizure induction by the CTZ, our immunohistochemistry results showed that both GAD and GAT-1 were significantly decreased across CA1, CA3, and dentate gyrus area of the hippocampus studied. In addition, both BDNF and its receptor TrkB were also decreased in hippocampus of the chronic CTZ seizure rats. Our results indicate that CTZ induced seizure is capable of developing to have recurrent seizure, and the decreased GABA synthesis and transport as well as the impaired BDNF-TrkB signaling pathway may contribute to the development of the recurrent seizure. Thus, CTZ seizure rats may provide a novel animal model for epilepsy study and anticonvulsant drug testing in the future.

The norbornenyl moiety of cyclothiazide determines the preference for flip-flop variants of AMPA receptor subunits.[Pubmed:10854736]

Neurosci Lett. 2000 Jun 23;287(2):161-5.

Cyclothiazide and two analogs in which the norbornenyl part was replaced with a cyclohexyl or a cyclohexenyl moiety were examined with regard to their preference for flop vs. flip splice variants of the (+/-)-alphaamino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor subunits GluR2, 3 and 4. The studies were carried out by measuring the effects of the drugs on the binding of [(3)H]AMPA or [(3)H]fluorowillardiine to membranes from HEK293 cells that stably express the AMPA receptor subunits. Cyclothiazide had four to nine times lower EC(50) values at flip than at flop receptors, as previously reported. In contrast, the two analogs showed little discrimination for GluR3 or GluR4 splice variants and a clear preference for the flop variant in the case of GluR2. These results indicate that it is the norbornenyl component of Cyclothiazide which confers the selectivity vis-a-vis flip-flop variants.

Allosteric regulation of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate receptors by thiocyanate and cyclothiazide at a common modulatory site distinct from that of 2,3-benzodiazepines.[Pubmed:9758228]

Neuroscience. 1998 Dec;87(3):615-29.

Allosteric regulators of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) receptors include 2,3-benzodiazepines such as GYKI 52466 and GYKI 53655 and the chaotropic anion thiocyanate that inhibit, and benzothiadiazines such as Cyclothiazide that potentiate AMPA receptor currents. Here we sought to determine whether the allosteric regulators modulate AMPA receptors at a common or distinct allosteric sites by comparing their actions on AMPA- and kainate-evoked currents in cultured rat hippocampal neurons and Xenopus oocytes expressing recombinant AMPA receptor subunits. GYKI 52466 and thiocyanate blocked AMPA-evoked currents in a concentration-dependent manner (IC50 values, 8.2 microM and 1.1 mM, respectively); in contrast, kainate-evoked currents were blocked by GYKI 52466, but were potentiated by high concentrations of thiocyanate (> or = 3 mM). Thiocyanate enhanced the rate of desensitization and slowed recovery from desensitization of AMPA-evoked currents, whereas GYKI 52466 failed to affect desensitization. Among neurons in the hippocampal cultures, there was cell-to-cell variability in the sensitivity to block of AMPA-evoked currents by thiocyanate that was correlated with the degree of potentiation by Cyclothiazide. Moreover, Cyclothiazide caused a parallel rightward shift in the concentration-response curve for thiocyanate block, and slowed the onset of thiocyanate block to a rate that was similar to that of Cyclothiazide dissociation. Together, these observations suggest that thiocyanate and Cyclothiazide act at non-distinct allosteric sites. GYKI 52466 blocked AMPA receptor responses to a similar extent, irrespective of the degree of Cyclothiazide potentiation. Moreover, the kinetics of GYKI 53655 block in the presence of Cyclothiazide were not consistent with a competitive interaction. As is the case for Cyclothiazide, SCN- exhibited greater affinity for flip than for flop AMPA receptor splice variants. In particular, GluR1flip/GluR2flip was especially sensitive to thiocyanate block. We conclude that thiocyanate, a flip-preferring allosteric modulator like Cyclothiazide, appears to act by enhancing desensitization at a site that may overlap the site where Cyclothiazide reduces desensitization, whereas 2,3-benzodiazepines act at a distinct site and the block does not involve a modification of desensitization.

Cyclothiazide acts at a site on the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor complex that does not recognize competitive or noncompetitive AMPA receptor antagonists.[Pubmed:7529311]

J Pharmacol Exp Ther. 1995 Jan;272(1):38-43.

Activation of the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) subtype of ionotropic glutamate receptors by certain agonists, including AMPA and glutamate, has been shown to result in a rapid desensitization of the receptor. This desensitization is profoundly inhibited by the benzothiadiazide diuretic, Cyclothiazide. We previously reported that Cyclothiazide potentiates AMPA-induced [3H]norepinephrine ([3H]NE) release from rat hippocampal slices. We used this system to investigate the possible interaction of Cyclothiazide with various AMPA receptor antagonists, including the competitive antagonist LY293558 and the 2,3-benzodiazepine noncompetitive antagonist GYKI 53655. Cyclothiazide significantly potentiated both AMPA- and KA-induced [3H]NE release from slices of the rat hippocampus. LY293558 and GYKI 53655 inhibited the potentiated and nonpotentiated AMPA- and KA-induced [3H]NE release in a concentration-dependent manner. The IC50 values for inhibition of AMPA- or KA-induced [3H]NE release by either antagonist were not affected by the presence of Cyclothiazide. Thus, Cyclothiazide seems to interact at a site on the AMPA receptor complex which differs from either the glutamate recognition site or the 2,3-benzodiazepine allosteric site.

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