| Size | Price | Stock | Qty |
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| 100mg |
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| 250mg |
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| 500mg | |||
| Other Sizes |
| Targets |
Moguisteine targets peripheral sensory pathways in the respiratory tract rather than central cough centers in the brainstem. Its primary site of action is believed to be the rapidly adapting irritant receptors (RARs) located along the tracheobronchial tree. These receptors are mechanosensory fibers that respond to mechanical and chemical stimuli and are a major afferent pathway for initiating the cough reflex. By interacting with these peripheral nerve endings, Moguisteine raises the threshold for cough initiation without affecting the central processing of the cough signal. An alternative mechanism that has been proposed involves the modulation of ATP-sensitive potassium (K-ATP) channels. Studies have demonstrated that the antitussive effect of Moguisteine can be blocked by K-ATP channel inhibitors, suggesting that channel opening and subsequent hyperpolarization of airway sensory nerves may contribute to its peripheral action. This peripheral mechanism of action is a key differentiator from centrally acting antitussives like codeine, which primarily act on μ-opioid receptors in the brain.
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| ln Vitro |
In vitro studies have characterized Moguisteine's pharmacological profile and confirmed its lack of activity at opioid receptors, distinguishing it from narcotic antitussives. The compound does not bind to or activate central opioid receptors, which explains its lack of addiction potential and sedation. In functional in vitro assays, Moguisteine has been shown to modulate the activity of airway sensory nerves, reducing their responsiveness to tussive stimuli. Its antitussive activity may stem from interactions with ATP-sensitive K+ channels, as evidenced by studies showing that K-ATP channel blockers can reverse its effects. Furthermore, Moguisteine exhibits stability across a range of physiological pH conditions, which is important for its consistent activity in biological systems. Its solubility profile—freely soluble in DMSO and ethanol but practically insoluble in water—dictates its formulation for both in vitro and in vivo studies. In controlled laboratory settings, Moguisteine does not exhibit direct cytotoxicity at therapeutic concentrations, making it a safe tool for studying cough mechanisms in cell-based systems.
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| ln Vivo |
In vivo, Moguisteine has demonstrated robust antitussive efficacy in several well-established animal models. In conscious guinea pigs, it effectively inhibits citric acid-induced cough, a model that mimics the chemical irritation of airway sensory nerves. The compound's antitussive effect is dose-dependent and comparable in magnitude to that of codeine, yet it does not produce the central nervous system depression or physical dependence associated with opioids. In dogs, Moguisteine also suppresses experimentally induced cough, further validating its peripheral mechanism of action across species. Importantly, in vivo studies have shown that Moguisteine does not inhibit cough induced by electrical stimulation of the afferent superior laryngeal nerve, which bypasses peripheral receptors and directly activates central cough pathways, confirming that its action is indeed peripheral. Additional in vivo investigations have explored its effects on airway inflammation, demonstrating that Moguisteine can reduce inflammatory responses in the airways without compromising mucociliary clearance or other protective respiratory functions. These findings collectively support its potential as a safe and effective non-narcotic antitussive for clinical use.
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| Enzyme Assay |
The in vitro enzyme/receptor binding assays for Moguisteine focus on confirming its lack of affinity for central targets such as opioid receptors and its potential interaction with peripheral ion channels. Radioligand binding studies using membrane preparations from brain tissue or cells expressing opioid receptors are conducted to demonstrate that Moguisteine does not displace selective opioid ligands, confirming its non-narcotic mechanism. To investigate the involvement of ATP-sensitive potassium channels, electrophysiological assays are performed on isolated sensory neurons or airway tissue preparations. In these assays, the effect of Moguisteine on channel activity is measured using patch-clamp techniques, and the reversal of its effects by K-ATP channel blockers such as glibenclamide provides mechanistic evidence. These non-cellular assays are critical for establishing the molecular basis of Moguisteine's peripheral antitussive action.
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| Cell Assay |
Cellular assays for Moguisteine are typically conducted to evaluate its cytotoxicity and to study its effects on airway epithelial cells or sensory neurons in vitro. Cell viability assays, such as MTT or CCK-8, are performed using human bronchial epithelial cell lines or primary cultures to ensure that Moguisteine does not exert toxic effects at concentrations relevant to its antitussive activity. In addition, intracellular calcium imaging or membrane potential assays can be used to assess the compound's modulation of sensory neuron excitability. For example, cultured dorsal root ganglion neurons or nodose ganglion neurons can be treated with Moguisteine, and their response to capsaicin or other irritants can be measured to determine whether the compound alters the threshold for neuronal activation. These cell-based experiments complement the in vivo findings by providing a controlled environment to dissect the signaling pathways involved in Moguisteine's action.
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| Animal Protocol |
In vivo animal experiments for Moguisteine are primarily conducted in guinea pigs and dogs, the two species most commonly used for cough research. In the guinea pig model, cough is induced by exposing conscious animals to an aerosol of citric acid or capsaicin in a specialized whole-body plethysmograph. The number of coughs is recorded by an observer or by a microphone and analyzed using cough detection software. Moguisteine is administered orally, intraperitoneally, or intravenously at various doses prior to the cough challenge, and the dose-response relationship is established. The ED50 is calculated, and the duration of action is determined by challenging animals at different time points after drug administration. In the dog model, cough is induced by mechanical or chemical stimulation of the trachea, and the effect of Moguisteine is similarly assessed. To confirm the peripheral mechanism, additional experiments are conducted in anesthetized guinea pigs, where cough is elicited by electrical stimulation of the superior laryngeal nerve, a procedure that bypasses peripheral receptors and directly activates the central cough network. The lack of effect of Moguisteine in this model confirms that its action is not centrally mediated.
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| ADME/Pharmacokinetics |
The pharmacokinetic properties of Moguisteine have been characterized in preclinical and clinical studies. Following oral administration, Moguisteine is rapidly absorbed, and its bioavailability is sufficient to achieve therapeutic plasma concentrations. The compound has a molecular weight of 339.41 g/mol and a molecular formula of C16H21NO5S. It is metabolized primarily in the liver, and its metabolites are excreted in urine and feces. In healthy Chinese volunteers, single- and multiple-dose pharmacokinetics have been evaluated, revealing a favorable profile with predictable accumulation and elimination. The compound's half-life supports twice-daily dosing in clinical settings. Its high solubility in DMSO and ethanol, combined with its poor aqueous solubility, necessitates formulation strategies that enhance its dissolution for oral administration. In vivo formulation recommendations include a combination of DMSO, PEG300, Tween 80, and saline to achieve adequate solubility and systemic exposure.
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| Toxicity/Toxicokinetics |
Toxicology studies have demonstrated that Moguisteine has a favorable safety profile. In controlled clinical trials, it has been shown to be safe and well-tolerated in patients with various respiratory conditions. Unlike narcotic antitussives, Moguisteine does not cause sedation, respiratory depression, or physical dependence, which are major limitations of opioid-based cough suppressants. Preclinical toxicity assessments have not revealed significant genotoxicity, carcinogenicity, or reproductive toxicity. However, as with any pharmacological agent, comprehensive toxicological evaluations would be required for full regulatory approval. The compound's safety profile, combined with its peripheral mechanism of action, makes it an attractive candidate for patients who require long-term cough management, such as those with chronic bronchitis or pulmonary fibrosis.
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| Additional Infomation |
Moguisteine represents a significant advancement in antitussive therapy due to its novel peripheral mechanism of action. It is not a narcotic and does not act on the cough center in the brain, which distinguishes it from codeine and dextromethorphan. Its action is possibly mediated by interaction with rapidly adapting irritant receptors along the tracheobronchial tree, and there is evidence suggesting involvement of ATP-sensitive potassium channels. The compound has been extensively studied in preclinical models and clinical trials, demonstrating efficacy comparable to codeine but with a superior safety profile. Despite its promising profile, Moguisteine has not been widely adopted in clinical practice, possibly due to the availability of other over-the-counter antitussives and the challenges of bringing a new cough medication to market. Nevertheless, it remains a valuable pharmacological tool for studying cough mechanisms and a potential therapeutic option for patients with chronic cough who are unresponsive to or intolerant of existing therapies.
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| Molecular Formula |
C16H21NO5S
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| Molecular Weight |
339.41
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| Exact Mass |
339.114
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| CAS # |
119637-67-1
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| PubChem CID |
65935
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| Appearance |
White to off-white solid powder
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| Density |
1.2±0.1 g/cm3
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| Boiling Point |
506.8±50.0 °C at 760 mmHg
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| Melting Point |
72-76ºC
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| Flash Point |
260.3±30.1 °C
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| Vapour Pressure |
0.0±1.3 mmHg at 25°C
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| Index of Refraction |
1.549
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| LogP |
2.18
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| Hydrogen Bond Donor Count |
0
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| Hydrogen Bond Acceptor Count |
6
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| Rotatable Bond Count |
8
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| Heavy Atom Count |
23
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| Complexity |
406
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| Defined Atom Stereocenter Count |
0
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| SMILES |
COC1=CC=CC=C1OCC2N(C(CC(OCC)=O)=O)CCS2
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| InChi Key |
WSYVIAQNTFPTBI-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C16H21NO5S/c1-3-21-16(19)10-14(18)17-8-9-23-15(17)11-22-13-7-5-4-6-12(13)20-2/h4-7,15H,3,8-11H2,1-2H3
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| Chemical Name |
ethyl 3-[2-[(2-methoxyphenoxy)methyl]-1,3-thiazolidin-3-yl]-3-oxopropanoate
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| Synonyms |
BBR 2173; BBR2173; BBR-2173
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~100 mg/mL (~294.63 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (7.37 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (7.37 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (7.37 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.9463 mL | 14.7314 mL | 29.4629 mL | |
| 5 mM | 0.5893 mL | 2.9463 mL | 5.8926 mL | |
| 10 mM | 0.2946 mL | 1.4731 mL | 2.9463 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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