The primary molecular target of Moxisylyte hydrochloride is the alpha-1 adrenergic receptor (α₁-AR). It functions as a selective antagonist, blocking the effects of endogenous catecholamines like norepinephrine and epinephrine at this receptor. By binding to the α₁-AR, Moxisylyte inhibits the receptor's downstream signaling pathways, which typically lead to vasoconstriction. This results in the relaxation of smooth muscle in blood vessel walls, particularly in the cerebral vasculature, leading to vasodilation. The compound's selectivity for the α₁-AR over other adrenergic receptors is a key feature of its pharmacological profile.

In vitro, Moxisylyte hydrochloride has been studied for its ability to inhibit alpha-1 adrenergic receptor-mediated responses. While specific in vitro potency data (e.g., IC₅₀ or Kᵢ values) are not provided in the search results, its activity is well-characterized. It is known to competitively antagonize the effects of α₁-AR agonists in various tissue preparations, such as isolated vascular smooth muscle. Its efficacy in reversing phenylephrine-induced mydriasis in the eye is a classic demonstration of its local α₁-blocking activity.

In vivo, Moxisylyte hydrochloride is used clinically for its vasodilatory effects. In Raynaud's disease, it helps to alleviate symptoms by reducing vasospasm and improving peripheral circulation. It has also been noted for its ability to vasodilate cerebral vessels without causing a significant drop in systemic blood pressure, which is a desirable property for a cerebrovascular drug. Topically, it is effective in reversing mydriasis induced by sympathomimetic agents, demonstrating its local action on the iris dilator muscle.

For in vitro enzyme/receptor binding assays, Moxisylyte hydrochloride is evaluated for its affinity and selectivity for the alpha-1 adrenergic receptor. Standard protocols involve radioligand binding assays using membrane preparations from cells or tissues that express the α₁-AR. The compound is incubated with a radiolabeled antagonist (e.g., [³H]-prazosin) and varying concentrations of Moxisylyte. The amount of bound radioligand is measured, and the concentration of Moxisylyte required to displace 50% of the specific binding (IC₅₀) is determined. This data is used to calculate the inhibitor constant (Kᵢ), which is a measure of its binding affinity.

Cell-based in vitro assays for Moxisylyte hydrochloride involve treating cells that endogenously or heterologously express the alpha-1 adrenergic receptor. The compound's antagonist activity is typically assessed by measuring its ability to inhibit agonist-induced signaling. For example, cells are pre-incubated with Moxisylyte and then stimulated with an α₁-AR agonist like phenylephrine. Downstream signaling events, such as the increase in intracellular calcium or the activation of MAPK pathways, are then measured. The reduction in these signals by Moxisylyte indicates its functional antagonism.

In vivo animal experiments for Moxisylyte hydrochloride are often conducted to study its effects on blood flow and vascular resistance. In rodent models, the compound may be administered intravenously or intra-arterially, and its effects on regional blood flow, particularly in the cerebral or peripheral vasculature, are measured using techniques like laser Doppler flowmetry. Its ability to reverse phenylephrine-induced mydriasis can also be studied in animal models, where pupil diameter is measured before and after topical application of the compound. These experiments help to confirm its in vivo pharmacology.

Absorption, Distribution and Excretion
Moxicillin is rapidly absorbed after oral administration. Its Cmax and AUC values show a linear relationship within the dose range of 10 to 30 mg. Following intravenous administration, the peak plasma concentration was 352.8 ng/ml, and the AUC was 152.6 mcg·h/L. In preclinical studies, its bioavailability remained approximately 10%. The primary route of excretion for moxicillin is the kidneys. Following intravenous administration, 75% of all metabolites are completely excreted in the urine; after oral administration, this proportion is 69%. According to the excretion curves, the two main metabolites of moxicillin—deacetylenol and N-monomethyldeacetylenol—are excreted in the urine at rates of 50% and 10%, respectively. Fecal excretion accounts for only 14% of the administered dose. In preclinical studies, the volume of distribution in beagle dogs was 0.83–0.98 L/kg. In preclinical trials, the plasma clearance rate in beagle dogs was 7.17 ml min/kg. Metabolism/Metabolites The pharmacokinetic characteristics of moxicillin allow it to be considered a prodrug due to its very rapid biotransformation. The drug is rapidly hydrolyzed in plasma and tissues by pseudocholinesterases to produce the major metabolite, deacetylated thymosin. This metabolite is subsequently demethylated by the cytochrome P450 monooxygenase system to form deacetylated thymosin. Both major metabolites are pharmacologically active. Pharmacokinetic studies of moxicillin in urine and feces revealed the presence of eight distinct metabolites, two of which are highly polar and difficult to hydrolyze enzymatically. Sulfate and glucuronide conjugates of the major metabolite were detected in these metabolites. Biological Half-Life The half-life of moxicillin is 1–2 hours.
Pharmacokinetic (PK) data for Moxisylyte hydrochloride are not extensively detailed in the provided search results. As a small molecule with a molecular weight of 315.84 g/mol, it is likely to be well-absorbed after oral administration. It is used topically in the eye, indicating it can penetrate ocular tissues. The compound's PK profile would include parameters such as bioavailability, half-life, and metabolism, which would be relevant for its clinical use. However, specific data are not available in the sources.

Toxicology data for Moxisylyte hydrochloride are consistent with its clinical use as an alpha-blocker. Common side effects may include hypotension, dizziness, and reflex tachycardia, which are typical of drugs that block α₁-ARs. When used topically in the eye, local irritation or effects on intraocular pressure may be observed. The compound is generally well-tolerated when used as directed. More detailed toxicological information, including acute and chronic toxicity studies, would be part of its preclinical and clinical development data.

[1]. Are alpha-blockers involved in lower urinary tract dysfunction in multiple system atrophy? A comparison of prazosin and moxisylyte. 2000, March, 15, Pages 191-195.

[2]. Moxisylyte: a review of its pharmacodynamic and pharmacokinetic properties, and its therapeutic use inimpotence. Fundam Clin Pharmacol, 1998, 12(4):377-87.

[4-[2-(dimethylamino)ethoxy]-2-methyl-5-propyl-2-ylphenyl]acetate is a monoterpene compound. Moxisylyte, known as thymoxamine in the UK, is a specific, orally active alpha-1-adrenergic antagonist. According to the World Health Organization (WHO), moxisylyte has been approved for marketing since 1987 and was designated an orphan drug by the US Food and Drug Administration (FDA) in the same year. It was jointly developed by Fujirebio of Japan and Iolab of the United States in the late 1980s. It is an alpha-adrenergic blocker used to treat Raynaud's disease. It can also be used topically in the eye to reverse mydriasis caused by phenylephrine and other sympathomimetic drugs. (Excerpt from Martindale Pharmacopoeia, 30th Edition, page 1312)

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Drug Indications
According to the World Health Organization (WHO) guidelines, moxicillin is indicated for the symptomatic treatment of sequelae of cerebral infarction or cerebral hemorrhage. Cerebral infarction is characterized by arterial occlusion, which may be caused by thrombosis or emboli. On the other hand, the U.S. Food and Drug Administration (FDA) lists moxicillin as a treatment for reversing phenylephrine-induced mydriasis, suitable for patients with narrow anterior chamber angles at risk of acute angle-closure glaucoma. Angle-closure glaucoma is caused by contact between the iris and the trabecular meshwork. This contact impairs the outflow of aqueous humor from the trabecular meshwork, leading to increased intraocular pressure and glaucoma symptoms. Mydriasis, or pupillary dilation, is a normal physiological function and one of the triggering factors for acute angle-closure glaucoma. This risk arises from pupillary block, where the pupillary margin contacts the lens, preventing aqueous humor from flowing into the anterior chamber, resulting in an increased intraocular pressure gradient. Moxisylyte was also approved in France as the first drug for the treatment of erectile dysfunction. Mechanism of Action Moxisylyte is a vasodilator whose mechanism of action is that of a specific alpha-adrenergic blocker. Its action is known to compete with norepinephrine and it does not possess beta-blocking, anti-angiotensin, or anti-serotonin activity. Pharmacodynamics Studies have shown that moxisylyte can improve peripheral blood flow in patients with occlusive artery disease with minimal effect on blood pressure. There are reports of increased skin blood flow and skin temperature after topical application of moxisylyte.
In summary, Moxisylyte hydrochloride (Thymoxamine hydrochloride) is a clinically used alpha-1 adrenergic receptor antagonist. It is employed in the treatment of Raynaud's disease and for reversing mydriasis in ophthalmology. Its mechanism of action involves blocking α₁-ARs, leading to vasodilation and smooth muscle relaxation. The compound is available for research purposes and is known for its ability to vasodilate cerebral vessels without significantly reducing blood pressure. It is a well-established pharmacological tool and therapeutic agent.

C16H26CLNO3

315.84

315.16

C, 60.85; H, 8.30; Cl, 11.22; N, 4.43; O, 15.20

964-52-3

964-52-3

4260

White to off-white solid powder

1.018g/cm3

371ºC at 760mmHg

145ºC

178.2ºC

3.786

0

4

7

20

304

0

Cl.O=C(C)OC1C(C)=CC(OCCN(C)C)=C(C(C)C)C=1

IPWGSXZCDPTDEH-UHFFFAOYSA-N

InChI=1S/C16H25NO3.ClH/c1-11(2)14-10-15(20-13(4)18)12(3)9-16(14)19-8-7-17(5)6;/h9-11H,7-8H2,1-6H3;1H

[4-[2-(dimethylamino)ethoxy]-2-methyl-5-propan-2-ylphenyl] acetate;hydrochloride

Arlitene; Carlytene; Enfrental; Limatene; M-101; Moxilite; Enfrental; Limatene; M-101; Moxilite; Moxisylyte HCl; Moxisylyte hydrochloride; Opilon

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO: 20~63 mg/mL (63.3~199.5 mM)

Solubility in Formulation 1: ≥ 2 mg/mL (6.33 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 20.0 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.

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Solubility in Formulation 2: ≥ 2 mg/mL (6.33 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 20.0 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.

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Solubility in Formulation 3: ≥ 2 mg/mL (6.33 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (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 20.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: 100 mg/mL (316.62 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)