α1 adrenoceptor
Benoxathian HCl targets α1-adrenoceptors, where it acts as an antagonist. By blocking these receptors, it may cause vasodilation and a reduction in blood pressure. It has also been described as an acetylcholinesterase inhibitor, suggesting it may target the cholinergic system as well. This dual activity could have implications for neurological disorders.

In vitro, Benoxathian HCl is a selective α1-adrenoceptor antagonist. It has also been shown to inhibit acetylcholinesterase activity. Specific IC50 values for its activity at these targets are not provided in the available sources. Its activity is characterized in receptor binding and enzyme inhibition assays.

Benoxathian hydrochloride (10 nM; paraventricular nucleus injection) totally reverses 2.5, 5.0, or 10.0 mg/kg phenylpropanolamine (IP)-induced anorexia in rats [1].
In vivo, Benoxathian HCl has been studied for its potential antihypertensive effects. It may also have applications in researching anorexia. Specific in vivo data, such as efficacy in animal models, are not provided in the available sources.

A cell-free assay for Benoxathian HCl would involve measuring its inhibition of acetylcholinesterase or its binding affinity to α1-adrenoceptors. For acetylcholinesterase, the enzyme is incubated with a substrate (e.g., acetylthiocholine) in the presence of varying concentrations of the compound, and the rate of substrate hydrolysis is measured. For receptor binding, membrane preparations are incubated with a radiolabeled ligand and the compound.

Cellular assays for Benoxathian HCl would typically involve measuring its effects on α1-adrenoceptor-mediated signaling or acetylcholinesterase activity in cell lines. Cells expressing the receptors can be used to measure downstream signaling, such as calcium mobilization. Specific protocols are not detailed.

Microinjection of the alpha-1 adrenergic receptor antagonist benoxathian (0, 2.5, 5.0 or 10.0 nmol) into the PVN was found to have no effect on baseline feeding behavior. Microinjection of 10.0 nmol benoxathian into the PVN completely reversed the anorexia induced by 2.5, 5.0 or 10.0 mg/kg PPA (IP), yet did not alter the hypodipsia produced by PPA. These data strongly suggest that PPA anorexia is mediated by an alpha-1 adrenergic satiety mechanism within the PVN.[1]
In vivo animal experiments for Benoxathian HCl are not described in the available sources. As a research compound with potential antihypertensive and neurological applications, it could be evaluated in animal models of hypertension or Alzheimer's disease. However, no specific protocols are provided.

Benoxathian HCl is a small molecule with a molecular weight of 397.92. It is soluble in water. Specific pharmacokinetic parameters, such as half-life and bioavailability, are not provided in the available sources. T

oxicity data for Benoxathian HCl are not provided in the available sources. As a research compound, it is intended for research use only and not for human consumption. Standard laboratory safety precautions should be observed.

[1]. Wellman PJ, et al. Reversal of phenylpropanolamine anorexia in rats by the alpha-1 receptor antagonist benoxathian. Pharmacol Biochem Behav. 1991 Apr;38(4):905-8.

Adrenergic alpha receptor antagonists: These drugs bind to alpha adrenergic receptors without activating them, thus blocking the effects of endogenous or exogenous adrenergic agonists. Adrenergic alpha receptor antagonists are used to treat hypertension, vasospasm, peripheral vascular disease, shock, and pheochromocytoma. Antihypertensive drugs: These are drugs used to treat acute or chronic vascular hypertension, regardless of their pharmacological mechanism. Antihypertensive drugs include: diuretics (especially thiazide diuretics); adrenergic beta receptor antagonists; adrenergic alpha receptor antagonists; angiotensin-converting enzyme inhibitors; calcium channel blockers; ganglion blockers; and vasodilators. Phenylehrenololamine (PPA) is a phenethylamine anorexic drug that acts primarily as a direct agonist on alpha-1 adrenergic receptors and also possesses some alpha-2 adrenergic activity. Direct injection of PPA and the α1 receptor agonist 1-phenylephrine into the paraventricular nucleus (PVN) of rats inhibited feeding. This study aimed to verify whether systemic PPA inhibited feeding by acting on the α1 receptor population in the PVN. To this end, we performed unilateral PVN localization-guided cannulation in adult male rats. The results showed that microinjection of the α1 adrenergic receptor antagonist phenoxythiazide (0, 2.5, 5.0 or 10.0 nmol) into the PVN had no effect on the baseline feeding behavior of rats. Microinjection of 10.0 nmol of phenoxythiazide into the paraventricular nucleus (PVN) completely reversed the anorexia induced by 2.5, 5.0 or 10.0 mg/kg PPA (intraperitoneal injection), but did not change the PPA-induced reduction in water intake. These data strongly suggest that PPA-induced anorexia is mediated by an α-1 adrenergic satiety mechanism in the PVN. [1]
Benoxathian HCl (CAS: 92642-97-2) is a selective α1-adrenoceptor antagonist. It has also been described as an acetylcholinesterase inhibitor. It has been studied for its potential antihypertensive effects and for applications in neurological disorders such as Alzheimer's disease. Its molecular formula is C19H23NO4S·HCl and its molecular weight is 397.92. It is not an approved drug and is strictly for research purposes.

C19H23NO4S.HCL

397.91616

397.111

92642-97-2

10386130

Typically exists as solid at room temperature

500.7ºC at 760 mmHg

256.6ºC

4.418

2

6

8

26

374

0

COC1=C(C(=CC=C1)OC)OCCNCC2CSC3=CC=CC=C3O2.Cl

OWRADFDDJVNMGL-UHFFFAOYSA-N

InChI=1S/C19H23NO4S.ClH/c1-21-16-7-5-8-17(22-2)19(16)23-11-10-20-12-14-13-25-18-9-4-3-6-15(18)24-14;/h3-9,14,20H,10-13H2,1-2H3;1H

N-(2,3-dihydro-1,4-benzoxathiin-2-ylmethyl)-2-(2,6-dimethoxyphenoxy)ethanamine;hydrochloride

Benoxathian hydrochloride; 92642-97-2; Benoxathian HCl; Benoxathian (hydrochloride); BenoxathianHydrochloride; Benzoxathian hydrochloride; NIOSH/DM2930000; 2-[[[2-(2,6-Dimethoxyphenoxy)ethyl]-amino]-methyl]-1,4-benzoxathian hydrochloride;

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 : ~250 mg/mL (~628.27 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (5.23 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 20.8 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: ≥ 2.08 mg/mL (5.23 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 20.8 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: ≥ 2.08 mg/mL (5.23 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 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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