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Buy methoxetamine MXE is a recently synthesised arylcyclohexamine ketamine analogue postulated to be a N-methyl D-aspartate (NMDA) receptor antagonist and a dopamine reuptake inhibitor.
What Does Methoxetamine Look Like?
Like many other synthetics, it is usually sold as an odorless white powder. A quick internet search shows that this drug can be purchased from overseas manufacturers who claim that it is a “research chemical” that can legally be sold to anyone. Twenty-five grams can be ordered for less than $200 paid with bitcoin or Western Union money order.
why Buy methoxetamine MXE ?
MXE was designed in part in an attempt to avoid the urotoxicity associated with ketamine abuse; it was thought the compound’s increased potency and reduced dose would limit the accumulation of urotoxic metabolites in the bladder.Like ketamine, MXE has been found to produce bladder inflammation and fibrosis after high dose, chronic administration in mice (although the dosages used were quite large). Reports of urotoxicity in humans have yet to appear in the medical literature
A. Chemical Name
IUPAC Name: (RS)2-(3-methoxyphenyl)-2-(ethylamino)cyclohexanone
CA Index Name: N/A
B. Chemical Structure
- Molecular Formula: C15H21NO2
- Molecular Weight: 247.33 g/mol (Monoisotopic mass: 247.157)
- Melting point: 227-233°C (hydrochloride salt)
- Boiling point: 389,084°C at 760 mm Hg
The synthesis of methoxetamine was achieved by 4 steps through simple reactions involving an aromatic nitrile, a Grignard reagent, bromination, imine formation through reaction with a suitable amine, followed by the application of heat to the product to allow ring expansion of 1-[(ethylimino)(3-methoxyphenyl)methyl]-1- cyclopentanol.
c. Chemical description
Methoxetamine is an arylcyclohexylamine substance which shares some structural similarities to ketamine. In methoxetamine, the 2-chloro group on the phenyl ring and the N-methylamino group of ketamine have been replaced by a 3-methoxy and a N-ethylamino group respectively.
D. Chemical properties
Methoxetamine hydrochloride (salt) is soluble in organic solvents like ethanol (10mg/mL) at 25° C, DMSO (14 mg/mL) and dimethyl formamide (5 mg/mL) and in aqueous, nonorganic solvents like PBS (5 mg/mL).
E. Chemical identification
Hayes et al.4 reported the synthesis and analysis of MXE. They used NMR, FTIR and GC-MS to describe the structure of methoxetamine. In a factsheet of the Belgium Early Warning System reference is made to the identification and the analytical profile of methoxetamine using GC-MS, LC-MS and LC-MS/MS.
Roth et al. used the resources of the National Institute of Mental Health “Psychoactive Drug Screening Program” to obtain a neurochemical profile of methoxetamine and to compare it with those of ketamine and PCP. The results confirmed that methoxetamine has significant affinity for glutamate NMDA receptors. The pKi values for phencyclidine, ketamine and methoxetamine are 7.23 0.07, 6.18 0.07 and 6.59 0.06 respectively.
Interaction with the NMDA receptor is thought to be the key factor underlying the mechanism of action of ketamine, phencyclidine and other dissociative anaesthetics and may explain their psychotomimetic effects in human users.
Furthermore methoxetamine binds to the serotonin transporter (SERT) with a pKi of 6.32 0.05. Ketamine does not bind to the serotonin transporter. As the affinity of methoxetamine for SERT is quite similar to its affinity for the NMDA receptor, it is not unlikely that inhibition of SERT may contribute to both its psychopharmacological profile and the additional features seen in acute methoxetamine toxicity.
Routes of administration and dosage
Methoxetamine is generally administrated orally, by insufflation, or injected (both intramuscular and intravenously). Rectal and sublingual administration have also been reported.
So far there have only been two studies that have investigated the metabolism of methoxetamine. No studies have assessed other pharmacokinetic parameters such as absorption, distribution or excretion. By using their standard urine screening approaches Meyer et al.
could identify the phase I and II metabolites of methoxetamine in both rat and human urine. A total of eight metabolites were described allowing postulation of the following metabolic pathways: Ndeethylation, O demethylation, hydroxylation, as well as combinations hereof, followed
by glucuronidation or sulfation. The initial metabolic step in humans, the N deethylation,
was catalyzed by CYP2B6 and CYP3A4. Menzies et al. used human liver microsomal cell preparations and human urine in order to identify the phase I and II metabolites of methoxetamine.The following metabolites were described in the in vitro studies:
normethoxetamine, O-desmethylmethoxetamine, dihydromethoxetamine, dehydromethoxetamine and several structural isomers of hydroxymethoxetamine and hydroxynormethoxetamine.
Phase II glucuronide conjugates included those of Odesmethylmethoxetamine, O-desmethylnormethoxetamine and Odesmethylhydroxymethoxetamine.
In urine collected from three individuals presenting with acute methoxetamine toxicity the presence of the majority of these phase I and II metabolites was also confirmed. With the exception of the absence of the Odesmethylhydroxynormethoxetamine metabolite in all three of the patient urine samples.
This may be due to this metabolite being conjugated or to other factors such as the timing of the urine collection relative to methoxetamine consumption. There was also concordance in the Phase II metabolites between the in vitro and in vivo samples.
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