Buy Methaqualone Cas-72-44-6

Methaqualone is a sedative–hypnotic medication that was widely prescribed during the mid-20th century. It was marketed under various brand names, including Quaalude (/ˈkweɪluːd/ KWAY-lood) and Sopor, typically containing 300 mg of methaqualone per tablet. A combination drug known as Mandrax was sold primarily in Europe, containing 250 mg of methaqualone and 20 mg of diphenhydramine in a single tablet.

Methaqualone belongs to the quinazolinone class of compounds. Its commercial production was discontinued in many countries during the mid-1980s due to widespread misuse, addiction, and associated public health concerns.

Methaqualone’s sedative–hypnotic properties were first identified in 1955. It gained popularity during the 1960s and 1970s for the treatment of insomnia, and as a general sedative and muscle relaxant. However, due to its abuse potential, it was eventually withdrawn from medical use.

The drug was classified as pregnancy category D, meaning there was evidence of risk to the human fetus, and it was not recommended during pregnancy.^[2]

Like other GABAergic substances, prolonged use of methaqualone can lead to drug tolerance, physical dependence, and withdrawal symptoms upon cessation.^[3]

An overdose of methaqualone can lead to coma and death.^[4] Additional effects are delirium, convulsions, hypertonia, hyperreflexia, vomiting, kidney failure, and death through cardiac or respiratory arrest. Methaqualone overdose resembles barbiturate poisoning, but with increased motor difficulties and a lower incidence of cardiac or respiratory depression. The standard single tablet adult dose of Quaalude brand of methaqualone was 300 mg when made by Lemmon. A dose of 8000 mg is lethal and a dose as little as 2000 mg could induce a coma if taken with an alcoholic beverage.^[5]

Methaqualone acts primarily as a sedative, reducing anxiety and inducing sleep. It binds to GABA_A receptors, where it functions as a positive allosteric modulator at many receptor subtypes, enhancing the inhibitory effects of the neurotransmitter GABA. It shows negligible affinity for a wide array of other potential targets, including other receptors and neurotransmitter transporters.^[6] This action is similar to that of benzodiazepines like diazepam.

Unlike most benzodiazepines, however, methaqualone may also act as a negative allosteric modulator at certain GABA_A receptor subtypes, producing excitatory effects in neurons expressing those receptors. As such, methaqualone is considered a mixed GABA_A receptor modulator.^[6]

The binding site for methaqualone on the GABA_A receptor complex is distinct from those of benzodiazepines, barbiturates, and neurosteroids, though it may partially overlap with the etomidate binding site.^[6]

Methaqualone reaches peak plasma concentrations within a few hours of administration. Its elimination half-life ranges between 20 and 60 hours, contributing to its sedative effects and potential for accumulation with repeated dosing.