Side effects
The usual dose of 350 mg is unlikely to engender prominent side effects other than somnolence, and mild to significant euphoria or dysphoria, but the euphoria is generally short-lived due to the fast metabolism of carisoprodol into meprobamate and other metabolites; the euphoria derived is, according to new research, most likely due to carisoprodols inherent, potent anxiolytic effects that are far stronger than those produced by its primary metabolite, meprobamate, which is often misblamed for the drug-seeking associated with carisoprodol, as carisoprodol itself is responsible for the significantly more intense central nervous system effects than meprobamate alone. Carisoprodol has a qualitatively different set of effects to that of meprobamate (Miltown). The medication is well tolerated and without adverse effects in the majority of patients for whom it is indicated. In some patients, however, and/or early in therapy, carisoprodol can have the full spectrum of sedative side effects and can impair the patients ability to operate a firearm, motor vehicles, and other machinery of various types, especially when taken with medications containing alcohol, in which case an alternative medication would be considered. The intensity of the side effects of carisoprodol tends to lessen as therapy continues, as is the case with many other drugs.
As mentioned above, carisoprodol appears to have strong anxiolytic effects on its own; however, a large part of its effects also come from the fact that it is metabolized into meprobamate: at least a 25% of the carisoprodol administered will be transformed into meprobamate which means that meprobamate is 3.25× stronger than carisoprodol (although this rate varies from person to person according to their levels of CYP2C19 enzymes in their livers with some people having considerably higher levels) or, in other words, 200 mg of meprobamate (which is the lowest standard dose) is equivalent to 650 mg of carisoprodol. As such, meprobamate is believed to play a significant role in the effects of carisoprodol and meprobamates long half-life results in bioaccumulation following extended periods of carisoprodol administration. It is slightly soluble in water and freely soluble in ethanol, chloroform and acetone. The drugs solubility is practically independent of pH. History
On 1 June 1959, several American pharmacologists convened at Wayne State University in Detroit, Michigan to discuss a newly discovered structural analogue of meprobamate. The substitution of one hydrogen atom with an isopropyl group on one of the carbamyl nitrogens was intended to yield a drug with new pharmacological properties. It had been developed by Frank Berger at Wallace Laboratories and was named carisoprodol.Building on meprobamates pharmacological effects, carisoprodol was intended to have better muscle relaxing properties, less potential for addiction, and a lower risk of overdose.