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Grandaxin ® (Tofisopam) is a non-sedating anxiolytic drug with unique pharmacological action.
Tofisopam was first synthesized in 1966 in Hungary, and is successfully used for anxiety management since 1970’s.
As of today, Grandaxin is used in 15 countries across the world, including Russia, Japan, Hungary and the Czech Republic. Although this drug is not approved for use in the North America, its R-enantiomer is in stage II clinical trials for the treatment of irritable bowel syndrome.
Grandaxin is a benzodiazepine tranquilizer; however, its pharmacological action differs from that of typical benzodiazepine derivatives. Tofisopam belongs to the 2,3-benzodiazepines family, a unique class of psychoactive substances also known as homophthalazines. Unlike 1,4- benzodiazepine derivatives (e.g Diazepam), Tofisopam does not have sedative and anticonvulsant properties and is not habit-forming.
Grandaxin does not impair cognitive functions; moreover, it has a mild stimulant action and is able to potentiate the effect of dopaminergic stimulants.
Tofisopam has a complicated mechanism of action. It does not bind to benzodiazepine receptors and has a limited affinity to the peripheral benzodiazepine receptors, but shown to improve the binding of 1,4-benzodiazepines to their receptors.
The drug acts as a PDE inhibitor with highest affinity to PDE-4A1, PDE-10A1, PDE-3 and PDE-2A3 which can be responsible for its moderate antipsychotic action.
Several studies suggest that the behavioral effects of Grandaxin are likely to be mediated through its effect on dopaminergic and opioid neurotransmission. Tofisopam appears to increase the sensitivity of dopamine receptors and modulate opioid signal transduction in the brain without the danger of addiction.
Tofisopam may increase the plasma concentration of the drugs metabolized by CYP3A4. Does potentiate the effects of CNS depressants (e.g analgesics, anesthetics, antidepressants, H1-antihistamines, sedatives and antipsychotics).
Hepatic enzyme inducers (alcohol, nicotine, barbiturates, anticonvulsants) may enhance the metabolism of Tofisopam, thus decreasing its efficacy.
Some antifungal drugs (Ketoconazole, Itraconazole) may inhibit the metabolism of Tofisopam and increase its concentration in blood plasma.
Some antihypertensive drugs (Clonidine, calcium channel blockers) may potentiate the effect of Tofisopam. Beta-blockers may inhibit the metabolism of the drug without affecting its efficacy significantly.
Tofisopam may increase plasma levels of Digoxin.
Benzodiazepines may affect the anticoagulant effect of warfarin.
Long-term treatment with disulfiram may inhibit the metabolism of Tofisopam.
Antacids may affect the absorption of Tofisopam. Omeprazole and Cimetidine does inhibit the metabolism of Tofisopam.
Oral contraceptives may inhibit the metabolism of Tofisopam.
Tofisopam does decrease the depressant effect of alcohol on the central nervous system.