Russia has produced a large number of strange psychotherapeutics with complex and poorly understood mechanisms of actions.
Is their design targeted towards these ligands or activities (like BDNF promotion, etc.) or do they just create a ton of these and test them on animals (or perhaps Ukrainians) and determine the activity. And the early use of psychiatric peptides seems either unnecessarily complex or very advanced.
Examples of compounds with such vague activities for instance are fabomotizole and mebicar but there are countless. Perhaps these weird russian drugs are designed to treat the unique sadness that only a cold Soviet winter can produce:
Fabomotizole
Its mechanism of action remains poorly defined however, with GABAergic, NGF- and BDNF-release-promoting, MT1 receptor agonism, MT3 receptor antagonism, and sigma agonism suggested as potential mechanisms. Fabomotizole was shown to inhibit MAO-A reversibly and there might be also some involvement with serotonin receptors.
Mebicar
Mebicar has an effect on the structure of limbic-reticular activity, particularly on hypothalamus emotional zone, as well as on all 4 basic neuromediator systems – γ aminobutyric acid (GABA), choline, serotonin and adrenergic activity. Mebicar decreases the brain noradrenaline level, exerts no effect on the dopaminergic systems, increases the brain serotonin level, and does not elicit cholinolytic action.[3]
*(This question came to me after i took 20mg of fabomotizole about an hour ago and it did seem to have definite anxiolytic activity, really damping down some amphetamine induced anxiety.)
Is their design targeted towards these ligands or activities (like BDNF promotion, etc.) or do they just create a ton of these and test them on animals (or perhaps Ukrainians) and determine the activity. And the early use of psychiatric peptides seems either unnecessarily complex or very advanced.
Examples of compounds with such vague activities for instance are fabomotizole and mebicar but there are countless. Perhaps these weird russian drugs are designed to treat the unique sadness that only a cold Soviet winter can produce:
Fabomotizole
Its mechanism of action remains poorly defined however, with GABAergic, NGF- and BDNF-release-promoting, MT1 receptor agonism, MT3 receptor antagonism, and sigma agonism suggested as potential mechanisms. Fabomotizole was shown to inhibit MAO-A reversibly and there might be also some involvement with serotonin receptors.
Mebicar
Mebicar has an effect on the structure of limbic-reticular activity, particularly on hypothalamus emotional zone, as well as on all 4 basic neuromediator systems – γ aminobutyric acid (GABA), choline, serotonin and adrenergic activity. Mebicar decreases the brain noradrenaline level, exerts no effect on the dopaminergic systems, increases the brain serotonin level, and does not elicit cholinolytic action.[3]
*(This question came to me after i took 20mg of fabomotizole about an hour ago and it did seem to have definite anxiolytic activity, really damping down some amphetamine induced anxiety.)
Last edited:
. Who knows what they mean by that, maybe they are referring to the TMN (tuberomammillary nucleus) or more likely the lateral hypothalamus and associated orexin system
