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Trade name:-
Specifications:25mg (calculated as C17H27NO2)；50mg (calculated as C17H27NO2)
Dosage form:tablet
* Please be kindly noted products are supplied for RLD supplies/ Reference listed drugs/ Comparator Drug Clinical trials. We do not sell to patients.
| Name | Venlafaxine Hydrochloride Tablets |
|---|---|
| Trade name | - |
| Specifications | 25mg (calculated as C17H27NO2)；50mg (calculated as C17H27NO2) |
| Dosage form | tablet |
| Licensee | Teva Pharmaceuticals USA Inc |
| Remarks | American Orange Book |
| Category | Reference Listed Drugs (RLDs) |
Flupirtine maleate is a selective neuronal potassium channel opener. It is a non-opioid analgesic that acts on the central nervous system and does not produce dependence and tolerance. Flupirtine maleate activates the G protein-coupled K+ channel on the nerve cell membrane, and K+ efflux stabilizes the resting membrane potential and reduces cell membrane activity; thereby indirectly inhibiting the activation of NMDA receptors. The therapeutic concentration of flupirtine maleate does not bind to α1, α2, 5HT1, 5HT2, dopamine, benzodiazepines, opioids, central M and N receptors. Flupirtine maleate has three main effects on the central nervous system: analgesia selectively opens the voltage-independent K+ channels of nerve cells, K+ outflows, resting membrane potential tends to stabilize, and neurons are not easily excited. This indirect antagonism to NMDA receptors reduces Ca2+ influx, and the sensitive effect caused by the increase in intracellular Ca2+ concentration is buffered. In this way, the nociceptive pain impulse conduction is inhibited when the neurons are excited. Muscle relaxation At therapeutic concentrations, the uptake of Ca2+ by mitochondria enhances the above-mentioned analgesic effect. This may be related to the muscle relaxation caused by the inhibition of the nerve impulse conduction of motor neurons and interneurons, but this muscle relaxation is mainly a decrease in muscle tone. Impact on pain prolongation (Chronificationprocesses) Pain prolongation is actually a nerve conduction disease caused by neuronal remodeling. Intracellular pathology induces the remodeling of neuronal function and strengthens the response to subsequent impulses through the so-called "wind-up" mechanism. NMDA receptors have a special significance (gene expression) for triggering this change. The indirect blockade of flupirtine maleate on NMDA receptors is an inhibitory effect that counteracts persistent pain. If the pain has persisted, then the stability of the cell membrane potential will gradually eliminate pain memories and reduce pain sensitivity.
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