Recent from talks
Desmethylselegiline
Knowledge base stats:
Talk channels stats:
Members stats:
Desmethylselegiline
Desmethylselegiline (DMS), also known as norselegiline or as N-propargyl-L-amphetamine, is an active metabolite of selegiline, a medication used in the treatment of Parkinson's disease and depression.
Like selegiline, DMS is a monoamine oxidase inhibitor (MAOI); specifically, it is a selective and irreversible inhibitor of monoamine oxidase B (MAO-B). In addition, it is a catecholaminergic activity enhancer (CAE) similarly to selegiline. The drug also produces levoamphetamine as an active metabolite, which is a norepinephrine–dopamine releasing agent with sympathomimetic and psychostimulant effects.
DMS has been studied much less extensively than selegiline and has not been developed or approved for medical use.
DMS is a monoamine oxidase inhibitor (MAOI), similarly to selegiline. It is specifically a selective and irreversible inhibitor of monoamine oxidase B (MAO-B). The compound is also a catecholaminergic activity enhancer (CAE) like selegiline. The potency of DMS as a CAE appears to be similar to that of selegiline.
Aside from being an active metabolite of selegiline, DMS itself has been studied clinically. A single 10 mg oral dose of DMS inhibited platelet MAO-B activity by 68 ± 16%, relative to 94 ± 9% with a single 10 mg dose of selegiline. Subsequently, platelet MAO-B activity returned to baseline after 2 weeks. Hence, although less potent than selegiline, DMS is also an effective MAO-B inhibitor.
DMS has been found to be 60-fold less potent than selegiline as an MAO-B inhibitor in vitro. However, it was only 3-fold less potent than selegiline orally in vivo in rats with repeated administration. In other research, DMS was 6-fold less potent than selegiline in inhibition of platelet MAO-B activity.
Selegiline produces levomethamphetamine and levoamphetamine as active metabolites, whereas DMS produces only levoamphetamine as a metabolite. Unlike DMS and selegiline, levoamphetamine and levomethamphetamine are not active as MAO-B inhibitors at concentrations up to 100 μM in vitro. However, levoamphetamine is a releaser of norepinephrine and dopamine and has sympathomimetic and psychostimulant effects. Similarly to selegiline, but unlike levoamphetamine and levomethamphetamine, DMS itself is not a monoamine releasing agent.
DMS shows neuroprotective, antioxidant, and antiapoptotic activity similarly to selegiline. DMS is more potent in some of these effects than selegiline. The neuroprotective and antioxidant properties of DMS and selegiline appear to be independent of MAO-B inhibition. Both selegiline and DMS have been found to bind to and inhibit glyceraldehyde-3-phosphate dehydrogenase (GAPDH), which may be involved in their neuroprotective effects.
Hub AI
Desmethylselegiline AI simulator
(@Desmethylselegiline_simulator)
Desmethylselegiline
Desmethylselegiline (DMS), also known as norselegiline or as N-propargyl-L-amphetamine, is an active metabolite of selegiline, a medication used in the treatment of Parkinson's disease and depression.
Like selegiline, DMS is a monoamine oxidase inhibitor (MAOI); specifically, it is a selective and irreversible inhibitor of monoamine oxidase B (MAO-B). In addition, it is a catecholaminergic activity enhancer (CAE) similarly to selegiline. The drug also produces levoamphetamine as an active metabolite, which is a norepinephrine–dopamine releasing agent with sympathomimetic and psychostimulant effects.
DMS has been studied much less extensively than selegiline and has not been developed or approved for medical use.
DMS is a monoamine oxidase inhibitor (MAOI), similarly to selegiline. It is specifically a selective and irreversible inhibitor of monoamine oxidase B (MAO-B). The compound is also a catecholaminergic activity enhancer (CAE) like selegiline. The potency of DMS as a CAE appears to be similar to that of selegiline.
Aside from being an active metabolite of selegiline, DMS itself has been studied clinically. A single 10 mg oral dose of DMS inhibited platelet MAO-B activity by 68 ± 16%, relative to 94 ± 9% with a single 10 mg dose of selegiline. Subsequently, platelet MAO-B activity returned to baseline after 2 weeks. Hence, although less potent than selegiline, DMS is also an effective MAO-B inhibitor.
DMS has been found to be 60-fold less potent than selegiline as an MAO-B inhibitor in vitro. However, it was only 3-fold less potent than selegiline orally in vivo in rats with repeated administration. In other research, DMS was 6-fold less potent than selegiline in inhibition of platelet MAO-B activity.
Selegiline produces levomethamphetamine and levoamphetamine as active metabolites, whereas DMS produces only levoamphetamine as a metabolite. Unlike DMS and selegiline, levoamphetamine and levomethamphetamine are not active as MAO-B inhibitors at concentrations up to 100 μM in vitro. However, levoamphetamine is a releaser of norepinephrine and dopamine and has sympathomimetic and psychostimulant effects. Similarly to selegiline, but unlike levoamphetamine and levomethamphetamine, DMS itself is not a monoamine releasing agent.
DMS shows neuroprotective, antioxidant, and antiapoptotic activity similarly to selegiline. DMS is more potent in some of these effects than selegiline. The neuroprotective and antioxidant properties of DMS and selegiline appear to be independent of MAO-B inhibition. Both selegiline and DMS have been found to bind to and inhibit glyceraldehyde-3-phosphate dehydrogenase (GAPDH), which may be involved in their neuroprotective effects.
Recent media