Neuserone-OA: 5HT1A Ago-Allosteric Modulator Neurogenic
First-in-Class 5HT1A Positive Allosteric Modulator/Co-Agonist, Neurogenic & Acetylcholine Releaser
Research Indications for antidepressant, anxiolytic, pro-social, memory and cognition, neurogenic, and neuroprotectant research
Solution Format: 100mg/ml 5ml/10ml
13 Item Items
In Stock
Warning: Last items in stock!
Availability date:
Neuserone-OA 99%
Neuserone-OA: 5HT1A Ago-Allosteric Modulator Neurogenic
First-in-Class 5HT1A Positive Allosteric Modulator/Co-Agonist, Neurogenic & Acetylcholine Releaser
Research Indications for antidepressant, anxiolytic, pro-social, memory and cognition, neurogenic, and neuroprotectant research
Solution Format: 100mg/ml 5ml/10ml
Recipient :
* Required fields
or Cancel
Neuserone-OA: 5HT1A Ago-Allosteric Modulator
5HT1A Positive Allosteric Modulator/Co-Agonist, Neurogenic, & Acetylcholine Releaser
Per animal studies conducted within this novel first-in-class agent and discovered pathways the following have been demonstrated and theorized:
rapid-onset antidepressant effects
neurogenesis (hippocampal)
rapid-acting pronounced anxiolysis
potent pro-social efficacy
improves memory and cognition
potently enhance neuroplasticity
potently enhances memory acquisition and consolidation
neuroprotective positive effects on amyloid metabolism
potent Alzheimer's Disease efficacy
may display efficacy within schizophrenia, ADHD, and OCD related conditions
appears to inhibit weight gain
no adverse contraindicated pathways or notable adverse effects appear present
potential adverse effects include headaches, gastrointestinal discomfort
Neuserone-OA Future Human Clinical Trials as extrapolated from animal data:
Data indicates dose arms of 10mg and 15mg once or twice per day (q.d. or b.i.d.) for efficacy within the given indications. Intranasal administration within animal paradigms so assayed would appear to display a viability for dose administration via that route at 4mg once or twice per day (q.d. or b.i.d.).
Format of Supply for in vivo animal research:
500mg Neuserone-OA supplied as a 125mg/ml 4ml solution in special carrier that separates. Swirl to form a coherent miscible suspension before drawing for research. Note, the main active is fully in solution and will be within any dilution as so noted using appropriate dilutants. Dilute as desired with water, glycerine, alcohol, or any combination thereof. Though not essential, glycerine is recommended to be added to hold the full miscible suspension of the carrier mixture for a longer duration after swirling.
USAGE: For Research Use Only! Not For Use in Humans.
Adjunct Potentials: SNRB-OX, Exetamine-OA, et al.
Glutamatergic neurotransmission has been implicated in affective disorders, possibly through the modulation of monoaminergic mechanisms. The aim of this study was to investigate the effect of coadministration of the noncompetitive NMDA antagonist dizocilpine (MK-801) with different, primarily noradrenergic and serotonergic antidepressants on forced swimming test (FST) and open-field behavior in rats. Acute administration of dizocilpine at doses of 0.02- 0.1 mg/kg did not show any effect in the open-field test or FST. Acute administration of citalopram (5 mg/kg), fluoxetine (20 mg/kg), desipramine (20 mg/kg) and maprotiline (20 mg/kg) did not influence FST, although coadministration of dizocilpine with serotonergic but not noradrenergic antidepressants caused a significant reduction of immobility. In the open-field test, fluoxetine had no effect on horizontal activity but significantly reduced the number of rearings. The coadministration of dizocilpine with fluoxetine elicited significant horizontal locomotor activation and attenuated the effect of fluoxetine on vertical activity. The combined administration of other antidepressants with dizocilpine tended to increase horizontal activity similar to that recorded with fluoxetine plus dizocilpine, but these effects were not statistically significant. Thus, the present results indicated that the coadministration of serotonergic antidepressants with NMDA receptor antagonists may induce faster and more pronounced antidepressant activity when compared to treatment with antidepressants alone. In contrast, the NMDA antagonists did not potentiate the antidepressant-like effects of noradrenergic antidepressants.