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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

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$ 59.96


$ 85.65

  • 500mg
  • 1g

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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.

Methods Find Exp Clin Pharmacol. 2010 Mar;32(2):123-8. doi: 10.1358/mf.2010.32.2.1481727.

The effect of the NMDA receptor antagonist dizocilpine on behavioral manifestations of serotonin and adrenergic antidepressants in rats.


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.