Einstepam: The Treatment of Depression

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Introduction

The modern world is burdened by several mental illnesses, with one of them being depression. Depression is a condition affecting people across all age groups, ethnicities and sex. The treatment and management of mild to severe major depressive episodes mainly entail the prescription of antidepressants. The treatment of depression has greatly revolutionized since the development of tricyclic antidepressants and monoamine oxidase inhibitors in the 1950s. This paper aims to comprehensively examine a hypothetical drug, Eistenpam, which is a more effective and safer version of the antidepressants that have been approved by the FDA.

Information about Its Origins

The treatment options for depression are centered on using antidepressant agents, most of which have monoaminergic-based targets. These include tricyclic antidepressants, selective serotonin reuptake inhibitors, monoamine oxidase inhibitors, and selective norepinephrine reuptake inhibitors. The positive effects of these agents are based on the inhibition of the metabolism or reuptake of monoaminergic neurotransmitters, such as norepinephrine, serotonin, and dopamine (Neis et al., 2015). Nevertheless, the efficacy of the drug treatment is limited because of the low remission rates, delayed onset of therapeutic effects, and increased treatment refractoriness. In several studies, the monoaminergic agents have been observed to have a time lag of two or more weeks before their therapeutic effects begin manifesting (Camargo & Rodrigues, 2019).

As a result, this demonstrated a greater need to develop a more effective antidepressant agent, which was ketamine. Ketamine, a glutamatergic agent, became a popular alternative that is fast-acting. Although glutamate is not a monoaminergic agent, early results indicated the presence of high glutamate plasma levels in patients diagnosed with mood disorders (Camargo & Rodrigues, 2019). This prompted the theory of the existence of an impaired relationship between synaptic plasticity and glutamatergic neurotransmission. Ketamine is a novel pharmacotherapeutic agent as its therapeutic effects have been seen to occur within 4 hours of use.

Regardless of its promising outcomes, the drug has its drawbacks; for instance, prolonged use leads to toxicity, and its oral bioavailability is low. Therefore, it is often administered intravenously (Camargo & Rodrigues, 2019). Consequentially, this triggered research of other compounds that might have a similar mechanism of action as ketamine, the rapid-acting antidepressant. Einstenpam, whose active compound is agmatine, was identified as the most promising as it is both rapid-acting and safer.

How It Is Used and What It Is Used For

Einstenpam is a glutamatergic agent used to treat depression, anxiety, and other related conditions. It will be administered orally. According to Freitas, Neis, and Rodrigues (2016), oral agmatine has been comparatively more potent in treating stress and depression than conventional antidepressants. Furthermore, its effects are increased when co-administered at sub-effective doses (Camargo & Rodrigues, 2019).

How the Drug Works In the Body

Overall, as a rapid-acting antidepressant, Einstenpam’s mechanism of action is based on its ability to inhibit NMDA receptors and isoforms of NOS in the brain (Camargo & Rodrigues, 2019). Specifically, this begins with the antagonism of the N-methyl-D-aspartate (NMDA) receptors in GABAergic interneurons. This prevents the inhibitory actions of the system on the glutamatergic tonus. Consequentially, the glutamatergic neurons secrete glutamate in the synaptic cleft that activates the alpha-amino-3-hydroxy-methyl-5-4-isoxazole proponoic acid (AMPA) receptors. In turn, the stimulation of AMPA receptors triggers the transient influx of sodium ions that causes cell depolarization and activates the voltage-dependent calcium gated channels. This stimulates the exocytosis of synaptic vesicles containing the brain-derived neurotrophic factor from the synaptic cleft, thereby activating the tropomyosin receptor kinase B.

A sequence of events is triggered, which finally culminate into the activation of mTOR. mTOR regulates the translation of several proteins, facilitating synaptogenesis and the formation of new dendritic spines. This results in an overall antidepressant effect.

The Effects of the Body and Brain

Agmatine, the primary ingredient in Einstenpam, is synthesized from L-arginine in a reaction catalyzed by arginine decarboxylase. The agent is widely distributed in mammalian tissues. In the central nervous system, it is mainly present in the cytoplasm of the neuronal network in the forebrain and rostral brainstem. In the brain, it inhibits the NMDA receptors and isoforms of NOS. Nonetheless, it remains unclear how the brain neurochemistry is altered in response to Einstepam treatment (Bergin et al., 2019). On the other hand, its effects on other parts of the body are vast and varied.

For instance, agmatine protects the retinal ganglion cells in the eyes from apoptosis. In the stomach, it buffers the pH; hence, it helps to prevent the hydrochloric acid from damaging the parietal cells as it has relatively strong alkalinity. Furthermore, in the kidney, it can enhance the glomerular filtration rate, which might be attributed to the activation of I2 imidazoline receptors. Lastly, the drug does not affect the male sex organs; therefore, it has no potential to cause sexual dysfunction. This is because it interacts with the alpha-2A receptors in the ductus deferens at both the pre and post-synaptic levels resulting in electricity-induced twitches.

Course of Treatment for This Drug

Since administering Einstepam has not been associated with any impacts on its efficacy, the course of treatment is straightforward. Patients will be given the recommended doses in which they are to take for a specific duration, either short or extended, until the mental illness is managed. Furthermore, the dosage is stable as the therapeutic effects of the drug begin manifesting in a period as short as four hours.

Costs to the Consumer

Unlike ketamine, which is expensive due to the fact that it can only be administered intravenously and received in a ketamine-certified treatment facility, Einstepam has shown oral efficacy (Neis et al., 2015). Therefore, it does not require the tablets to be taken in a certified facility, which lessens the costs in terms of treatment and time.

Potential Risks and Benefits

As a therapy, Einstepam treatment is regarded as relatively safe as it has not been associated with any toxicity nor adverse effects. The efficacy of Einstenpam is influenced by the traditional pharmaceutical antidepressants, including Wellbutrin and SSRIs (Freitas et al., 2016). Wellbutrin reduces its concentration while SSRI drugs do the vice versa. Therefore, caution should be taken when using Einstenpam in combination with other antidepressants. However, some of the probable side effects are nausea, stomach upset, and diarrhea.

Long term use contraindications

Empirical evidence has indicated no apparent adverse effects on behavior or signs of toxicity (Bergin et al., 2019). In a clinical experiment, no adverse effects of agmatine sulfate administered to several patients at a high daily dose of 2,670 mg for five years were reported (Bergin et al., 2019). Overall, it has not been associated with physical dependence, abuse, and tolerance.

Restrictions

It is not advisable to combine Einstepam with alcohol. Moreover, special precautions should be taken when administered to lactating and pregnant women. Diabetic patients should also be monitored as Einstepam can lower blood sugar levels.

Conclusion

Einstepam is a new drug that appears promising in terms of safety and efficacy in treating depression, anxiety, and other related mood disorders, compared to the monoaminergic-based agents and glutamatergic agents, such as ketamine. This is because of its high emission rates, limited adverse effects, early onset of therapeutic effects, and the relatively low treatment cost. The drug acts by inhibiting the NMDA receptors and isoforms of NOS in the brain from inducing antidepressant effects. Nevertheless, its impact on lactating and pregnant mothers should be further evaluated as they are a highly vulnerable population.

References

Bergin, D.H., Jing, Y., Williams, G., Mockett, B., Hu, Z., Abraham, C., & Liu, P. (2019). Safety and neurochemical profiles of acute and sub-chronic oral treatment with agmatine sulfate. Scientific Reports, 9(1), 1-33. Web.

Camargo, A., & Rodrigues, A. (2019). Novel targets for fast antidepressant responses: Possible role of endogenous neuromodulators. Psychology and Counselling, 3, 1-13. Web.

Freitas, A., Neis, V., & Rodrigues, A. (2016). Agmatine, a potential novel therapeutic strategy for depression. European Neurpsychopharmacology, 26, 1885-1899. Web.

Neis, V., Moretti, M., Manosso, L., Lopes, M., Leal, R., & Rodrigues, A. (2015). Agmatine enhances antidepressant potency of MK-801 and conventional antidepressants in mice. Pharmacology Biochemistry and Behavior, 130, 9-14. Web.

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