The Perfect Drug
Depression causes sleep and eating disorders and deficiencies in cognition and energy, associated with thoughts of guilt, worthlessness, and suicide. Antidepressants are routinely among the three most widely prescribed types of medicines in the United States, according to the Centers for Disease Control and Prevention (Katzung, 2017). This essay discusses the “perfect drug,” an antidepressant named Xarapine, that has reduced adverse effects like increased tendency to cause suicide, headache, and insomnia.
Basic Pharmacology of the Antidepressant
Though xarapine a selective serotonin reuptake inhibitor (SSRI), it has reduced side effects, making it the drug of choice for the management of major depressive disorder (MDD). Its primary mode of action is the serotonin transporter’s inhibition, which makes it ideal for treating pain disorders such as neuropathies and fibromyalgia. The drug binds the serotonin and norepinephrine transporters, but unlike the normal SSRI, it does not have much affinity for other receptors (Katzung, 2017). It has venlafaxine and desvenlafaxine, which are bicyclic compounds compared to duloxetine present in tricyclic antidepressants.
Antidepressants have numerous pharmacokinetic characteristics, with the majority exhibiting relatively quick oral absorption. Most drugs, such as Xarapine, reach peak plasma levels in 2-3 hours and are strongly linked to plasma proteins (Davies & Read, 2019). The active product of xarapine metabolism is norxarapine, which has a higher intracellular concentration than xarapine. The excretion half-life of norxarapine is about three times that of xarapine, contributing to the prolonged half-life of all SSRIs. Xarapine is a potent inhibitor of the CYP2D6 isoenzyme, which increases the possibility of interactions with other drugs.
All currently available antidepressants enhance monoamine neurotransmission, with the most common mechanism being inhibition of serotonin and norepinephrine transporters activities. The wide availability of monoamines for binding in the neuromuscular junction causes a chain reaction of events that promotes the transcription of some proteins while inhibiting the expression of others (Luethi et al., 2019). SSRIs, such as Xarapine, block the transporter by attaching to the serotonin transporter (SERT) receptor at a location other than the serotonin binding site; at therapeutic levels, around 80% of the active transporter is inhibited, as is explained by Luethi.
Xarapine inhibits serotonin reabsorption (reuptake) into neurons, increasing the availability of serotonin, which promotes neuronal communication. The 5-HT1A receptor on the somatodendritic portion of the raphe nuclei serotonergic neuron is an instance of an autoreceptor. This autoreceptor activation is by serotonin excess, which slows the activation level of this neuron’s action potentials “negative feedback loop” (Gould, Zarate, and Thompson, 2019). Unlike tricyclic and selective norepinephrine antidepressants, xarapine has only little effect on other neurotransmitters.
Clinical Effects on Users
As previously stated, Xarapine can be used to manage major depressive disorder in people with depression since it produces remission of all symptoms. Xarapine inhibits serotonin reabsorption (reuptake) into neurons. This increases the availability of serotonin, which promotes neuronal communication. Most medications do not provide their full effectiveness until 1-2 months; however, Xarapine achieves remission in this time frame.
Although Xarapine is beneficial, it has some common side effects like every other antidepressant, which can be predictable from its potent inhibition of the SERT (Wichniak et al., 2017). Xarapine improves serotonergic tone throughout the body, not only in the brain. Nausea, gastrointestinal discomfort, diarrhea, and other gastrointestinal symptoms are frequently connected with increased stomach activity. Another side effect of Xarapine includes headaches and insomnia or hyper insomnia, though mildly affecting a small population.
A common and unfortunate consequence of MDD is suicide attempts; Xarapine can reduce the chances of suicide occurrence by 50% in patients deemed suicidal. Most cases of suicide from antidepressants are from arrhythmias induced from lethal overdosing (Hengartner and Plöderl, 2019). In addition, blood pressure abnormalities and anticholinergic symptoms, such as altered mental state and convulsions, are occasionally observed in overdose. Xarapine has a reduced cholinergic effect making it safe even on relatively higher doses.
Davies, J., & Read, J. (2019). A systematic review into the incidence, severity and duration of antidepressant withdrawal effects: are guidelines evidence-based? Addictive Behaviors, 97, 111-121. Web.
Gould, T. D., Zarate Jr, C. A., & Thompson, S. M. (2019). Molecular pharmacology and neurobiology of rapid-acting antidepressants. Annual Review of Pharmacology and Toxicology, 59, 213-236. Web.
Hengartner, M. P., & Plöderl, M. (2019). Newer-generation antidepressants and suicide risk in randomized controlled trials: A re-analysis of the FDA database. Psychotherapy and Psychosomatics, 88(4), 247-248. Web.
Katzung, B. G. (2017). Basic and clinical pharmacology 14th edition. McGraw Hill Professional.
Luethi, D., Widmer, R., Trachsel, D., Hoener, M. C., & Liechti, M. E. (2019). Monoamine receptor interaction profiles of 4-aryl-substituted 2, 5-dimethoxyphenethylamines (2C-BI derivatives). European Journal of Pharmacology, 855, 103-111. Web.
Wichniak, A., Wierzbicka, A., Walęcka, M., & Jernajczyk, W. (2017). Effects of antidepressants on sleep. Current Psychiatry Reports, 19(9), 1-7. Web.