Sertraline

A: Sertraline is classified as a selective serotonin reuptake inhibitor (SSRI) [1-16]. It primarily acts by inhibiting the serotonin transporter (SERT), a protein responsible for removing serotonin from the synapse, the space between nerve cells [, ]. This inhibition leads to an increased concentration of serotonin in the synapse, enhancing serotonergic neurotransmission [1-3, 5, 16-20].

A: this compound has a molecular formula of C17H17Cl2N and a molecular weight of 306.23 g/mol [].

A: Yes, several studies utilize High-Performance Liquid Chromatography (HPLC) coupled with various detection methods, such as UV spectrophotometry and electron-capture detection, for the quantification of this compound and its metabolites in biological samples [, , , ]. These techniques rely on specific spectroscopic properties of this compound for detection and analysis.

ANone: this compound is not known to exhibit catalytic properties. As a pharmaceutical compound, its primary function is to modulate biological processes rather than catalyze chemical reactions.

A: While the provided research doesn't delve into specific computational studies, it highlights the importance of pharmacogenetic factors, such as CYP2D6*2 and CYP2C19 polymorphisms, in influencing this compound clearance []. This suggests the potential for applying computational approaches, like QSAR modeling and molecular docking simulations, to further understand this compound's interactions with its targets and predict its metabolic fate.

A: Although the provided research doesn't explicitly discuss this compound analogues, it emphasizes the stereoselective nature of its biological activity. One study describes the separation of its four stereoisomers, (1S, 4S)-, (1R, 4R)-, (1S, 4R)-, and (1R, 4S)-isomers, highlighting the importance of the (1S, 4S) configuration for therapeutic efficacy []. This suggests that even minor changes in this compound's three-dimensional structure can significantly affect its binding affinity to SERT and, consequently, its potency and selectivity.

A: One study investigated a novel Self-Micro Emulsifying Drug Delivery System (SMEDDS) for this compound hydrochloride []. This formulation approach aims to enhance the solubility and bioavailability of the drug, potentially leading to improved therapeutic outcomes.

ANone: The research papers primarily focus on the scientific and clinical aspects of this compound. Information on specific SHE regulations, compliance, and risk minimization practices is not discussed.

A: this compound is known to be slowly absorbed following oral administration, reaching peak plasma concentrations between 6 and 8 hours []. It exhibits high plasma protein binding (up to 97%) and undergoes extensive first-pass metabolism, primarily through demethylation to its active metabolite, N-desmethylthis compound []. Both this compound and N-desmethylthis compound are further metabolized through hydroxylation and conjugation, with a terminal elimination half-life of approximately 26 hours [].

A: Yes, genetic polymorphisms in drug-metabolizing enzymes significantly influence this compound clearance. For example, individuals carrying the CYP2D6*2 polymorphism exhibit a 23.1% decrease in this compound clearance compared to those without this polymorphism []. Similarly, patients with intermediate or poor CYP2C19 metabolizer phenotypes show reduced this compound clearance, requiring dose adjustments to achieve therapeutic levels [].

A: N-desmethylthis compound possesses pharmacological activity comparable to this compound, contributing to the drug's prolonged therapeutic effect [, , ]. The formation of this active metabolite is influenced by genetic variations in metabolizing enzymes, leading to interindividual differences in this compound's pharmacokinetic and pharmacodynamic profile [, ].

A: The forced swim test, a widely used preclinical model for assessing antidepressant activity, is frequently employed to evaluate this compound's effects on behavioral despair in rodents []. Studies have consistently shown that this compound significantly reduces immobility time in this test, indicating its potential to alleviate depressive symptoms [, ].

A: Numerous randomized controlled trials have demonstrated this compound's efficacy in treating major depressive disorder in various patient populations, including adults [, , , , , , ] and the elderly [, ]. These trials have shown that this compound effectively reduces depressive symptoms, as measured by validated scales like the Hamilton Depression Rating Scale (HAMD) and Clinical Global Impression (CGI) scales [, , , , , , , ].

A: While the provided research doesn't extensively cover resistance mechanisms, it highlights that a significant portion of patients with major depressive disorder do not achieve adequate response to SSRI monotherapy, including this compound [, , , , ]. Factors contributing to treatment resistance in depression are complex and multifaceted, potentially involving genetic variability in drug targets, altered neurotransmitter systems, and individual differences in disease pathophysiology [, , , , ].

ANone: The provided research primarily focuses on the therapeutic benefits and mechanisms of this compound. Detailed information regarding its toxicology, adverse effects, and safety profile, including potential long-term effects, is not discussed in these studies.

ANone: The research papers primarily focus on the pharmacological and clinical aspects of this compound. Specific details regarding these aspects are limited or not addressed within the provided research context.

A: The introduction of this compound and other SSRIs marked a significant milestone in the treatment of depression and other psychiatric disorders [1-3, 5, 8, 14, 16-20]. These drugs offered improved tolerability and a more favorable side effect profile compared to previous generations of antidepressants, such as tricyclic antidepressants and monoamine oxidase inhibitors [, , , ]. Research on this compound has also highlighted the importance of personalized medicine, as genetic variations in drug-metabolizing enzymes influence its pharmacokinetic profile, emphasizing the need for individualized treatment approaches to optimize efficacy and minimize adverse effects [].

A: The study of this compound exemplifies the collaborative nature of modern pharmaceutical research, involving expertise from pharmacology, medicinal chemistry, clinical medicine, neuroscience, and genetics [1-20]. For instance, understanding this compound's mechanism of action requires insights from pharmacology and neuroscience, while optimizing its formulation and delivery relies on collaborations between pharmaceutical scientists and medicinal chemists [, , , ]. Additionally, investigating the influence of genetic factors on this compound's pharmacokinetics and efficacy necessitates collaboration between geneticists and clinicians [, ]. These cross-disciplinary efforts are crucial for advancing our understanding of this compound's therapeutic potential and developing novel treatment strategies for depression and other mental health conditions.