Oseltamivir

Q1: How does oseltamivir interact with its target and what are the downstream effects?

A1: this compound phosphate itself is a prodrug, meaning it is inactive until metabolized in the body. [, , ] It is converted by hepatic esterases into its active metabolite, this compound carboxylate. [] this compound carboxylate functions by selectively inhibiting neuraminidase, an enzyme crucial for the replication and release of influenza A and B viruses. [, , , ] By blocking neuraminidase, this compound prevents the release of newly formed viral particles from infected cells, thereby inhibiting the spread of the virus within the host. []

Q2: What is the molecular formula, weight, and available spectroscopic data for this compound?

A2: Unfortunately, the provided research papers do not delve into the specific spectroscopic characterization of this compound. While the molecular formula (C16H28N2O4) and weight (312.4 g/mol) are widely available in drug databases, the papers focus primarily on clinical and biological aspects rather than detailed spectroscopic analysis.

Q3: The provided research does not seem to cover aspects like material compatibility, catalytic properties, or computational studies of this compound. Why is that?

A3: You are right to point that out. The research focuses primarily on this compound's application as an antiviral drug. Therefore, aspects like material compatibility and stability, which are more relevant to material science, are not discussed. Similarly, this compound does not function as a catalyst, hence the lack of studies on catalytic properties. While computational chemistry could offer insights into this compound's interactions, the available research emphasizes experimental studies on its biological activity and pharmacokinetics.

Q4: How do structural modifications of this compound impact its activity, potency, and selectivity?

A4: Although the provided research doesn't focus on synthesizing this compound analogs, it highlights a crucial structure-activity relationship. The conversion of this compound phosphate to its active form, this compound carboxylate, is essential for its antiviral activity. [, , ] Studies demonstrate that mutations affecting the carboxylesterase 1 enzyme, responsible for this conversion, can significantly impair this compound's efficacy. [] This underscores the importance of the carboxylate moiety for the drug's interaction with neuraminidase and its subsequent antiviral effect.

Q5: Can you elaborate on the pharmacokinetics of this compound, including its absorption, distribution, metabolism, and excretion (ADME)?

A7: this compound is administered orally as a prodrug and is rapidly absorbed. [] It undergoes rapid conversion to its active metabolite, this compound carboxylate, primarily by hepatic esterases. [, ] this compound carboxylate demonstrates high bioavailability and is widely distributed in the body, reaching therapeutic concentrations in various sites, including the lungs. [, ] It is primarily eliminated renally, with dose adjustments recommended for patients with renal impairment. [, ]

Q6: What is the impact of co-administration of other drugs, such as probenecid, on this compound's pharmacokinetics?

A9: Research shows that co-administration with probenecid, a drug that inhibits renal tubular secretion, can increase plasma concentrations of this compound carboxylate. [] While this interaction may allow for reduced this compound doses, it could also increase the risk of drug interactions and potentially impact tolerability. []

Q7: What in vitro and in vivo models have been used to evaluate the efficacy of this compound against influenza viruses?

A10: Several studies utilized both in vitro and in vivo models to evaluate this compound's efficacy. In vitro studies often employed Madin-Darby canine kidney cells infected with various influenza A strains, including H1N1, H3N2, and H5N1 subtypes. [, , ] These studies measured parameters like viral titer reduction, inhibition of viral neuraminidase activity, and the emergence of drug resistance mutations. [, , ] In vivo studies predominantly used mouse models infected with different influenza A strains to assess this compound's therapeutic and prophylactic efficacy. [, , ] These studies typically monitored survival rates, body weight changes, lung viral titers, and the extent of lung damage as indicators of treatment effectiveness. [, , ]

Q8: Have there been any clinical trials evaluating the effectiveness of this compound in treating influenza in humans?

A11: Yes, numerous clinical trials have assessed this compound's effectiveness in treating influenza in humans. Many studies focused on its use in various populations, including adults, children, and specific high-risk groups like hospitalized patients. [, , , , , , , , , ] These trials assessed outcomes like time to alleviation of symptoms, reduction in viral shedding, incidence of influenza-related complications (e.g., pneumonia, otitis media), hospitalization rates, and mortality. [, , , , , , , , , ] The research emphasizes that early initiation of this compound treatment is crucial for maximizing its therapeutic benefits. []

Q9: What are the known mechanisms of resistance to this compound, and is there any evidence of cross-resistance with other antiviral drugs?

A12: A significant concern is the emergence of this compound resistance, primarily attributed to mutations in the viral neuraminidase gene. [, , , , ] The most prevalent mutation is H275Y, initially observed in seasonal H1N1 viruses and later identified in pandemic H1N1 2009 strains. [, , , ] This mutation alters the binding site of neuraminidase, reducing this compound's ability to inhibit the enzyme effectively. [] Research indicates that this compound-resistant strains can emerge both in vitro and in vivo, highlighting the potential for resistance development during treatment. [, ] Studies investigating other antiviral drugs, like amantadine and ribavirin, demonstrate that combinations of these drugs with this compound can exhibit synergistic effects against certain influenza strains. [, ] This suggests that combination therapy might be a viable strategy for combating the emergence of drug resistance. [, ]

Q10: Due to the focus on scientific aspects, the provided research excludes detailed information on toxicology, drug delivery strategies, and biomarkers related to this compound. Why is this information absent?

A10: The research primarily aims to provide insights into the scientific basis of this compound's action, focusing on its mechanism, efficacy, and resistance development. While understanding its toxicology, drug delivery, and biomarkers is crucial for clinical practice, these topics are beyond the scope of these specific research papers.

Q11: What analytical techniques are commonly employed to characterize and quantify this compound?

A14: Several analytical methods were employed throughout the research. High-performance liquid chromatography (HPLC) coupled with various detection methods, such as UV detection, was widely used to quantify this compound and its metabolite in biological samples. [] Genotyping assays, particularly real-time polymerase chain reaction (PCR) techniques, were utilized to identify specific mutations in the influenza virus genome associated with this compound resistance. [, , ] These techniques enabled researchers to track the emergence and spread of drug-resistant strains. [, , ]