Vicriviroc

A: Vicriviroc is a CCR5 antagonist, meaning it binds to the CCR5 receptor on the surface of CD4+ cells []. By doing so, it blocks the interaction between the HIV-1 envelope glycoprotein gp120 and CCR5, preventing viral entry into the cell [, , ].

A: The primary downstream effect is the inhibition of HIV-1 replication by preventing viral entry [, ]. Blocking CCR5 also inhibits the signaling cascade typically initiated by chemokine binding, potentially affecting immune cell migration and activation [, ].

A: The molecular formula of this compound is C27H39F3N6O2. Its molecular weight is 536.63 g/mol [].

A: Yes, studies have utilized various spectroscopic techniques to characterize this compound, including NMR spectroscopy and X-ray analysis. These studies have provided insights into the 3D properties and conformational behavior of the molecule, particularly concerning the arrangement at the planar amido function and the conformational preferences of the piperazine and piperidine rings [].

ANone: The provided research focuses primarily on this compound's biological activity and pharmacological properties. Therefore, detailed information regarding material compatibility and stability under various conditions is limited within these studies.

A: this compound acts as a receptor antagonist and does not exhibit catalytic properties []. Its primary mechanism involves competitive binding to the CCR5 receptor, inhibiting HIV-1 entry.

A: Yes, computational chemistry and modeling have been employed to understand the interactions of this compound with the CCR5 receptor []. Models have been developed to simulate the binding of this compound to the transmembrane domain of CCR5 and analyze its impact on receptor conformation and interaction with HIV-1 gp120 [].

A: Research has shown that even single amino acid substitutions in the V3 loop region of the HIV-1 envelope glycoprotein gp120 can significantly impact this compound resistance []. Specific mutations, such as K305R and K319T, have been linked to altered resistance and infectivity profiles [].

A: While specific stability data is limited within the provided research, it is known that this compound is metabolized primarily by the CYP3A4 enzyme system [, ]. Co-administration with CYP3A4 inhibitors or inducers may necessitate dose adjustments []. Formulation strategies, such as the development of intravaginal rings, have been explored to achieve sustained drug delivery and potentially improve bioavailability [].

ANone: The research primarily focuses on the scientific and clinical aspects of this compound. Detailed information regarding specific SHE regulations and compliance is not extensively discussed.

A: this compound exhibits good oral bioavailability and a long half-life, permitting once-daily dosing [, , , ]. It is primarily metabolized by the CYP3A4 enzyme system, necessitating dose adjustments when co-administered with CYP3A4 inhibitors or inducers [, , , ]. Studies in humans, monkeys, and rats reveal that the drug is metabolized through O-demethylation, N-dealkylation, oxidation, and glucuronidation [].

A: Studies have shown a correlation between higher this compound concentrations, particularly the minimum plasma concentration (Cmin), and a greater decrease in HIV-1 RNA levels []. Subjects with a Cmin above 54 ng/mL exhibited a significantly larger mean decrease in viral load compared to those with a lower Cmin []. This correlation suggests a concentration-dependent antiviral effect of this compound.

A: Yes, this compound has demonstrated potent antiviral activity in both in vitro and in vivo studies. In vitro, it effectively inhibits the replication of various HIV-1 isolates, including drug-resistant strains, and exhibits synergistic effects with other antiretroviral agents []. In clinical trials, this compound, when administered with a boosted protease inhibitor-containing regimen, significantly reduced HIV-1 RNA levels in treatment-experienced patients compared to placebo, with sustained efficacy observed over 48 weeks []. Furthermore, studies have explored its potential in treatment-naïve patients [, ].

A: Resistance to this compound primarily arises from mutations within the HIV-1 envelope glycoprotein, specifically the V3 loop region [, , , ]. These mutations can reduce the binding affinity of this compound to CCR5, thereby diminishing its antiviral activity.

A: Cross-resistance to other CCR5 antagonists, such as TAK-779, has been reported in HIV-1 isolates with reduced susceptibility to this compound []. This suggests that mutations conferring resistance to one CCR5 antagonist might confer resistance to others within the same class.

A: Research has investigated intravaginal rings containing this compound and MK-2048, a novel nucleoside reverse transcriptase translocation inhibitor, for sustained drug delivery to prevent HIV-1 infection []. This approach aims to achieve high drug concentrations in the vaginal mucosa while minimizing systemic exposure.

A: Liquid chromatography coupled with mass spectrometry (LC-MS) is a primary method used to identify and quantify this compound and its metabolites in biological samples []. This technique provides high sensitivity and selectivity for analyzing drug concentrations in various matrices.

ANone: The provided research focuses primarily on this compound's biological activity, pharmacology, and clinical effects. Therefore, information regarding environmental impact, dissolution/solubility, analytical method validation, alternatives, recycling/waste management, research infrastructure/resources, and related aspects is limited within these studies.

ANone: this compound emerged as part of the research effort to develop new antiretroviral therapies, specifically targeting the HIV-1 entry process. It represents a second-generation CCR5 antagonist, building upon earlier research on compounds like SCH-C. Despite its initial promise, this compound faced challenges in phase III clinical trials, leading to the discontinuation of its development as a treatment for HIV-1 infection. Nevertheless, the knowledge gained from this compound research has contributed to the understanding of HIV-1 entry mechanisms and the development of other antiretroviral drugs.

A: While the primary focus of this compound research has been on HIV-1 treatment, the knowledge gained has broader implications. For instance, understanding the role of CCR5 in viral entry and the mechanisms of CCR5 antagonist action can inform research on other viruses that utilize this receptor, such as some flaviviruses []. Additionally, this compound's effects on CCR5 signaling and immune cell migration could have implications for understanding and potentially treating inflammatory and autoimmune diseases.