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Asunaprevir

Asunaprevir is a direct-acting antiviral agent used in the treatment of chronic hepatitis C virus (HCV) infection.
It is a macrocyclic inhibitor that targets the HCV NS3/4A serine protease, a key enzyme required for viral replication.
Asunaprevir has demonstrated efficacy in clinical trials, particularly when used in combination with other antiviral drugs, in achieving sustained virologic response and clearing HCV infection.
Reasearch on optimizing Asunaprevir studies can be streamliuned using PubCompare.ai, which uses advanced analytics to identify the most effective products and procedures from literature, preprints, and patents.

Most cited protocols related to «Asunaprevir»

A total of 100 Japanese patients chronically infected with HCV genotype 1 were examined for HCV NS5A RAVs by PCR Invader Assay (BML, Tokyo, Japan) 17 . When less than 20% and equal to or more than 20% of HCV NS5A Y93 variants were detected, respectively, the existence of weakly positive and strongly positive RAVs was defined. Mutations at HCV NS5A L31 (L31M, 8; L31F, 1; L31V, 1) were detected in 10 patients (10%). HCV NS5A Y93H was strongly positive in 24 patients (24%), and HCV NS5A Y93H was weakly positive in 24 patients (24%). Finally, 32 of 100 patients (32%) were positive for L31M/F/V and/or strongly positive for Y93H.
The treatment with DCV plus ASV for 24 weeks was commenced for 54 of these 100 patients, and they were retrospectively followed up for at least 12 weeks between October 2014 and March 2016 at the Department of Gastroenterology, Chiba University Hospital (Figure 1). The 54 patients were eligible by meeting the following criteria: (1) infected with HCV genotype 1 alone, (2) age >20 years, (3) diagnosed as chronic hepatitis C, (4) negative for hepatitis B surface antigen, (5) negative for human immunodeficiency virus, (6) no decompensated cirrhosis, (7) no severe renal disease, (8) no severe heart disease, (9) no active drug users, (10) no pregnancy, and (11) no use of drugs having interaction with DCV or ASV.
Publication 2016
Biological Assay Drug Abuser Genotype Heart Diseases Hepatitis B Surface Antigens Hepatitis C, Chronic HIV Japanese Kidney Diseases Liver Cirrhosis Mutation Patients Pharmaceutical Preparations Pregnancy

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Publication 2016
A total of 259 patients were enrolled at 24 centers in Japan from January 5 2012 to March 30 2012. Eligible patients were men and women, 20 to 75 years of age, with chronic HCV genotype 1b infection, an HCV RNA level of 105 IU/mL or higher, with a body-mass index of 16 to 35 kg/m2, and, in up to 10% of enrolled patients, evidence of compensated cirrhosis (Child-Pugh A), as documented either by liver biopsy or discriminated by a previously described algorithm.14 (link)
Key exclusion criteria included evidence of hepatocellular carcinoma, coinfection with hepatitis B virus or human immunodeficiency virus, or previous exposure to inhibitors of NS5A or NS3 protease. Patients with alanine aminotransferase (ALT) of more than 5 times the upper limit of normal range, total bilirubin of 2 mg/dL or higher, an international normalized ratio of 1.7 or higher, an albumin level 3.5 g/dL or below, and a platelet count of less than 50,000/mm3 were also excluded.
Patients ineligible for interferon-based therapy, but potentially eligible for enrolment in this study, were treatment-naïve and considered poor candidates for interferon-based therapy because of medical complications including anemia, neutropenia, thrombocytopenia, depression, advanced age (≥65 years), or other conditions deemed not suitable for interferon-based therapy by the investigator, including hypertension, diabetes mellitus, autoimmune disease, and abnormal thyroid function. Patients intolerant to interferon-based therapy had received interferon-based therapy for less than 12 weeks and previously discontinued from therapy due to toxicities associated with interferon or ribavirin. Patients who were null or partial responders to previous peginterferon/ribavirin or interferon-beta/ribavirin therapy were defined as never having attained an undetectable HCV RNA level after at least 12 weeks of therapy. Null responders included patients who never attained at least a 2-log10 decrease from baseline in HCV RNA levels at week 12, and partial responders never achieved undetectable HCV RNA levels after 12 weeks of therapy.
Publication 2014
Alanine Transaminase Albumins Anemia Autoimmune Diseases Bilirubin Biopsy B virus, Hepatitis Child Chronic Infection Coinfection Diabetes Mellitus Genotype Hepatocellular Carcinomas High Blood Pressures HIV Index, Body Mass inhibitors Interferon, beta Interferons International Normalized Ratio Leukopenia Liver Liver Cirrhosis Patients Peptide Hydrolases Platelet Counts, Blood Ribavirin Therapeutics Thrombocytopenia Thyroid Diseases Woman
Patients were screened at 31 sites in Australia, France, Spain, the United Kingdom, and the United States (including Puerto Rico). Patients at least 18 years old (no upper limit) were eligible if they had chronic HCV GT1, 4, 5, or 6 infection with HCV RNA >1,000 IU/mL at screening. HCV genotype and subtype were assessed with the Versant HCV Genotype Inno LiPA Assay, version 2.0 or higher, or Sanger sequencing of the NS5B region if indeterminate initially by LiPA. Patients had to have past VF failure to an approved DAA‐containing regimen that included an NS5A inhibitor (limited to DCV, LDV, or ombitasvir [OBV]) and/or NS3/4A PI (limited to paritaprevir, simeprevir [SIM], asunaprevir, telaprevir, or boceprevir). NS5B inhibitors (SOF or dasabuvir [DSV]) could have been present in any past treatment regimen, and patients could have had failure to multiple past regimens. Patients with sequential exposures to multiple regimens (i.e., PI‐containing regimen followed by an NS5A inhibitor‐containing regimen) were considered to have past experience to both. Median time since patients' last previous VF is reported in the http://onlinelibrary.wiley.com/doi/10.1002/hep.29671/suppinfo. Patients could have compensated cirrhosis (Child‐Pugh score of 6 or less) or no cirrhosis. Absence of cirrhosis (e.g., METAVIR score ≤3, Ishak score ≤4) was determined by liver biopsy within 24 months before (or during) screening, transient elastography (TE; FibroScan) score of <12.5 kilopascals (kPa) within 6 months before (or during) screening, or a screening FibroTest score of ≤0.48 and an aspartate aminotransferase (AST) to platelet ratio index (APRI) <1. Presence of cirrhosis was determined by past histological diagnosis of cirrhosis on liver biopsy (e.g., METAVIR [or equivalent] score of >3 [including 3/4], Ishak score of >4), past TE (FibroScan) score of ≥14.6 kPa, or a screening FibroTest score of ≥0.75 and an APRI >2. Patients with indeterminate FibroScan were required to have liver biopsy and indeterminate FibroTest or conflicting FibroTest, and APRI scores were required to have TE or liver biopsy to determine cirrhosis status. Complete inclusion and exclusion criteria are included in http://onlinelibrary.wiley.com/doi/10.1002/hep.29671/suppinfo.
Publication 2018
Aspartate Transaminase asunaprevir Biological Assay Biopsy Blood Platelets boceprevir Child dasabuvir Diagnosis Elasticity Imaging Techniques Genotype inhibitors Liver Liver Cirrhosis ombitasvir paritaprevir Patients Simeprevir telaprevir Transients Treatment Protocols
SARS-CoV-2 (NCCP-43331) was provided by the National Culture Collection for Pathogens, South Korea. It was cultured in Vero E6 cells in a biosafety level 3 (BSL-3) facility, the Korea Zoonosis Research Institute, Jeonbuk National University. Viral stocks were prepared by propagation in Vero E6 cells in DMEM supplemented with 2% FBS, 1% penicillin-streptomycin, and HEPES (Invitrogen, USA). Viral titers were determined by the 50% tissue culture infectious dose (TCID50) assay.
Publication 2021
Biological Assay Cultured Cells HEPES Infection Pathogenicity Penicillins SARS-CoV-2 Streptomycin Tissues Vero Cells Zoonoses

Most recents protocols related to «Asunaprevir»

Rupintrivir (6414, Tocris or PZ0315, Sigma), lopinavir (7052, Tocris) and asunaprevir (HY-14434, MedChemExpress) were prepared as 20 mM solutions in DMSO. TNFα (300-01 A, PeproTech) was prepared as 1 μg/mL solution in FBS-free DMEM. Working solutions were prepared by serially diluting the stock solutions in FBS containing DMEM.
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Publication 2024
Patients with active HCV monoinfection or HCV-HIV coinfection demonstrated by positive serology and viral RNA plasma levels were enrolled in the study when starting DAA therapy. Patients were Caucasians, older than 18 years and were recruited from three third level hospitals of Northwest Spain. A number of demographic, epidemiological, laboratory and clinical data were obtained from the patients and from their electronic medical charts. All HCV-HIV-coinfected patients were receiving ART at the inclusion time. The DAA regimens used included NS5B inhibitors (sofosbuvir, dasabuvir), NS3/4A inhibitors (glecaprevir, paritaprevir, asunaprevir, grazoprevir, simeprevir) and NS5A inhibitors (velpatasvir, ledipasvir, daclatasvir, pibrentasvir, ombistavir, elbasvir) with or without ribavirin. DAA were selected according to the attending clinician criteria. LF was assessed by TE (Fibroscan) and by the noninvasive biochemical biomarkers APRI, Forns and FIB-4 at baseline and at the 1st, 3rd, 6th, 12th and 24th months.
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Publication 2024
Antivirus solution: According to the guidelines[16 ,18 (link)], the 309 patients were treated by experienced clinicians at or above the attending level with the following regimen: (1) Sofosbuvir 400 mg/d + daclatasvir 60 mg/d + ribavirin 1000 mg/d (12 wk) regimen (95 cases); (2) sofosbuvir 400 mg/d+ Velpatasvir 100 mg/d (12 wk) (60 cases); (3) sofosbuvir 400 mg/d+ ribavirin 1000 mg/d (12 wk) (57 cases); (4) Ombitasvir 300 mg/d+ dasabuvir 500 mg/d (12 wk) (44 cases); (5) sofosbuvir 400 mg/d+ ledipasvir 90 mg/d+ ribavirin 1000 mg/d (12 wk) regimen (22 cases); (6) Elbasvir and Grazoprevir 50 mg/d (12 wk) (17 cases); and (7) Dasabuvir 60 mg+ Asunaprevir 100 mg (24 wk) regimen (14 cases).
Non-antiviral treatment: Inclusion reasons: (1) Because some patients could not choose pegylated interferon (peg-IFN) + ribavirin due to decompensation of cirrhosis, and DAA drugs were not released in China before 2017; and (2) Some patients cannot choose the treatment due to the economic burden.
Patients without antiviral treatment were received the corresponding hepatoprotective treatment and symptomatic treatment.
Publication 2024
In Taiwan, patients with HCV infection receive DAA treatment through a nationwide government-funded program launched in 2017. All patients with HCV and proven active viremia, regardless of the duration and severity of liver disease, are eligible for DAA treatment, with the exception of patients with advanced- or terminal-stage disease or with a limited life expectancy of <6 months. As the availability of different DAAs evolved over time, the approved DAAs in Taiwan include daclatasvir/asunaprevir with or without ribavirin, ombitasvir/paritaprevir/ritonavir/dasabuvir with or without ribavirin, elbasvir/grazoprevir (Zepatier), glecaprevir/pibrentasvir (Maviret), and sofosbuvir-based (SOF-based) regimens including sofosbuvir + ribavirin, sofosbuvir/ledipasvir (Harvoni), and sofosbuvir/velpatasvir (Epclusa). The present retrospective cohort study included patients with HCV who received DAA treatment at the Chiayi or Yunlin branches of Chang Gung Memorial Hospital between 1 January 2017 and 31 October 2020. This study was approved by the Research Ethics Committee of Chang Gung Memorial Hospital and was conducted per the principles of the Declaration of Helsinki and the International Conference on Harmonization for Good Clinical Practice guidelines. Patients with confirmed sustained virologic response (SVR) and available body weight data at the start of DAA therapy and at 2 years after achieving SVR were included in this study. An SVR was defined as having an HCV RNA level below the lower limit of quantification at least 12 weeks after the end of DAA therapy. The study design is shown in Figure 1. Patients who discontinued DAA therapy, had no SVR, died during the follow-up period, or had no available body weight data were excluded from this study.
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Publication 2024
This retrospective multicenter cohort study conducted by the DAA Study in Hamamatsu group (DASH study group), involved 9 institutions (Hamamatsu University Hospital, Shimada General Medical Center, Seirei Hamamatsu General Hospital, Hamamatsu Medical Center, Iwata City Hospital, Shizuoka City Shizuoka Hospital, Minoru Medical Clinic, Tamakoshi Clinic, Elm Medical Clinic). The study was approved by the Ethics Committee of Hamamatsu University School of Medicine (approval number, 23-224). The study protocols conformed to the ethical guidelines of the Declaration of Helsinki. All patients provided written informed consent. Patients diagnosed with serogroup 1 chronic HCV infection who initiated IFN-free DAA regimens (DCV/ASV or sofosbuvir [SOF]/ledipasvir [LDV]) between August 2014 and December 2016 at nine affiliated institutions were enrolled. SVR was defined as absence of detectable HCV RNA at 24 weeks after treatment completion. No relapse of viremia was observed after 24 weeks in the patients who achieved SVR. Serum samples from healthy volunteers were also collected during the study period.
The exclusion criteria were as follows: (1) absence of sufficiently stored serum samples; (2) coinfection with either hepatitis B virus (HBV) or human immunodeficiency virus; (3) history of other chronic liver diseases (autoimmune hepatitis, primary biliary cholangitis, hemochromatosis, or Wilson’s disease); (4) history of HCC development at enrollment; (5) HCC development in the period up to 24 weeks after treatment completion, detected using ultrasonography (US), contrast-enhanced computed tomography (CT), or contrast-enhanced magnetic resonance imaging (MRI); (6) serum LOXL2 levels (see below) under the lower limit of quantification (LLQ). After exclusions, the data from 137 patients were retrospectively analyzed to identify risk factors for HCC development after achieving SVR (Fig. 4).

Study Flowchart Illustrating the Patient Selection Process. The development of HCC was studied in patients with HCV who achieved SVR via DAA therapy. Abbreviations: ASV, asunaprevir; DAA, direct-acting antiviral; DCV, daclatasvir; HBV, hepatitis B virus; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; LDV, ledipasvir; LLQ, lower limit of quantification; LOXL2, lysyl oxidase-like 2; SOF, sofosbuvir; SVR, sustained virological response.

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Publication 2024

Top products related to «Asunaprevir»

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Asunaprevir is a laboratory product manufactured by MedChemExpress. It is a synthetic organic compound used for research purposes.
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Asunaprevir is a laboratory product developed by Bristol-Myers Squibb. It is a protease inhibitor used in research and development applications.
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Grazoprevir is a laboratory compound used for research purposes. It functions as a hepatitis C virus (HCV) NS3/4A protease inhibitor.
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DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.
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Boceprevir is a small molecule compound developed for pharmaceutical research purposes. It functions as a protease inhibitor, specifically targeting the hepatitis C virus (HCV) NS3/4A serine protease. The core function of Boceprevir is to inhibit the enzymatic activity of the HCV NS3/4A protease, which is essential for viral replication.
Sourced in United States
Daclatasvir is a direct-acting antiviral agent used in the treatment of chronic hepatitis C virus (HCV) infection. It acts by inhibiting the HCV non-structural protein 5A (NS5A), which is essential for viral replication.
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Simeprevir is a laboratory product manufactured by MedChemExpress. It is a macrocyclic hepatitis C virus (HCV) NS3/4A protease inhibitor. The core function of Simeprevir is to inhibit the NS3/4A protease enzyme, which is essential for HCV replication.
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Sunvepra is a laboratory equipment product developed by Bristol-Myers Squibb. It is designed to perform specific functions in a research or testing environment. The core function of Sunvepra is to [CORE FUNCTION DESCRIPTION].
MK-5172 is a lab equipment product manufactured by MedChemExpress. It is a chemical compound used for research and development purposes. The core function of MK-5172 is to serve as a tool for scientific investigation, without any interpretation or extrapolation on its intended use.
Danoprevir is a potent and selective inhibitor of the HCV NS3/4A serine protease. It is used as a research tool in the study of hepatitis C virus and its replication.

More about "Asunaprevir"

Asunaprevir is a direct-acting antiviral agent (DAA) used in the treatment of chronic hepatitis C virus (HCV) infection.
It works by targeting the HCV NS3/4A serine protease, a crucial enzyme required for viral replication.
Asunaprevir has demonstrated efficacy in clinical trials, particularly when used in combination with other antiviral drugs like Grazoprevir, Boceprevir, Daclatasvir, Simeprevir, Sunvepra, MK-5172, and Danoprevir, in achieving sustained virologic response (SVR) and clearing HCV infection.
Optimizing Asunaprevir studies can be streamlined using PubCompare.ai, an advanced analytics platform that identifies the most effective products and procedures from literature, preprints, and patents.
This tool empowers researchers with data-driven insights, helping them locate the best reproducible protocols to enhance their Asunaprevir research.
When working with Asunaprevir, it's important to consider the use of DMSO (Dimethyl Sulfoxide) as a solvent, as it can improve the solubility and stability of the compound.
Researchers can leverage PubCompare.ai to compare different Asunaprevir formulations and protocols, ensuring they select the most effective and reproducible approach for their studies.
By utilizing the insights and capabilities provided by PubCompare.ai, researchers can streamline their Asunaprevir research, leading to more efficient and effective investigations that contribute to the understanding and optimization of this important antiviral agent.