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Daclatasvir (BMS790052; EBP883)

Alias: BMS-790052; Daclatasvir; BMS790052; Daclatasvir; 1009119-64-5; BMS-790,052; BMS790,052; EBP 883; Daclatasvir [USAN]; BMS 790,052; methyl N-[(2S)-1-[(2S)-2-[5-[4-[4-[2-[(2S)-1-[(2S)-2-(methoxycarbonylamino)-3-methylbutanoyl]pyrrolidin-2-yl]-1H-imidazol-5-yl]phenyl]phenyl]-1H-imidazol-2-yl]pyrrolidin-1-yl]-3-methyl-1-oxobutan-2-yl]carbamate; BMS 790052; EBP883; EBP 883; EBP-883; BMS 790052; Daclatasvir [USAN];Daklinza (trade name)
Cat No.:V0724 Purity: ≥98%
Daclatasvir (formerly BMS-790052; EBP-883; trade name Daklinza), adirect-acting antiviral agent, is aselective inhibitor of HCV NS5A (nonstructural protein) with an EC50 of 9-50 pM.
Daclatasvir (BMS790052; EBP883)
Daclatasvir (BMS790052; EBP883) Chemical Structure CAS No.: 1009119-64-5
Product category: HCV Protease
This product is for research use only, not for human use. We do not sell to patients.
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50mg
100mg
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Other Forms of Daclatasvir (BMS790052; EBP883):

  • Daclatasvir dihydrochloride
  • Daclatasvir-d6
Official Supplier of:
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Daclatasvir (formerly BMS-790052; EBP-883; trade name Daklinza), a direct-acting antiviral agent, is a selective inhibitor of HCV NS5A (nonstructural protein) with an EC50 of 9-50 pM. In order to treat hepatitis C (HCV), daclatasvir has been used in conjunction with sofosbuvir, another antiviral medication, to lower the levels of HCV RNA in the serum. 2014 saw the EU approve it after it was developed by BMS. The HCV nonstructural protein NS5A is inhibited by daclatasvir. According to a recent study, it targets two stages of the viral replication process, allowing HCV RNA to rapidly decline. Daclatasvir has been tested in combination regimens with ribavirin and pegylated interferon, as well as with other direct-acting antiviral medications like sofosbuvir and asunaprevir.

Biological Activity I Assay Protocols (From Reference)
Targets
HCV NS5A (EC50 = 9 pM-50 pM)
ln Vitro
BMS-790052 is among the strongest HCV replication inhibitors found to date. For HCV genotype 1a and 1b replicons, the mean EC50 values of BMS-790052 are 50 and 9 pM, respectively. BMS-790052 is inactive against a panel of 10 RNA and DNA viruses, with an EC50 greater than 10 μM, and exhibits a therapeutic index (CC50/EC50) of at least 105. This validates the HCV specificity of BMS-790052.[1] BMS-790052, with EC50 values ranging from 1 to 15 pM, inhibits both transient and stable HCV genome replication in Huh7 cells expressing the HCV genotype 1b replicons. It has been demonstrated that BMS-790052 (100 pM or 1 nM) modifies the subcellular localization and biochemical fractionation of NS5A.[2] With an EC50 of 7–13 pM, BMS-790052 suppresses hybrid replicons carrying HCV genotype–4 NS5A genes. In the hybrid replicons, residue 30 of NS5A plays a crucial role in BMS-790052-mediated resistance.[3]
ln Vivo
Humanized liver chimeric mice, with an estimated 40% chimeric liver, receive intravenous injections of 100 µL of human serum samples positive for HCV. Every one to four weeks following the vaccination, their blood is drawn from an external jugular vein. With a lower measurement range of 3.2 log IU/mL serum, the COBAS TaqMan HCV test measures the HCV RNA levels in 100-fold diluted serum. Once serum HCV RNA levels plateau, mice are given 40 mg/kg of Asunaprevir plus 30 mg/kg of Daclatasvir, 15 mg/kg of Ledipasvir plus 50 mg/kg of GS-558093, or 50 mg/kg of GS-558093 plus 400 mg/kg of Telaprevir orally once a day for four weeks.
In a randomized, double-blind, placebo-controlled, single ascending-dose study, Daclatasvir/BMS-790052 was administered at six dose levels to healthy, non-HCV-infected subjects over a range of 1 to 200 mg as an oral solution. The compound was safe and well tolerated up to 200 mg with no clinically relevant adverse effects. After oral administration, BMS-790052 was readily absorbed, with dose-proportional exposures over the studied dose range, and all subjects had drug concentrations greater than the protein-binding-adjusted EC90 for genotypes 1a and 1b, as measured in the replicon assay, at and beyond 24 h post-dose (Fig. 3). (The protein binding-adjusted EC90 figures were derived from an analysis of the effect of the addition of human serum on antiviral activity in replicons. In the presence of 40% human serum, the EC90 for BMS-790052 is 383 pM (0.28 ng ml-1) for the genotype 1a replicon and 49 pM (0.04 ng ml-1) for the genotyope 1b replicon.) [1]
In a randomized, double-blind, placebo-controlled, single ascending-dose study, Daclatasvir/BMS-790052 was administered to subjects with genotype 1 chronic HCV at doses of 1, 10 and 100 mg as an oral solution. All subjects were infected with HCV genotype 1a except for two subjects at 10 mg and three subjects at 100 mg who were infected with genotype 1b. BMS-790052 was safe and well tolerated in HCV-infected subjects after single oral doses up to 100 mg. Specifically, there were no deaths, serious adverse events, discontinuations due to adverse events or clinically relevant adverse effects. Headache was the most frequent adverse event, reported by four subjects after administration of BMS-790052. In HCV-infected subjects, BMS-790052 had a mean plasma elimination half-life ranging from 10 to 14 h, and plasma drug levels were similar to those in non-HCV-infected subjects. After single oral doses of 10–100 mg BMS-790052, all subjects had 24-h plasma concentrations above the tenfold protein binding-adjusted EC90 for HCV genotypes 1a and 1b, suggesting the possibility for once daily administration. The plasma HCV RNA levels were measured for up to 6 days after administration; the mean decline from the time of administration to 144 h post-dose is shown in Fig. 4. A single milligram dose of BMS-790052 produced a mean 1.8 log10 reduction (range 0.2–3.0 log10) in HCV viral load measured 24 h after drug administration. Both the 10 and 100 mg doses produced a greater antiviral effect, with mean plasma viral RNA falling by 3.2 log10 (range 2.9–4.0 log10) and 3.3 log10 (range 2.7–3.6 log10), respectively, at 24 h post-dose. Moreover, the 100 mg dose resulted in a mean maximal HCV RNA decline of 3.6 log10 (range 3.0–4.1 log10) and a prolonged antiviral response was observed in two subjects infected with genotype 1b virus, with an HCV RNA measurement that reached the lower limit of quantification (less than 25 IU ml-1) in one subject and 35 IU ml-1 in the other measured at hour 144. Genotypic analysis of samples taken at baseline (T0), 24 (T24) and 144 (T144) hours post-dose revealed that, in general, a marked reduction in viral load was required to detect major HCV variants. Substitutions were observed at amino-acid positions identified using the in vitro replicon system (Supplementary Tables 12–14): M28T, Q30H/R and L31M for genotype 1a, and Y93H for genotype 1b, results that suggest the usefulness of the replicon system for assessing resistance in response to inhibitor pressure in vivo. Follow-up samples were available for only one of these subjects, which revealed that HCV RNA had returned to near baseline; however, genotype analysis was not performed on this sample. As would be anticipated based on the in vitro replicon potency of BMS-790052, a greater and more sustained decline in HCV RNA was observed for subjects infected with genotype 1b (mean 3.6 log10 reduction (range 3.1–4.0 log10) and mean 3.1 log10 reduction (range 2.7–3.4 log10) in HCV viral load measured 24 h after a 10 and 100 mg dose, respectively) than for subjects infected with genotype 1a (mean 1.8 log10 reduction (range 0.2–3.0 log10), mean 2.9 log10 reduction (range 2.9–3.0 log10) and mean 3.6 log10 reduction (range 3.5–3.6 log10) in HCV viral load measured 24 h after a 1, 10 and 100 mg dose, respectively). The mean rates of decline for subjects who received 10 and 100 mg doses of BMS-790052 were similar up to 36 h after dosing, after which the mean decline was greater and more sustained in the subjects who received 100 mg. Subjects who received 1 mg of BMS-790052 had a lower mean decline in HCV RNA than subjects treated with 10 and 100 mg (Fig. 4). However, multiple-dose studies are needed to define the optimal dose range for maximal antiviral effect beyond the first phase of viral decline. The relationships between maximum decline from baseline in HCV RNA and drug pharmacokinetics exposures were explored using Pearson’s correlation coefficients. All estimated Pearson’s correlation coefficients were above 0.65, suggesting that the maximum declines in log10 HCV RNA and log pharmacokinetics exposures (BMS-790052 Cmax, AUC(0-T), AUC(INF), C12 and C24) were positively correlated; that is, that the maximum declines in log10 HCV RNA increase with the exposure to Daclatasvir/BMS-790052[1].
Enzyme Assay
The peptide (Ac-Asp-Glu-Asp [EDANS]-Glu-Glu-Abu-[COO] Ala-Ser-Lys [DABCYL]-NH2) contains a fluorescence donor {EDANS, 5-[(2-aminoethyl)amino]naphthalene-1-sulfonic acid} near one end of the peptide and an acceptor {DABCYL, 4-[(4-dimethylamino)phenyl]azo)benzoic acid} near the other end. Intermolecular resonance energy transfer between the donor and the acceptor quenches the fluorescence of the peptide, but as the NS3 protease cleaves the peptide, the products are released from resonance energy transfer quenching. The fluorescence of the donor increases over time as more substrate is cleaved by the NS3 protease. The assay reagent consists of 20 μM FRET peptide, 150 mM NaCl, and 5× luciferase cell culture lysis reagent diluted to 1× with dH2O. In a 96-well plate, HCV-Huh-7 cells are added and left to attach for the entire night (1×104 cells per well). The plate is incubated for 72 hours after BMS-790052 is added to the wells the following day. After that, the plate is cleaned with PBS and prepared for the FRET test by adding 30 μL of the previously mentioned FRET peptide assay reagent to each well. Signals are acquired by reading the plate in the kinetic mode with the Cytofluor 4000 instrument, which is programmed to operate in the automatic mode at 340 nm (excitation)/490 nm (emission) for 20 cycles or less. Once FRET is completed, each well is filled with 40 μL of luciferase substrate, and the amount of luciferase is evaluated.
Cell Assay
BMS-790052 is added to 96-well plates that have HCV replicon cells seeded in 200 µL media about 12 hours earlier.After being incubated for 72 hours, the cell plates are examined for cytotoxicity and replication activity. Following the measurement of cytotoxicity using CellTiter-Blue, the media and dye are removed, the plates are inverted, and the liquid that remains is blotted with paper towels. Renilla luciferase is used to measure the HCV genotype 1a cell lines' replication activity. After adding 1× Renilla luciferase lysis buffer (30 µL) to each well, the plates are incubated for 15 minutes with light shaking. The signals are then detected using a Top Count luminometer that is configured for light emission quantification after adding 40 µL of renilla luciferase substrate. The DMSO-only wells calculate 100% activity for each cell line; the average value for compound-containing wells is divided by the average value for DMSO-containing wells to determine the percentage activity for each inhibitor concentration.
Animal Protocol
At the termination of experiments, all mice were euthanized by CO2 inhalation. To evaluate in vivo efficacy of antiviral agents on HCV, NOD/SCID mice bearing HCV-replicating Huh7 xenografts were used21. Briefly, HCV RNA-transfected cells mixed with Matrigel were injected into the large lobes of the livers of anesthetized immunodeficient NOD/SCID male mice (5 weeks of age, 18–20 g body weight). Four weeks after implantation, compounds dissolved in saline were orally administered to mice using a feeding needle. Serum HCV titer was monitored by RT-qPCR.[Sci Rep. 2018 Aug 20;8(1):12469]
HCV-infected clinical study population [1]
In total, 16 subjects received treatment with Daclatasvir/BMS-790052 and two subjects received placebo. Subjects selected for this study included men and women aged 18–49 years, inclusive, who were chronically infected with HCV genotype 1 and were treatment naive or treatment non-responders, defined as subjects who received the current standard of care (interferon and/or ribavirin) and who continued to have a detectable HCV RNA level (including relapsers) or subjects who did not attain a 2 log10 decline in HCV RNA levels at 12 weeks and stopped treatment; or treatment-intolerant subjects, defined as subjects who were unable to tolerate the toxicities associated with interferon and/or ribavirin; and who had not received another NS5A replication co-factor inhibitor; and who were not co-infected with human immunodeficiency virus, hepatitis B virus or HCV other than genotype 1.
30 mg/kg; oral
Mice
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Studies demonstrated that peak plasma concentrations typically occurred within 2 hours after administration of multiple oral doses ranging from 1 - 100 mg once daily. Steady state is reached after approximately 4 days of once-daily daclatasvir administration. The absolute bioavailability of the tablet formulation is 67%.
Approximately 88% of total dose of daclatasvir is eliminated into bile and feces in which 53% remains as unchanged form, while 6.6% of the total dose is eliminated primarily unchanged in the urine.
The approximate volume of distribution of daclatasvir is 47 L in patients who was orally administered 60 mg tablet followed by 100 µg [13C,15N]-daclatasvir intravenously.
In subjects who received daclatasvir 60 mg tablet orally followed by 100 µg radiolabeled daclatasvir intravenously, the total clearance was 4.2 L/h.
Metabolism / Metabolites
Daclastavir is a substrate of CYP3A enzymes where its metabolism is predominantly mediated by CYP3A4 isoform. Oxidative pathways included δ-oxidation of the pyrrolidine moiety, resulting in ring opening to an aminoaldehyde intermediate followed by an intramolecular reaction between the aldehyde and the proximal imidazole nitrogen atom. High proportion of the drug in the plasma (greater than 97%) is in the unchanged form.
Biological Half-Life
Following multiple dose administration of daclatasvir in HCV-infected subjects, with doses ranging from 1 mg to 100 mg once daily, the terminal elimination half-life of daclatasvir ranged from approximately 12 to 15 hours.
Toxicity/Toxicokinetics
Hepatotoxicity
In large randomized controlled trials, daclatasvir was not associated with serum enzyme elevations during therapy. A difficulty in assessing side effects of daclatasvir and other anti-HCV agents, however, was that they are never used as monotherapy, but were also combined with agents active against other HCV targets, such as the viral protease (NS3) or polymerase (NS5B). Daclatasvir was also commonly used in combination with the more traditional agents used for hepatitis C, such as peginterferon and ribavirin, both of which have prominent adverse effects. In combination with asunaprevir (an HCV protease inhibitor), daclatasvir was associated with serum ALT elevations in 3% to 11% of patients and with several instances of acute hypersensitivity and hepatitis, some of which were severe. The cause of the hypersensitivity reaction, however, appeared to be asunaprevir. In combination with sofosbuvir, daclatasvir was not associated with serum enzyme elevations or with clinically apparent liver injury.
Daclatasvir has, however, been implicated in rare instances of acute decompensation of HCV related cirrhosis. The role of daclatasvir and the other HCV antivirals in this syndrome, however, was unclear. The liver injury usually arose within 2 to 6 weeks of starting therapy, but occasionally later and even after discontinuation of therapy. The injury was marked by worsening jaundice and signs of hepatic failure. In some instances, lactic acidosis was present early. In most but not all instances, the serum enzymes increased minimally if at all, despite the worsening hepatic failure. Several instances resulted in death or need for emergency liver transplantation. For this reason, it was recommended that patients with cirrhosis undergoing antiviral therapy with potent direct acting agents should be monitored carefully, particularly during the first few weeks of treatment.
Finally, reactivation of hepatitis B has occurred in rare patients being treated for chronic hepatitis C some of whom had received daclatasvir. The relationship of HBV reactivation to the antiviral treatment of HCV infection is not clear, but it may be due to clearance of HCV replication which allows HBV DNA levels to increase.
Likelihood score: C (probable rare cause of clinically apparent liver injury in patients with cirrhosis or preexisting hepatitis B virus coinfection).
Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Daclatasvir has been removed from the US market. It has not been studied in nursing mothers being treated for hepatitis C infection. Because it is 99% bound to maternal plasma proteins, amounts in breastmilk are likely to be very low. If daclatasvir used alone or in combination with sofosbuvir is required by the mother, it is not a reason to discontinue breastfeeding. Some sources recommend against breastfeeding when daclatasvir is used with ribavirin.
Hepatitis C is not transmitted through breastmilk and breastmilk has been shown to inactivate hepatitis C virus (HCV). However, the Centers for Disease Control recommends that mothers with HCV infection should consider abstaining from breastfeeding if their nipples are cracked or bleeding. It is not clear if this warning would apply to mothers who are being treated for hepatitis C.
Infants born to mothers with HCV infection should be tested for HCV infection; because maternal antibody is present for the first 18 months of life and before the infant mounts an immunologic response, nucleic acid testing is recommended.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.
Protein Binding
Daclatasvir is highly protein bound (99%).
References

[1]. Nature . 2010 May 6;465(7294):96-100.

[2]. Virology . 2011 May 25;414(1):10-8.

[3]. Antimicrob Agents Chemother . 2012 Mar;56(3):1588-90.

[4]. Antimicrob Agents Chemother . 2005 Apr;49(4):1346-53.

Additional Infomation
Pharmacodynamics
Daclatasvir is a direct-acting antiviral agent that targets the NS5A and causes a decrease in serum HCV RNA levels. It disrupts HCV replication by specifically inhibiting the critical functions of an NS5A protein in the replication complex. It is shown to cause downregulation of the hyperphosphorylation of NS5A. It does not appear to prolong the QT interval even when given at 3 times the maximum recommended dose.
The worldwide prevalence of chronic hepatitis C virus (HCV) infection is estimated to be approaching 200 million people. Current therapy relies upon a combination of pegylated interferon-alpha and ribavirin, a poorly tolerated regimen typically associated with less than 50% sustained virological response rate in those infected with genotype 1 virus. The development of direct-acting antiviral agents to treat HCV has focused predominantly on inhibitors of the viral enzymes NS3 protease and the RNA-dependent RNA polymerase NS5B. Here we describe the profile of BMS-790052, a small molecule inhibitor of the HCV NS5A protein that exhibits picomolar half-maximum effective concentrations (EC(50)) towards replicons expressing a broad range of HCV genotypes and the JFH-1 genotype 2a infectious virus in cell culture. In a phase I clinical trial in patients chronically infected with HCV, administration of a single 100-mg dose of BMS-790052 was associated with a 3.3 log(10) reduction in mean viral load measured 24 h post-dose that was sustained for an additional 120 h in two patients infected with genotype 1b virus. Genotypic analysis of samples taken at baseline, 24 and 144 h post-dose revealed that the major HCV variants observed had substitutions at amino-acid positions identified using the in vitro replicon system. These results provide the first clinical validation of an inhibitor of HCV NS5A, a protein with no known enzymatic function, as an approach to the suppression of virus replication that offers potential as part of a therapeutic regimen based on combinations of HCV inhibitors. [1]
The hepatitis C virus (HCV) non-structural (NS) 5A protein plays an essential role in the replication of the viral RNA by the membrane-associated replication complex (RC). Recently, a putative NS5A inhibitor, BMS-790052, exhibited the highest potency of any known anti-HCV compound in inhibiting HCV replication in vitro and showed a promising clinical effect in HCV-infected patients. The precise mechanism of action for this new class of potential anti-HCV therapeutics, however, is still unclear. In order to gain further insight into its mode of action, we sought to test the hypothesis that the antiviral effect of BMS-790052 might be mediated by interfering with the functional assembly of the HCV RC. We observed that BMS-790052 indeed altered the subcellular localization and biochemical fractionation of NS5A. Taken together, our data suggest that NS5A inhibitors such as BMS-790052 can suppress viral genome replication by altering the proper localization of NS5A into functional RCs.[2]
The antiviral profile of BMS-790052, a potent hepatitis C virus (HCV) replication complex inhibitor targeting nonstructural protein NS5A, is well characterized for HCV genotype-1. Here, we report that BMS-790052 inhibits hybrid replicons containing HCV genotype-4 NS5A genes with 50% effective concentrations (EC(50)s) ranging from 7 to 13 pM. NS5A residue 30 was an important site for BMS-790052-selected resistance in the hybrid replicons. Our results support the potential of BMS-790052 as a valuable component of combination therapy for HCV genotype-4 chronic infection.[3]
Daclatasvir is a member of the class of biphenyls that is a potent inhibitor of nonstructural protein 5A and is used (as its hydrochloride salt) for treatment of hepatitis C. It has a role as a nonstructural protein 5A inhibitor and an antiviral drug. It is a member of biphenyls, a member of imidazoles, a carbamate ester, a carboxamide and a valine derivative. It is a conjugate base of a daclatasvir(2+).
Daclatasvir is a direct-acting antiviral agent against Hepatitis C Virus (HCV) used for the treatment of chronic HCV genotype 1 and 3 infection. It is marketed under the name DAKLINZA and is contained in daily oral tablets as the hydrochloride salt form . Hepatitis C is an infectious liver disease caused by infection with Hepatitis C Virus (HCV). HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, and affecting 72% of all chronic HCV patients. Daclatasvir was the first drug with demonstrated safety and therapeutic efficacy in treating HCV genotype 3 without the need for co-administration of interferon or [DB00811]. It exerts its antiviral action by preventing RNA replication and virion assembly via binding to NS5A, a nonstructural phosphoprotein encoded by HCV. Binding to the N-terminus of the D1 domain of NS5A prevents its interaction with host cell proteins and membranes required for virion replication complex assembly. Daclatasvir is shown to target both the cis- and trans-acting functions of NS5A and disrupts the function of new HCV replication complexes by modulating the NS5A phosphorylation status. The most common critical NS5A amino acid substitutions that led to reduced susceptibility to daclatasvir therapy occured at position Q30 (Q30H/K/R) and M28 in genotype 1a patients and Y93H in genotype 3 patients. According to 2017 American Association for the Study of Liver Diseases (AASLD), 60mg of daclatasvir is recommended with 400mg [DB08934] for genotype 1a/b patients with or without cirrhosis as second-line therapy. The same dosing regimen can be used as first-line therapy in patients with genotype 3 without cirrhosis and second-line therapy in genotype 3 patients with compensated cirrhosis. Combination therapies that include daclatasir can be used for challenging-to-treat patients who have HIV-1 coinfection, advanced cirrhosis, or post-liver transplant recurrence of HCV. The therapy is intended to cure or achieve a sustained virologic response (SVR12), after 12 weeks of daily therapy. SVR and eradication of HCV infection is associated with significant long-term health benefits including reduced liver-related damage, improved quality of life, reduced incidence of Hepatocellular Carcinoma, and reduced all-cause mortality. Daclatasvir was FDA-approved in July 2015 for use with [DB08934] (Sovaldi) with or without [DB00811] to treat HCV genotype 1 and 3 infections. The SVR12 in HCV genotype 1a-infected treatment-naïve subjects without and with cirrhosis undergoing daclatasvir and [DB08934] therapy were 88% and 99%, respectively. The same dosing regimen in treatment-naïve patients with HCV genotype 3 infection with or without cirrhosis achieved SVR12 rates of 71% and 98%, respectively.
Daclatasvir is a Hepatitis C Virus NS5A Inhibitor. The mechanism of action of daclatasvir is as a P-Glycoprotein Inhibitor, and Organic Anion Transporting Polypeptide 1B1 Inhibitor, and Organic Anion Transporting Polypeptide 1B3 Inhibitor, and Breast Cancer Resistance Protein Inhibitor.
Daclatasvir is an orally available antiviral agent that inhibits the NS5A region of the hepatitis C virus (HCV) and was used in combination with other oral antiviral agents to treat chronic hepatitis C before its withdrawal in 2019. Elevations in serum enzyme levels during daclatasvir therapy are uncommon, and it has yet to be convincingly implicated in cases of idiosyncratic liver injury with jaundice. Nevertheless, successful all-oral regimens of antiviral therapy in patients with chronic hepatitis C and cirrhosis is occasionally complicated by hepatic decompensation and may cause reactivation of hepatitis B in susceptible patients coinfected with the hepatitis B virus (HBV).
Daclatasvir is an orally available inhibitor of the hepatitis C virus (HCV) non-structural protein 5A (NS5A) replication complex, with potential activity against HCV. Although the exact mechanism of action of daclatasvir has yet to be fully determined, this agent, upon oral administration and after intracellular uptake, appears to bind to domain I of the NS5A protein. This inhibits the activity of the NS5A protein and results in the disruption of the viral RNA replication complex, blockage of viral HCV RNA production, and inhibition of viral replication. NS5A, a zinc-binding and proline-rich hydrophilic phosphoprotein, plays a crucial role in HCV RNA replication. HCV is a small, enveloped, single-stranded RNA virus belonging to the Flaviviridae family.
DACLATASVIR is a small molecule drug with a maximum clinical trial phase of IV (across all indications) that was first approved in 2014 and is indicated for viral disease and chronic hepatitis c virus infection and has 7 investigational indications. This drug has a black box warning from the FDA.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C40H50N8O6
Molecular Weight
738.890
Exact Mass
738.385
Elemental Analysis
C, 65.02; H, 6.82; N, 15.17; O, 12.99
CAS #
1009119-64-5
Related CAS #
Daclatasvir dihydrochloride;1009119-65-6;Daclatasvir-d6;1801709-41-0;Daclatasvir-d16
PubChem CID
25154714
Appearance
Light yellow to yellow solid powder
Density
1.3±0.1 g/cm3
Boiling Point
1071.2±65.0 °C at 760 mmHg
Flash Point
601.7±34.3 °C
Vapour Pressure
0.0±0.3 mmHg at 25°C
Index of Refraction
1.595
LogP
5.44
Hydrogen Bond Donor Count
4
Hydrogen Bond Acceptor Count
8
Rotatable Bond Count
13
Heavy Atom Count
54
Complexity
1190
Defined Atom Stereocenter Count
4
SMILES
O=C([C@@H](NC(OC)=O)C(C)C)N1CCC[C@H]1C2=NC=C(N2)C3=CC=C(C=C3)C4=CC=C(C5=CN=C([C@@H]6CCCN6C([C@@H](NC(OC)=O)C(C)C)=O)N5)C=C4
InChi Key
FKRSSPOQAMALKA-CUPIEXAXSA-N
InChi Code
InChI=1S/C40H50N8O6/c1-23(2)33(45-39(51)53-5)37(49)47-19-7-9-31(47)35-41-21-29(43-35)27-15-11-25(12-16-27)26-13-17-28(18-14-26)30-22-42-36(44-30)32-10-8-20-48(32)38(50)34(24(3)4)46-40(52)54-6/h11-18,21-24,31-34H,7-10,19-20H2,1-6H3,(H,41,43)(H,42,44)(H,45,51)(H,46,52)/t31-,32-,33-,34-/m0/s1
Chemical Name
methyl N-[(2S)-1-[(2S)-2-[5-[4-[4-[2-[(2S)-1-[(2S)-2-(methoxycarbonylamino)-3-methylbutanoyl]pyrrolidin-2-yl]-1H-imidazol-5-yl]phenyl]phenyl]-1H-imidazol-2-yl]pyrrolidin-1-yl]-3-methyl-1-oxobutan-2-yl]carbamate dihydrochloride
Synonyms
BMS-790052; Daclatasvir; BMS790052; Daclatasvir; 1009119-64-5; BMS-790,052; BMS790,052; EBP 883; Daclatasvir [USAN]; BMS 790,052; methyl N-[(2S)-1-[(2S)-2-[5-[4-[4-[2-[(2S)-1-[(2S)-2-(methoxycarbonylamino)-3-methylbutanoyl]pyrrolidin-2-yl]-1H-imidazol-5-yl]phenyl]phenyl]-1H-imidazol-2-yl]pyrrolidin-1-yl]-3-methyl-1-oxobutan-2-yl]carbamate; BMS 790052; EBP883; EBP 883; EBP-883; BMS 790052; Daclatasvir [USAN];Daklinza (trade name)
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: ~148 mg/mL (~200.3 mM)
Water: <1 mg/mL
Ethanol: ~148 mg/mL (~200.3 mM)
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.5 mg/mL (3.38 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 2.5 mg/mL (3.38 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (3.38 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.


 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 1.3534 mL 6.7669 mL 13.5338 mL
5 mM 0.2707 mL 1.3534 mL 2.7068 mL
10 mM 0.1353 mL 0.6767 mL 1.3534 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

Calculator

Molarity Calculator allows you to calculate the mass, volume, and/or concentration required for a solution, as detailed below:

  • Calculate the Mass of a compound required to prepare a solution of known volume and concentration
  • Calculate the Volume of solution required to dissolve a compound of known mass to a desired concentration
  • Calculate the Concentration of a solution resulting from a known mass of compound in a specific volume
An example of molarity calculation using the molarity calculator is shown below:
What is the mass of compound required to make a 10 mM stock solution in 5 ml of DMSO given that the molecular weight of the compound is 350.26 g/mol?
  • Enter 350.26 in the Molecular Weight (MW) box
  • Enter 10 in the Concentration box and choose the correct unit (mM)
  • Enter 5 in the Volume box and choose the correct unit (mL)
  • Click the “Calculate” button
  • The answer of 17.513 mg appears in the Mass box. In a similar way, you may calculate the volume and concentration.

Dilution Calculator allows you to calculate how to dilute a stock solution of known concentrations. For example, you may Enter C1, C2 & V2 to calculate V1, as detailed below:

What volume of a given 10 mM stock solution is required to make 25 ml of a 25 μM solution?
Using the equation C1V1 = C2V2, where C1=10 mM, C2=25 μM, V2=25 ml and V1 is the unknown:
  • Enter 10 into the Concentration (Start) box and choose the correct unit (mM)
  • Enter 25 into the Concentration (End) box and select the correct unit (mM)
  • Enter 25 into the Volume (End) box and choose the correct unit (mL)
  • Click the “Calculate” button
  • The answer of 62.5 μL (0.1 ml) appears in the Volume (Start) box
g/mol

Molecular Weight Calculator allows you to calculate the molar mass and elemental composition of a compound, as detailed below:

Note: Chemical formula is case sensitive: C12H18N3O4  c12h18n3o4
Instructions to calculate molar mass (molecular weight) of a chemical compound:
  • To calculate molar mass of a chemical compound, please enter the chemical/molecular formula and click the “Calculate’ button.
Definitions of molecular mass, molecular weight, molar mass and molar weight:
  • Molecular mass (or molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
  • Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.
/

Reconstitution Calculator allows you to calculate the volume of solvent required to reconstitute your vial.

  • Enter the mass of the reagent and the desired reconstitution concentration as well as the correct units
  • Click the “Calculate” button
  • The answer appears in the Volume (to add to vial) box
In vivo Formulation Calculator (Clear solution)
Step 1: Enter information below (Recommended: An additional animal to make allowance for loss during the experiment)
Step 2: Enter in vivo formulation (This is only a calculator, not the exact formulation for a specific product. Please contact us first if there is no in vivo formulation in the solubility section.)
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+
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Calculation results

Working concentration mg/mL;

Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
             (2) Be sure to add the solvent(s) in order.

Clinical Trial Information
Antiviral Agents Against COVID-19 Infection
CTID: NCT04468087
Phase: Phase 2/Phase 3    Status: Completed
Date: 2024-03-22
Safety and Efficacy of Sofosbuvir-Based Regimens in the Treatment of Egyptian Patients With Hepatitis C Infection
CTID: NCT02992457
Phase: Phase 4    Status: Completed
Date: 2023-08-25
Efficacy and Safety Study of Pegylated Interferon Lambda-1a With Ribavirin and Daclatasvir, to Treat naïve Subjects With Chronic HCV Genotypes 1, 2, 3, and 4 Who Are Co-infected With HIV
CTID: NCT01866930
Phase: Phase 3    Status: Terminated
Date: 2023-06-13
Sofosbuvir, Daclatasvir, Ribavirin for Hepatitis C Virus (HCV) Cirrhotics
CTID: NCT02596880
Phase: Phase 3    Status: Completed
Date: 2023-04-20
Effect of New Oral Treatment for Hepatitis C Virus on Seminal Parameters
CTID: NCT05616598
Phase: Phase 2/Phase 3    Status: Completed
Date: 2023-02-08
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Efficacy and Safety of Therapy Against HCV Based on Direct-acting Antivirals in Real-life Conditions
CTID: NCT02333292
Phase:    Status: Completed
Date: 2022-06-29


Study to Evaluate the Safety and PK of Elpida® in Healthy Subjects and Patients With Hepatic Impairment and to Assess the Impact of Food Intake and Drug-Drug Interactions With Other Antiviral Drugs
CTID: NCT03706898
Phase: Phase 1    Status: Completed
Date: 2022-01-11
A Study Comparing Efficacy and Safety of ABT-493/ABT-530 to Sofosbuvir Dosed With Daclatasvir in Adults With HCV Genotype 3 Infection
CTID: NCT02640157
Phase: Phase 3    Status: Completed
Date: 2021-07-30
Role of Pegylated Interferon in Combination With DAAs to Cure Hepatitis C As Soon As Possible - Hepatitis C [ASAP-C]
CTID: NCT03480932
Phase: Phase 2/Phase 3    Status: Completed
Date: 2021-05-18
Evaluation of Daclatasvir (DCV) in Combination With Sofosbuvir (SOF) in Children With Chronic Hepatitis C (CHC) Infection
CTID: NCT03487848
Phase: Phase 2    Status: Terminated
Date: 2021-04-20
Safety of Sofosbuvir in People With Advanced Kidney Failure
CTID: NCT03883698
Phase: Phase 3    Status: Completed
Date: 2021-04-06
Sofosbuvir in Treatment of COVID 19
CTID: NCT04460443
Phase: Phase 2/Phase 3    Status: Unknown status
Date: 2020-12-08
A Drug-drug Interaction Study Between Daclatasvir and Metformin
CTID: NCT02565862
Phase: Phase 1    Status: Completed
Date: 2020-12-07
A Drug-drug Interaction Study Between Daclatasvir and Atazanavir/Ritonavir or Atazanavir/Cobicistat
CTID: NCT02565888
Phase: Phase 1    Status: Completed
Date: 2020-12-07
Sofosbuvir Containing Regimens in Treatment of COVID 19 Patients
CTID: NCT04497649
Phase: Phase 2/Phase 3    Status: Unknown status
Date: 2020-12-03
Phase III China GT 1b Interferon (IFN) Intolerant Prev Exclude Dual
CTID: NCT01995266
Phase: Phase 3    Status: Completed
Date: 2020-08-11
Safety and Efficacy Study in Subjects With Chronic HCV and Underlying Hemophilia
CTID: NCT01741545
Phase: Phase 3    Status: Completed
Date: 2020-08-11
Study of AT-527 in Combination With Daclatasvir in Subjects With Hepatitis C Virus (HCV) Infection
CTID: NCT04019717
Phase: Phase 2    Status: Completed
Date: 2020-05-04
Three-year Follow-up Study of Subjects Who Participated in a Previous Asunaprevir (BMS-650032) and/or Daclatasvir (BMS-790052) Chronic Hepatitis C Clinical Trial
CTID: NCT01492504
Phase:    Status: Completed
Date: 2019-11-27
An Efficacy, Safety and Pharmacokinetics Study of Simeprevir, Daclatasvir and Sofosbuvir in Participants With Chronic Hepatitis C Virus Genotype 1 or 4 Infection and Decompensated Liver Disease
CTID: NCT02262728
Phase: Phase 2    Status: Completed
Date: 2019-05-08
Study to Evaluate the Safety and Efficacy of Daclatasvir/Sofosbuvir/Ribavirin for 16 Versus 24 Weeks for HCV Genotype 3 Cirrhotics
CTID: NCT02304159
Phase: Phase 4    Status: Completed
Date: 2019-04-24
Comparative Study of Two Regiemns in Management of Sofosbuvir/Daclatasvir Failure
CTID: NCT03549832
Phase: N/A    Status: Completed
Date: 2019-03-19
Daclatasvir, Asunaprevir Plus Ribavirin for HCV Genotype 1b Without NS5A RAV
CTID: NCT03004625
Phase: Phase 3    Status: Completed
Date: 2019-01-09
Efficacy and Safety of All-Oral Combination of Narlaprevir/Ritonavir and Daclatasvir in Treatment-Naїve Patients With Chronic Hepatitis C Genotype 1b
CTID: NCT03485846
Phase: Phase 2    Status: Completed
Date: 2018-12-19
A Study of Pharmacokinetics, Efficacy, Safety, Tolerability, of the Combination of Simeprevir (TMC435), Daclatasvir (BMS-790052), and Ribavirin (RBV) in Patients With Recurrent Chronic Hepatitis C Genotype 1b Infection After Orthotopic Liver Transplantation
CTID: NCT01938625
Phase: Phase 2    Status: Completed
Date: 2018-11-21
Effect of Co-administration of Metformin and Daclatasvir on the Pharmacokinetis and Pharmacodynamics of Metformin
CTID: NCT03686722
Phase: Phase 1    Status: Completed
Date: 2018-10-12
Impact of Antiviral Therapy on Gastroesophageal Varices.
CTID: NCT02758509
Phase:    Status: Completed
Date: 2018-05-21
Interferon-free Antiviral Treatment of HCV-Positive Genotype 1b Related Indolent Non-Hodgkin Lymphomas
CTID: NCT02762448
Phase:    Status: Withdrawn
Date: 2018-04-19
SOF Plus DCV in Treating Chinese Treatment-experienced HCV Patients
CTID: NCT02473211
Phase: Phase 2/Phase 3    Status: Completed
Date: 2018-03-19
A Study to Evaluate the Safety and Efficacy of the Combined Single Dose of Dactavira Plus Or Dactavira in Egyptian Adults With Chronic Genotype 4 HCV Infection
CTID: NCT03186313
Phase: Phase 3 Sta
Immune phenotyping in chronic hepatitis C patients treated with Sofosbuvir and Daclatasvir combination with or without Ribavirin for 12 or 24 weeks -SODA study
CTID: null
Phase: Phase 3    Status: Completed
Date: 2015-04-16
Open-Label, Randomized Study of Daclatasvir, Sofosbuvir, and Ribavirin for 12 vs. 16 weeks in Treatment-Naïve and Treatment-Experienced Patients with Genotype 3 Chronic Hepatitis C Infection with Compensated Advanced Fibrosis/Cirrhosis (F3/F4)
CTID: null
Phase: Phase 3    Status: Completed
Date: 2015-02-13
A Phase 2, Open-label Study to Investigate the Efficacy and Safety of the Combination of Simeprevir and Daclatasvir in Chronic Hepatitis C Genotype 1b-Infected Subjects
CTID: null
Phase: Phase 2    Status: Completed
Date: 2014-12-05
Effect of ASV and DCV therapy on the quality of immune status in chronic HCV patients
CTID: null
Phase: Phase 4    Status: Ongoing
Date: 2013-12-19
A Phase 3 Evaluation of a daclatasvir/asunaprevir/BMS-791325 Fixed Dose Combination in Non-cirrhotic Subjects with Genotype 1 Chronic Hepatitis C
CTID: null
Phase: Phase 3    Status: Completed
Date: 2013-12-13
A Phase 3 Evaluation of a daclatasvir/asunaprevir/BMS-791325 Fixed Dose Combination in Subjects with Genotype 1 Chronic Hepatitis C and Compensated Cirrhosis
CTID: null
Phase: Phase 3    Status: Completed
Date: 2013-12-13
Phase 2, Open-Label Study to Investigate the Pharmacokinetics, Efficacy, Safety, and Tolerability of the Combination of Simeprevir (TMC435), Daclatasvir (BMS-790052) and Ribavirin (RBV) in Patients with Recurrent Chronic Hepatitis C Genotype 1b Infection after Orthotopic Liver Transplantation
CTID: null
Phase: Phase 2    Status: Completed
Date: 2013-12-12
Phase 3 open label study evaluating the efficacy and safety of pegylated interferon lambda-1a, in combination with ribavirin and daclatasvir, for treatment of chronic HCV infection with treatment naïve genotypes 1, 2, 3 or 4 in subjects co-infected with HIV.
CTID: null
Phase: Phase 3    Status: Completed
Date: 2013-08-13
MAGNITUDE - A Phase 3 Evaluation of the Safety and Efficacy of Lambda/RBV/DCV in Treatment Naïve Subjects with Chronic HCV Infection, who have Underlying Mild or Moderate Hemophilia or Patients who are Prior Relapsers to Pegylated interferon alfa/RBV
CTID: null
Phase: Phase 3    Status: Completed, Temporarily Halted, Prematurely Ended
Date: 2013-03-13
A Phase 3 Evaluation of Daclatasvir in Combination with Peginterferon Lambda-1a and Ribavirin (RBV) or Telaprevir in Combination with Peginterferon Alfa-2a and RBV in Patients with Chronic Hepatitis C Genotype 1b who are Treatment Naïve or Prior Relapsers to Alfa/RBV Therapy (The STRUCTURE Study)
CTID: null
Phase: Phase 3    Status: Completed
Date: 2013-01-18
A Phase 3, Randomized, Double-Blind, Controlled Study Evaluating the Efficacy and Safety of Peginterferon Lambda-1a, with and without Daclatasvir, Compared to Peginterferon Alfa-2a, Each in Combination with Ribavirin, in the Treatment of Naïve Genotype 2 and 3 Chronic Hepatitis C Subjects
CTID: null
Phase: Phase 3    Status: Completed
Date: 2012-11-20
A Phase 2, Open-Label Study of Daclatasvir (BMS-790052) and TMC435 in Combination With or Without Ribavirin (RBV) For Treatment-Naive Subjects or Null Responders to Prior Peginterferon Alfa (PegIFN)/RBV Therapy with Genotype 1 Chronic Hepatitis C
CTID: null
Phase: Phase 2    Status: Completed
Date: 2012-08-13
A Phase 3 Study with Asunaprevir and Daclatasvir (DUAL) for Null or Partial Responders to Peginterferon Alfa and Ribavirin (P/R), Intolerant or Ineligible to P/R Subjects and Treatment- Naive Subjects with Chronic Hepatitis C Genotype 1b Infection
CTID: null
Phase: Phase 3    Status: Completed
Date: 2012-07-12
A Phase 3, Open-Label Study with Asunaprevir and Daclatasvir Plus Peginterferon Alfa-2a (Pegasys) and Ribavirin (Copegus) (P/R) (QUAD) for Subjects Who Are Null or Partial Responders to Peginterferon Alfa 2a or 2b Plus Ribavirin with Chronic Hepatitis C Genotypes 1 or 4 Infection
CTID: null
Phase: Phase 3    Status: Completed
Date: 2012-06-13
A Phase 3 Evaluation of Daclatasvir (BMS-790052) in Combination with Peg-Interferon Alfa-2a and Ribavirin in Treatment-Naive Subjects with Chronic Hepatitis C Genotype 4
CTID: null
Phase: Phase 3    Status: Completed
Date: 2012-03-07
A Phase 3 Evaluation of BMS-790052 (Daclatasvir) Compared with Telaprevir in Combination with Peg-Interferon Alfa-2a and Ribavirin in Treatment-Naive Patients with Chronic Hepatitis-C
CTID: null
Phase: Phase 3    Status: Completed
Date: 2012-02-09
A Long-Term Follow-up Study of Subjects Who Participated in a Clinical Trial in Which Asunaprevir (BMS-650032) and/or Daclatasvir (BMS-790052) Was Administered for the Treatment of Chronic Hepatitis C.
CTID: null
Phase: Phase 3    Status: Completed
Date: 2012-02-09
A Phase 3, Open Label Study of Safety and Efficacy with BMS-790052 plus Peg-Interferon Alfa 2a and Ribavirin in Previously Untreated HCV Patients Coinfected with Human Immunodeficiency Virus (HIV) and Hepatitis C Virus (HCV)
CTID: null
Phase: Phase 3    Status: Completed
Date: 2012-01-11
An Open-Label Re-treatment Study with Peg-Interferon Alfa-2a, Ribavirin and BMS-790052 With or Without BMS-650032 for Subjects With Chronic Hepatitis C
CTID: null
Phase: Phase 2    Status: Completed
Date: 2011-09-30
A Phase 2B Study of BMS-790052 in Combination with Peginterferon Alfa-2a and Ribavirin in Chronic Hepatitis C Genotype 1 Infected Subjects Who are Null or Partial Responders to Prior Treatment with Peginterferon Alfa plus Ribavirin Therapy
CTID: null
Phase: Phase 2    Status: Completed
Date: 2010-09-06
Efficacy and safety of Simeprevir/PEG alpha-IFN-2a/RBV therapy for patients with chronic hepatitis C after resection of hepatocellular carcinoma
CTID: UMIN000012937
PhaseNot applicable    Status: Recruiting
Date: 2014-03-01
A Phase 3 Evaluation of Daclatasvir in Combination With Peginterferon Lambda-1a and Ribavirin (RBV) in Patients With Chronic Hepatitis C Genotype 1b Who Are Treatment naive or Prior Relapsers to Alfa/RBV Therapy
CTID: jRCT2080222042
Phase:    Status:
Date: 2013-03-14
A Phase 3, Comparative Study of Asunaprevir and Daclatasvir Combination Therapy versus Telaprevir Therapy in Japanese HCV subjects.
CTID: jRCT2080221958
Phase:    Status:
Date: 2012-11-19

Biological Data
  • Daclatasvir (BMS-790052)

    BMS-790052 alters the subcellular fractionation patterns of NS proteins.Virology.2011 May 25;414(1):10-8.
  • Daclatasvir (BMS-790052)

    BMS-790052 alters the subcellular localization of NS viral proteins.Virology.2011 May 25;414(1):10-8.
  • Daclatasvir (BMS-790052)

    BMS-790052 blocks HCV genome replication.Virology.2011 May 25;414(1):10-8.
  • Daclatasvir (BMS-790052)

    Reversal of BMS-790052-induced alterations on subcellular localization of NS proteins expressed from a replicon containing the BMS-790052-resistant mutation (Y93H) in NS5A.Virology.2011 May 25;414(1):10-8.
  • Daclatasvir (BMS-790052)

    BMS-790052 affects neither the in vitro replicase activity of pre-assembled RCs nor the self-dimerization of NS5A proteins.Virology.2011 May 25;414(1):10-8.
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