Telaprevir

679.85

679.85

1533716-785-6

655M5O3W0U

DTXSID40193304

C81603

White to off-white powder

J05AE|J - Antiinfectives for systemic use

29339900

log Kow = 1.73 (est)

1.3±0.1 g/cm3

1.584

In water, 0.0047 mg/mL|3.55e-02 g/L

Store at 25 °C (77 °F); excursions permitted to 15-30 °C (59-86 °F)

9.93X10-26 mm Hg at 25 °C (est)

Henry's Law constant = 7.81X10-31 atm-cu m/mol at 25 °C (est)

24/25

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including telaprevir, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

|Warning|H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P301+P312, P330, and P501|Aggregated GHS information provided by 11 companies from 2 notifications to the ECHA C&L Inventory.

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

Antiviral drugs have been recently recognized as one of the emerging contaminants in the environment. These are discharged after therapeutic use through human excretion. Effluent containing high concentration of antiviral drugs discharged from production facilities is also a cause of concern to nearby aquatic bodies. There is an increased interest in their removal because they are highly bioactive. Some antiviral drugs are resistant to conventional methods of degradation, and there is a risk of development of antiviral resistance in humans and animals if exposed repeatedly for long periods. To date, the potential human, animal, and ecological risks associated with the discharge of these antiviral compounds to the environment are not well documented. This study presents a brief summary on occurrence, ecotoxicological risks, and physicochemical properties of antiviral drugs in the environment. The needs regarding removal, disposal, and treatment of antiviral drugs are also addressed(1). /Antiviral drugs/

Serious skin reactions, including Stevens Johnson Syndrome, Drug Reaction with Eosinophilia and Systemic Symptoms, and Toxic Epidermal Necrolysis, have been reported in patients treated with telaprevir combination treatment. Use of [DB00811], [DB00008], [DB00022] and Telaprevir is associated with a further increase in anemia frequency than in [DB00811], [DB00008], and [DB00022] without telaprevir.

In large randomized controlled trials, triple therapy with telaprevir, peginterferon and ribavirin was associated with a high rate of adverse events that often required dose adjustments and led to early discontinuation in 5% to 20% of patients. However, serum ALT elevations and clinically apparent liver injury were not generally mentioned as adverse events of therapy. Telaprevir, however, was associated with a high rate of rash, which was sometimes associated with features of hypersensitivity, including rare instances of DRESS and Stevens Johnson syndrome. These severe cutaneous reactions are often accompanied by laboratory evidence of hepatic injury (ALT and alkaline phosphatase elevations). In reported cases, however, the rash and other features of hypersensitivity have overshadowed the hepatic injury and none were reported to be associated with jaundice.

Telaprevir is a strong inhibitor of CYP3A. Telaprevir is contraindicated when combined with drugs that are highly dependent on CYP3A for clearance and for which elevated plasma concentrations are associated with serious and/or life-threatening events (narrow therapeutic index). Telaprevir is contraindicated when combined with drugs that strongly induce CYP3A and thus may lead to lower exposure and loss of efficacy of telaprevir.|Potential pharmacokinetic interaction with drugs that are inducers or inhibitors of P-glycoprotein, with possible alteration in telaprevir concentrations.|Potential pharmacokinetic interaction with alfuzosin (increased alfuzosin concentrations). Concomitant use of telaprevir and alfuzosin is contraindicated because increased alfuzosin concentrations may result in hypotension or cardiac arrhythmia.|Potential pharmacokinetic interaction with antiarrhythmic agents (amiodarone, bepridil (no longer commercially available in US), flecainide, systemic lidocaine, propafenone, quinidine) may result in increased concentrations of the antiarrhythmic agent; potential for serious and/or life-threatening adverse effects. If telaprevir and antiarrhythmic agents are used concomitantly, use caution and clinical monitoring.|For more Interactions (Complete) data for Telaprevir (54 total), please visit the HSDB record page.

Telapravir is 59-76% bound to human plasma proteins following a single dose. It binds to both human serum albumin and α1-acid glycoprotein.

Telapravir's production and administration as an antiviral(1) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1.0X10+5(SRC), determined from a structure estimation method(2), indicates that telapravir is expected to be immobile in soil(SRC). Volatilization of telapravir from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 7.8X10-31 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Telapravir is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 9.9X10-26 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation date in soil were not available(SRC, 2013).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1.0X10+5(SRC), determined from a structure estimation method(2), indicates that telapravir is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 7.8X10-31 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 6(SRC), from an estimated log Kow of 1.73(6) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data in water were not available(SRC, 2013).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), telapravir, which has an estimated vapor pressure of 9.9X10-26 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase telapravir may be removed from the air by wet and dry deposition(SRC). Telapravir contains chromophores that absorb at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

Telapravir is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(1). Telapravir contains chromophores that absorb at wavelengths >290 nm(1) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 6 was calculated in fish for telapravir(SRC), using an estimated log Kow of 1.73(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of telapravir can be estimated to be 1.0X10+5(SRC). According to a classification scheme(2), this estimated Koc value suggests that telapravir is expected to be immobile.

The Henry's Law constant for telapravir is estimated as 8.8X10-31 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that telapravir is expected to be essentially nonvolatile from water and moist soil surfaces(2). Telapravir is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 9.9X10-26 mm Hg(SRC), determined from a fragment constant method(3).

It is not known whether telaprevir is excreted in human breast milk. When administered to lactating rats, levels of telaprevir were higher in milk compared to those observed in plasma. Rat offspring exposed to telaprevir in utero showed no effects on body weight at birth. However, when fed via milk from telaprevir-treated dams, body weight gain of pups was lower than pups fed milk from control dams. After weaning, rat pup body weight gain was similar in offspring from telaprevir-treated and control dams. Because of the potential for adverse reactions in nursing infants, nursing must be discontinued prior to initiation of treatment.The following adverse reactions have been identified during post-approval use of INCIVEK. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure. Skin and Subcutaneous Tissue Disorders: Toxic Epidermal Necrolysis (TEN) and Erythema Multiforme (EM).

Occupational exposure to telapravir may occur through inhalation and dermal contact with this compound at workplaces where telapravir is produced or used. Exposure to telapravir among the general population may be limited to those administered the drug. (SRC)

Telaprevir, when used in combination with [DB00811], [DB00008], and [DB00022] is indicated for use in the treatment of chronic HCV genotype 1 infection in adults.|FDA Label|Incivo, in combination with peginterferon alfa and ribavirin, is indicated for the treatment of genotype-1 chronic hepatitis C in adult patients with compensated liver disease (including cirrhosis):who are treatment naïve;who have previously been treated with interferon alfa (pegylated or non-pegylated) alone or in combination with ribavirin, including relapsers, partial responders and null responders.|Treatment of chronic hepatitis C

Telaprevir is an oral, direct acting hepatitis C virus (HCV) protease inhibitor that is used in combination with other antiviral agents in the treatment of chronic hepatitis C, genotype 1. Telaprevir has not been linked to instances of acute liver injury during therapy, but has been linked to cases of severe cutaneous reactions such as DRESS and Stevens Johnson syndrome which can be associated with mild hepatic injury. In addition, when combined with peginterferon and ribavirin, telaprevir has been associated with cases of hepatic decompensation in patients with preexisting cirrhosis.

Hepatitis C Agents

Oligopeptides|INCIVEK (telaprevir), in combination with peginterferon alfa and ribavirin, is indicated for the treatment of genotype 1 chronic hepatitis C in adult patients with compensated liver disease, including cirrhosis, who are treatment-naive or who have previously been treated with interferon-based treatment, including prior null responders, partial responders, and relapsers. /Included in US product label/

Fatal and non-fatal serious skin reactions, including Stevens Johnson Syndrome (SJS), Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS), and Toxic Epidermal Necrolysis (TEN), have been reported in patients treated with INCIVEK combination treatment. Fatal cases have been reported in patients with progressive rash and systemic symptoms who continued to receive INCIVEK combination treatment after a serious skin reaction was identified. For serious skin reactions, including rash with systemic symptoms or a progressive severe rash, INCIVEK, peginterferon alfa, and ribavirin must be discontinued immediately. Discontinuing other medications known to be associated with serious skin reactions should be considered. Patients should be promptly referred for urgent medical care.|Rash developed in 56% of patients receiving telaprevir during controlled clinical trials. Severe rash (e.g., generalized rash or rash with vesicles or bullae or ulcerations other than SJS) was reported in 4% of patients receiving telaprevir in conjunction with peginterferon alfa and ribavirin compared with less than 1% of patients receiving peginterferon alfa and ribavirin without telaprevir. Rash frequently was observed during the first 4 weeks of telaprevir treatment, but can occur at any time. Rash generally improves when telaprevir therapy is completed or discontinued; complete resolution may take weeks.|If a serious skin reaction occurs, telaprevir, peginterferon alfa, and ribavirin should be immediately discontinued and the patient promptly referred for urgent medical care. Patients with mild to moderate rash should be monitored for progression of rash or development of systemic symptoms. If rash progresses and becomes severe or if systemic symptoms develop, telaprevir should be discontinued; peginterferon alfa and ribavirin may be continued.|Telaprevir dosage should not be reduced and telaprevir should not be restarted if it was discontinued because of rash. If improvement is not observed within 7 days of discontinuing telaprevir, sequential or simultaneous interruption or discontinuance of peginterferon alfa and/or ribavirin should be considered. If medically indicated, earlier interruption or discontinuance of peginterferon alfa and ribavirin should be considered.|For more Drug Warnings (Complete) data for Telaprevir (18 total), please visit the HSDB record page.

Certain amino acid substitutions (mutations) in the HCV NS3 protease domain (V36A/M, T54A/S, R155K/T, A156S, A156V/T, R155T with D168N, V36A with T54A, V36M/A with R155K/T, T54S/A with A156S/T) have been associated with reduced in vitro susceptibility to telaprevir. HCV with reduced susceptibility to telaprevir have been selected in vitro and have emerged during telaprevir treatment. The majority of HCV isolates from patients in phase 3 clinical studies who did not achieve sustained virologic response (SVR) had treatment-emergent resistance mutations. The clinical impact of prior exposure to HCV protease inhibitors (including telaprevir) is not known. HCV with telaprevir resistance-associated mutations have been isolated from some individuals who have not been exposed to HCV protease inhibitors. Telaprevir treatment-emergent resistance mutations can also result in decreased in vitro susceptibility or cross-resistance to other HCV NS3/4A protease inhibitors (e.g., boceprevir). Cross-resistance is not expected between telaprevir and interferons or ribavirin.|HCV genotype 1b replicons with reduced susceptibility to telaprevir have been selected in cell culture and characterized for telaprevir genotypic and phenotypic resistance. Additionally, resistance to telaprevir was evaluated in both biochemical and HCV genotype 1b replicon assays using site-directed mutants and recombinant NS3/4A from telaprevir Phase 2 clinical trials isolates. Variants V36A/M, T54A/S, R155K/T, A156S, R155T+D168N, and V36A+T54A conferred 3- to 25-fold reduced susceptibility to telaprevir; and A156V/T variants and the V36M/A+R155K/T and T54S/A+A156S/T double variants conferred greater than 62-fold reduced susceptibility to telaprevir. No amino acid substitutions were observed at the proteolytic cleavage sites.

Telaprevir is classified as a direct-acting antiviral (DAA) and prevents viral replication in HCV genotype 1.

Telaprevir reaches peak plasma concentration 4-5hours after administration. Absolute bioavailability has not been determined. When taken with a normal fat meal (21g of fat), exposure increases by 235% compared to fasting conditions. With low (3.6g of fat) and high fat (56g of fat) meals, exposure increased 117% and 330% respectively.|Telaprevir is mainly eliminated in the feces (82%) with a smaller amount eliminated via expiration (9%) and very little in the urine (1%). 31.9% and 18.8% of drug in the feces was present as the parent compound and R-diastereomer of the parent compound respectively.|The estimated apparent volume of distribution for Telapravir is 252 litres with an inter-individual variability of 72%.|Telaprevir has an estimated aparent total body clearance of 32.4 liters per hour with an interindividual variability of 27.2%.|The pharmacokinetic properties of telaprevir have been evaluated in healthy adult subjects and in subjects with chronic hepatitis C. Following multiple doses of telaprevir (750 mg every 8 hr) in combination with peginterferon alfa and ribavirin in treatment-naive subjects with genotype 1 chronic hepatitis C, mean (SD) Cmax was 3510 (1280) ng/mL, Cmin was 2030 (930) ng/mL, and AUC8h was 22,300 (8650) ng.hr/mL.|Telaprevir is orally available, most likely absorbed in the small intestine, with no evidence for absorption in the colon. Maximum plasma concentrations after a single dose of telaprevir are generally achieved after 4 to 5 hours.|Telaprevir is a substrate for and inhibitor of P-glycoprotein transport.|The systemic exposure (AUC) to telaprevir was increased by 237% when telaprevir was administered with a standard fat meal (containing 533 kcal and 21 g fat) compared to when telaprevir was administered under fasting conditions. In addition, the type of meal significantly affects exposure to telaprevir. Relative to fasting, when telaprevir was administered with a low-fat meal (249 kcal, 3.6 g fat) and a high-fat meal (928 kcal, 56 g fat), the systemic exposure (AUC) to telaprevir was increased by approximately 117% and 330%, respectively.|For more Absorption, Distribution and Excretion (Complete) data for Telaprevir (13 total), please visit the HSDB record page.

Telaprevir is extensively metabolized via hydrolysis, oxidation, and reduction. The major metabolites of Telaprevir are pyrazinoic acid, a metabolite that underwent reduction at the α-ketoamide bond, and the R-diastereomer of telaprevir which is 30-fold less active than the parent compound were found to be the predominant metabolites. The primary enzyme involved in the metabolism of Telaprevir is CYP3A4. Some metabolism is performed by aldo-keto reductases and other reductases.|Telaprevir is extensively metabolized in the liver, involving hydrolysis, oxidation, and reduction. Multiple metabolites were detected in feces, plasma, and urine. After repeated oral administration, the R-diastereomer of telaprevir (30-fold less active), pyrazinoic acid, and a metabolite that underwent reduction at the alpha-ketoamide bond of telaprevir (not active) were found to be the predominant metabolites of telaprevir.

Telaprevir has a half-life of elimination of 4.0-4.7 hours after a single dose and an effective half life of 9-11 hours at steady state.|The mean elimination half-life after single-dose oral administration of telaprevir 750 mg typically ranged from about 4.0 to 4.7 hours. At steady state, the effective half-life is about 9 to 11 hours.

Telaprevir is a NS3/4a protease inhibitor used to inhibit viral HCV replication. NS3/4a protease is an integral part of viral replication and mediates the cleavage the virally encoded polyprotein to mature proteins (NS4A, NS4B, NS5A and NS5B). Telaprevir inhibits NS3/4A with an IC50 of 10nM.|Telaprevir is a peptidomimetic, selective hepatitis C virus (HCV) nonstructural 3/4A (NS3/4A) protease inhibitor. The drug is a direct-acting antiviral (DAA) agent with activity against HCV. Telaprevir contains an alpha-ketoamide functional group that covalently and reversibly binds the active serine site of HCV NS3/4 protease. By blocking proteolytic cleavage of NS4A, NS4B, NS5A, and NS5B from the HCV-encoded polyprotein, the drug inhibits HCV replication. Telaprevir has in vitro activity against HCV genotypes 1a, 1b, and 2, but is less active against genotypes 3a and 4a.|Telaprevir is an inhibitor of the HCV NS3/4A serine protease, necessary for the proteolytic cleavage of the HCV encoded polyprotein into mature forms of the NS4A, NS4B, NS5A and NS5B proteins and essential for viral replication. In a biochemical assay, telaprevir inhibited the proteolytic activity of the recombinant HCV NS3 protease domain with an IC50 value of 10 nM.

No specific antidote is available for overdose with telaprevir. Treatment of overdose with telaprevir consists of general supportive measures including monitoring of vital signs and observation of the clinical status of the patient. In the event of an overdose, it is reasonable to employ the standard supportive measures, such as, removing unabsorbed material from the gastrointestinal tract, employing clinical monitoring (including obtaining an electrocardiogram), and instituting supportive therapy if required. It is not known whether telaprevir is dialyzable by peritoneal or hemodialysis.|/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/|For more Antidote and Emergency Treatment (Complete) data for Telaprevir (7 total), please visit the HSDB record page.

/SIGNS AND SYMPTOMS/ The highest documented dose administered is 1875 mg every 8 hours for 4 days in healthy subjects with telaprevir alone. In that trial, the following common adverse events were reported more frequently with the 1875 mg q8h regimen compared to the 750 mg q8h regimen: nausea, headache, diarrhea, decreased appetite, dysgeusia, and vomiting.|/SIGNS AND SYMPTOMS/ Fatal and non-fatal serious skin reactions, including Stevens Johnson Syndrome (SJS), Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS), and Toxic Epidermal Necrolysis (TEN), have been reported in patients treated with INCIVEK combination treatment. Fatal cases have been reported in patients with progressive rash and systemic symptoms who continued to receive INCIVEK combination treatment after a serious skin reaction was identified. For serious skin reactions, including rash with systemic symptoms or a progressive severe rash, INCIVEK, peginterferon alfa, and ribavirin must be discontinued immediately. Discontinuing other medications known to be associated with serious skin reactions should be considered. Patients should be promptly referred for urgent medical care.|/CASE REPORTS/ /Investigators/ report a case of drug rash with eosinophilia and systemic symptoms (DRESS) due to telaprevir (VX-950), a specific inhibitor of the hepatitis C virus (HCV) serine protease. A 57-year-old woman with chronic hepatitis C was included in a phase 2 rollover study of VX-950. She received VX-950 in combination with pegylated interferon alfa-2a and ribavirin. Six weeks later, she developed a generalized pruritic maculopapular exanthema with malaise, fever, dyspnoea and lymph node swelling. She had an eosinophilia (up to 2.7 X 10(+9) cells/L), large activated lymphocytes and increased concentrations of aminotransferases. Histological examination of a cutaneous biopsy was consistent with a drug rash reaction. The HCV treatment was stopped, and she was treated with topical and oral steroids. Cutaneous and systemic symptoms disappeared within 1 month. Telaprevir was considered the culprit drug. The safety data of telaprevir is derived mainly from the PROVE1, PROVE2 and PROVE3 studies. They showed a high frequency of cutaneous side effects reported under the imprecise terms of pruritus and rash, leading to an increased rate of treatment discontinuation. It is important to be aware of the high incidence of cutaneous side effects and better describe them. Our observation suggests that potentially severe hypersensitivity reactions may belong to the spectrum of rashes induced by this drug.|/EPIDEMIOLOGY STUDIES/ Previous studies have reported telaprevir is effective for chronic hepatitis C virus infection, but the safety of a telaprevir-based regimen remains uncertain. A meta-analysis was performed to assess the safety of the addition of telaprevir to a standard regimen of pegylated interferon (peginterferon) plus ribavirin (combination telaprevir with peginterferon plus ribavirin, the TPR group) compared with the standard regimen group (peginterferon plus ribavirin, the PR group). Seven randomized controlled trials involving a total of 2808 patients were included in the meta-analysis. The addition oftelaprevir to the standard regimen was associated with a significantly increased risk of serious adverse events compared with the standard PR group (relative risk [RR]=1.56; 95% confidence interval [CI] 1.21, 2.03; p=0.0007; I2=0%). Telaprevir was also associated with increased risk of treatment discontinuation (RR=2.10; 95% CI 1.56, 2.83; p

incivek

INCIVEK (telaprevir) is supplied as purple film-coated capsule-shaped tablets containing 375 mg of telaprevir. Each tablet is debossed with the characters "V 375" on one side and is packaged as follows: 28-day packer contains 4 weekly cartons of 7 blister strips each (6 tablets per blister strip)

Human drugs -> Incivo -> EMA Drug Category|Antivirals for systemic use -> Human pharmacotherapeutic group|Human Drugs -> EU pediatric investigation plans|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients