March 5, 2012


By Kathie Beach
In 1988, my husband Kurt, a Smithfield Police Officer, responded to an emergency call and tried to save a child's life who had been born with spina bifida and had a trachometry in her throat to be able to breathe. On this day, the child was not breathing and her heart had stopped. Kurt proceeded mouth to trach breaths and CPR on her having to suck the blood and mucous out of the airwaves to try to give her oxygen. It was to no avail, the child, sadly died. The mother of that precious child knew Kurt did everything within his power to save her. She considers Kurt a hero. So do I.
In 1988 the police department was not trained on blood pathogens and Hepatitis C had not even been classified yet, being called Non A and Non B Hepatitis. Kurt's attempt to save a life put his life in jeopardy. Later, he found out the terrible news that he had contracted this disease when he came in contact with the child's infected blood due to multiple blood transfusions her condition had demanded.
All these years God has kept His hand on Kurt. Although he was diagnosed with Hepatitis C and aggressive chronic liver disease, he was able to work and go about his life. He worked hard and gave tirelessly of whatever was required of him. He endured countless tests, procedures and experimental therapies to try to rid his body of the disease. The doctors were amazed by his stamina, his faith and his encouraging ways. He bounced back again and again and I suppose we always thought he would. Then in May of this year he ended up at Obici hospital for a five day stay. From there he went to MCV where his team of doctors did extensive tests and evaluations. Another stay at Obici and another round at MCV and then finally this week we are told by his team of doctors that Kurt needs a new liver and we need to prepare him for a live donor as a wait for a DD (deceased donor) is in the 100,000s. They did not mince words that Kurt could die waiting for a liver donor.
Kurt needs a living donor liver transplant.
This is a procedure that involves the removal of the recipient's (Kurt) native liver and replacing it with a potion of the living donor's liver. Both Kurt's and the donor's livers will regenerate to normal functional volume within weeks. AMAZING!
Kurt has a wonderful team of doctors who have monitored him over the years and when they convened they said he is a perfect candidate for this operation. The doctor went so far as to say 'Kurt, you will feel like a new man. Able to work, play and live and you will feel better than you have in years.'
My hero needs a hero, he needs a living donor.
(Just to clarify...this was an email petition sent out to friends and family in 2008. Kurt received a living liver donor in 2009 after 3 failed deceased donor attempts.)

Treatment of chronic hepatitis C genotype 1 with triple therapy comprising telaprevir or boceprevir

Review article | Published 24 February 2012, doi:10.4414/smw.2012.13516
Cite this as: Swiss Med Wkly. 2012;142:w13516

Swiss Association for the Study of the Liver1

1 Current Council Members of the Swiss Association for the Study of the Liver are listed in

Abbreviations: AASLD, American Association for the Study of Liver Diseases; BOC, boceprevir; CHC, chronic hepatitis C; EASL, European Association for the Study of the Liver; HBV, hepatitis B virus; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; HIV, human immunodeficiency virus; PEG-IFN-α, pegylated interferon-α; RBV, ribavirin; SVR, sustained virological response; SASL, Swiss Association for the Study of the Liver; TPV, telaprevir.


Hepatitis C virus (HCV) infection is a leading cause of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma worldwide. Two first-generation protease inhibitors, telaprevir and boceprevir, have recently been approved for the treatment of chronic hepatitis C genotype 1. Triple therapy comprising pegylated interferon-α, ribavirin and telaprevir or boceprevir increases sustained virological response rates to ~70% and allows to shorten treatment duration in ~½ of treatment-naïve patients with chronic hepatitis C genotype 1. Sustained virological response rates in treatment-experienced patients depend on the response to previous treatment, ranging from >80% in previous relapsers to ~30% in previous null responders. These advances come at the expense of new adverse effects and increased cost. In addition, treatment of chronic hepatitis C will become more complex. In these times of changing medical practice, the present expert opinion statement by the Swiss Association for the Study of the Liver shall provide guidance on the treatment of chronic hepatitis C with triple therapy comprising telaprevir or boceprevir.

Key words: boceprevir; chronic hepatitis C; HCV; hepatitis C virus; interferon; protease inhibitor; ribavirin; telaprevir


Hepatitis C virus (HCV) infection is a leading cause of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma (HCC) [13]. An estimated 120–200 million individuals worldwide and about 1% of the general population in Switzerland are chronically infected with HCV. About 50% of the chronic HCV infections in Switzerland are due to genotype 1 [4]. While the incidence of acute hepatitis C has declined significantly since the introduction of anti-HCV screening of blood and blood products in 1990, the number of patients presenting with decompensated cirrhosis and HCC is expected to increase further, attaining a peak around 2020 [1, 5]. More than 50% of the individuals at risk may currently be unaware of their infection. Strategies to increase testing and detection rates are currently being explored (e.g., screening of populations at risk vs. birth cohort screening) [6, 7].

Fifty to 80% of acutely infected individuals develop persistent infection. Of these, 2–20% will develop liver cirrhosis within the first 20 years, and accumulating evidence suggests that disease progression may increase in a nonlinear fashion thereafter [8]. Once cirrhosis is established, the rate of HCC development is 1–6% per year. Factors associated with more frequent and rapid progression to cirrhosis are, among others, higher age at the time of infection, male sex, alcohol consumption, coinfections with the human immunodeficiency virus (HIV) or hepatitis B virus (HBV), nonalcoholic fatty liver disease and smoking. Comprehensive management of chronic hepatitis C (CHC) takes these factors into consideration and aims at improving the ones that can be modified (alcohol abstinence; weight loss, regular physical activity and other measures to control the metabolic syndrome; vaccination against HBV [and hepatitis A virus]; smoking cessation including cannabis) [9].

While non-invasive methods for fibrosis assessment are actively being pursued [10], liver biopsy remains the reference for grading and staging of CHC. The Metavir and Ishak scoring systems are most often applied. Fibrosis stages are classified from 0 (absence of fibrosis) to 4 (cirrhosis) in the Metavir system [11], and from 0 to 6 in the Ishak system [12].

The decision to treat CHC is based on the analysis of numerous variables and should take into account the specific situation of each patient. Treatment is clearly recommended for patients with Metavir fibrosis stage ≥2 who do not have any contraindications. For other patients, decisions will have to be made on an individual basis. Additional factors that come into consideration are, among others, the (biological) age and general condition of the patient, the patient’s personal and professional plans, the duration of HCV infection, the risk of developing cirrhosis, the likelihood of response to therapy, and comorbidity.

For the last 10 years, standard therapy of CHC consisted of pegylated interferon-α (PEG-IFN-α) combined with ribavirin (RBV) for (16-)24-48(-72) weeks, yielding sustained virological response (SVR) rates of 40–50% in patients infected with HCV genotype 1 and ~80% in patients infected with genotypes 2 and 3. Definitions of virological response patterns are provided in table 1.

Polymorphisms near the IL28B gene have recently been identified as strong predictors of the outcome of IFN-α-based antiviral therapy (reviewed in [13, 14]). A number of laboratories offer IL28B genetic testing, but its role in clinical practice and decision making, if any, remains to be defined.

A first generation of directly acting antivirals, the NS3-4A protease inhibitors telaprevir (TPV; Incivo®) and boceprevir (BOC; Victrelis®), has recently been approved for the treatment of CHC genotype 1. TPV and BOC have to be combined with PEG-IFN-α and RBV in order to avoid the rapid selection of HCV strains resistant to antiviral therapy [15, 16]. Triple therapy comprising TPV or BOC increases SVR rates to ~70% in treatment-naïve patients with CHC genotype 1 [1719]. In treatment-experienced patients, SVR rates depend on the virological response to previous therapy with PEG-IFN-α and RBV, ranging from >80% in patients with previous relapse to ~50% in patients with previous partial response and ~30% in patients with previous null response [2022]. Treatment schedules comprising TPV or BOC have more side effects than PEG-IFN-α and RBV, and should be managed carefully.

A significant increase in the number of patients with CHC to be treated is expected for 2012, with triple therapy regimens that are more complex, as discussed below [23]. These expected developments represent a significant challenge and will stretch current resources.

The present Swiss Association for the Study of the Liver (SASL) expert opinion statement is not intended as guideline but shall provide some guidance on the management of CHC genotype 1 and the use of TPV and BOC. It is based on the results of recently published phase III clinical trials performed in treatment-naïve and treatment-experienced patients (ADVANCE [17], ILLUMINATE [19] and REALIZE [20] for TPV as well as SPRINT-2 [18], RESPOND-2 [21] and PROVIDE [22] for BOC), and take into account the recently updated American Association for the Study of Liver Diseases (AASLD) Practice Guidelines [3] as well as the labels approved by the US Food and Drug Administration, the European Medicinal Agency, and Swissmedic. Current European Association for the Study of the Liver (EASL) Clinical Practice Guidelines [2] are expected to be updated shortly. In addition, different national guidelines are in preparation. Therefore, as recommendations are emerging and as real-life data and practical experience on the use of TPV and BOC are still limited, it is strongly recommended to initiate and pursue triple therapy comprising TPV or BOC only in close collaboration with an expert centre.

Click to enlarge


Practical use of telaprevir and boceprevir

TPV is available in the form of 375-mg film-coated tablets and has to be taken at a dose of 750 mg every 8 hours (i.e., two tablets every 8 hours), with a meal or a snack containing ~20 g of fat to increase bioavailability. BOC is available in the form of 200-mg capsules and has to be taken at a dose of 800 mg every 8 hours (i.e., 4 capsules every 8 hours), with a meal or a snack. Dosing every 8 ± 1 hour rather than 3 times per day is important to maintain inhibitory drug serum concentrations and to avoid antiviral resistance development. TPV and BOC should never be used alone, and doses should never be reduced. When used alone, these drugs will not be effective and will cause emergence of HCV strains with resistance to antiviral therapy that could be difficult to treat subsequently. RBV can be taken with the first dose of TPV or BOC in the morning and with the last dose of TPV or BOC in the evening.

TPV and BOC are only approved for use in patients with HCV genotype 1 infection. The development of antiviral resistance is more frequent in subtype 1a than 1b but this should not influence therapeutic decision making.

Both TPV and BOC have a strong potential for drug-drug interactions, as they affect the metabolism of other drugs metabolised through cytochrome P450 3A4 (CYP3A4) and other pathways [24]. See package inserts, continuously updated online databases (e.g.,, Epocrates, Medscape) and Leise et al. [25] for known drug-drug interactions and contraindicated drugs. Commonly used drugs that are contraindicated in combination with TPV or BOC include, among others, atorvastatin, lovastatin, simvastatin, sildenafil, alfuzosin, carbamazepin, phenytoin, oral midazolam, and St. John’s wort. Among the drugs commonly used to manage adverse effects of therapy, paracetamol and metoclopramide (but not domperidone) are allowed. TPV and BOC may decrease citalopram levels and efficacy.

Main adverse effects of TPV include anemia, nausea and diarrhea, skin rashes and pruritus as well as anorectal disorders. Rash should be managed in collaboration with an experienced dermatologist and should follow recommendations that have recently been summarised [26]. TPV has to be discontinued if rash progresses and becomes severe. Rare cases of DRESS (drug-related eosinophilia with systemic symptoms) and Stevens Johnson syndrome/toxic epidermal necrolysis have been observed. If either one is suspected, all drugs have to be stopped immediately, followed by emergency dermatological consultation.

Main adverse effects of BOC include anemia, with a significant number of patients requiring concomitant erythropoietin treatment in phase II and III clinical trials, as well as dysgeusia.

Anemia can develop rapidly and become very pronounced with both TPV and BOC, especially in patients with cirrhosis. Therefore, close monitoring is recommended. Anemia should be managed by timely RBV dose reduction and, if needed, blood transfusions and/or erythropoetin.

Data on the safety and efficacy of TPV and BOC in patients with HIV coinfection are emerging. TPV and BOC should be used only in close collaboration with an expert in these patients.

There is no data in liver transplant recipients, hemodialysis patients and children, and the use of TPV and BOC in these situations is currently proscribed.

In registration trials, TPV was used with PEG-IFN-α2a 180 µg per week plus RBV 1000–1200 mg per day and BOC was used with PEG-IFN-α2b 1.5 µg/kg per week plus RBV 600–1400 mg per day. However, both forms of PEG-IFN-α may be used with RBV and either TPV or BOC.

PEG-IFN-α is contraindicated in decompensated cirrhosis.

Strict contraception must be followed during and for 6 months after the end of triple therapy because of the potential teratogenicity of RBV.

Who should be treated with triple therapy comprising TPV or BOC?

Triple therapy will represent a new standard for most treatment-naïve patients with CHC genotype 1 as well as treatment-experienced patients with a relapse or partial response to previous therapy with PEG-IFN-α and RBV (table 2).

Treatment of CHC is expected to change significantly within the next few years, with the arrival of better tolerated and even more efficacious new drugs as well as the advent of IFN-free/sparing regimens [2730]. These developments shall significantly improve the outlook for our patients. Therefore, deferring treatment may be considered in patients who’s treatment can be safely postponed.

Treatment-naïve patients with favourable baseline predictors (HCV RNA <4 x 105 IU/ml, absence of advanced fibrosis or cirrhosis) who achieve a rapid virological response (RVR; see table 1) have excellent chances to achieve SVR with 24 weeks of therapy with PEG-IFN-α and RBV alone [31]. Therefore, a 4-week lead-in with PEG-IFN-α and RBV may be considered in patients with the above-mentioned favourable baseline predictors and treatment continued without adding TPV or BOC for a total of 24 weeks in those who achieve RVR.

Lead-in with PEG-IFN-α and RBV may also be considered if there are doubts concerning the tolerance or adherence to PEG-IFN-α and RBV backbone therapy.

There is currently only limited data on the use of BOC in patients with previous null response. In general, retreatment of previous null responders has to be considered carefully, as SVR rates remain limited, especially in patients with cirrhosis. Inclusion of such patients into clinical trials involving quadruple therapy or IFN-sparing regimens may be considered. Lead-in with PEG-IFN-α and RBV may be considered in previous null responders, especially in cirrhotics, with the addition of TPV or BOC only in case of ≥1 log decline of HCV RNA at week 4. Subanalysis of the REALIZE trial revealed that 54% of the patients with ≥1 log decline after 4 weeks of lead-in with PEG-IFN-α and RBV achieved SVR with triple therapy comprising TPV, compared to only 15% of those with a decline of HCV RNA <1 log [32].

Careful monitoring and stopping rules, as detailed below, shall reduce the risk of selecting HCV strains resistant to antiviral therapy. While long-term consequences of the selection of such strains are presently unknown, antiviral resistance is likely to affect future treatment options [15, 16].


Figure 1 Telaprevir-based triple therapy. (A) Treatment-naïve patients with CHC genotype 1 and treatment-experienced patients with previous relapse. (B) Treatment-experienced patients with CHC genotype 1 and previous partial or null response. eRVR, extended rapid virological response (see table 1 for definitions of virological response patterns); P, pegylated interferon-α; R, ribavirin; T, telaprevir; wks, weeks.


Figure 2 Boceprevir-based triple therapy. (A) Treatment-naïve patients with CHC of genotype 1 without cirrhosis. (B) Treatment-experienced patients with CHC genotype 1 and previous relapse or partial response without cirrhosis. (C) All cirrhotic patients and prior null responders. B, boceprevir; BPR = B + P + R; P, pegylated interferon-α; R, ribavirin; RVR8, rapid virological response at week 8 (see table 1 for definitions of virological response patterns); wks, weeks.

Click to enlarge


Specific treatment algorithms

Telaprevir-based triple therapy

• Treatment-naïve patients and previous relapsers with CHC genotype 1 (fig. 1A)

Non-cirrhotic patients who achieve eRVR

12 weeks TPV + PEG-IFN-α + RBV

+ 12 weeks PEG-IFN-α + RBV

Non-cirrhotic patients who do not achieve eRVR and all cirrhotic patients

12 weeks TPV + PEG-IFN-α + RBV

+ 36 weeks PEG-IFN-α + RBV

• Previous partial and null responders with CHC genotype 1 (fig. 1B)

  • 12 weeks TPV + PEG-IFN-α + RBV
  • + 36 weeks PEG-IFN-α + RBV

Lead-in with PEG-IFN-α and RBV may be considered in previous null responders, especially in cirrhotics, with the addition of TPV only in case of ≥1 log decline of HCV RNA at week 4.

Stopping rules:

  • Stop all therapy if HCV RNA >1000 IU/ml at either week 4 or 12 of triple therapy.
  • Stop all therapy if HCV RNA detectable at wk 24.
  • Stop all therapy if previously negative HCV RNA becomes confirmed positive again under treatment.

Boceprevir-based triple therapy

• Treatment-naïve patients with CHC genotype 1 (fig. 2A and 2C)

Non-cirrhotic patients who achieve RVR8

4 weeks PEG-IFN-α + RBV lead-in

+ 24 weeks BOC + PEG-IFN-α + RBV

Non-cirrhotic patients who do not achieve RVR8

4 weeks PEG-IFN-α + RBV lead-in

+ 24 weeks BOC + PEG-IFN-α + RBV

+ 20 weeks PEG-IFN-α + RBV

Cirrhotic patients

4 weeks PEG-IFN-α + RBV lead-in

+ 44 weeks BOC + PEG-IFN-α + RBV

• Previous relapsers or partial responders with CHC genotype 1* (fig. 2B and 2C)

Non-cirrhotic patients who achieve RVR8

4 weeks PEG-IFN-α + RBV lead-in

+ 32 weeks BOC + PEG-IFN-α + RBV

Non-cirrhotic patients who do not achieve RVR8

4 weeks PEG-IFN-α + RBV lead-in

+ 32 weeks BOC + PEG-IFN-α + RBV

+ 12 weeks PEG-IFN-α + RBV*

Cirrhotic patients

4 weeks PEG-IFN-α + RBV lead-in

+ 44 weeks BOC + PEG-IFN-α + RBV

* For patients with prior null response, 4 weeks of lead-in with PEG-IFN-α + RBV, followed by 44 weeks of triple therapy with BOC + PEG-IFN-α + RBV is recommended.

Stopping rules:

  • Consider stopping therapy in patients with cirrhosis and <1 log drop of HCV RNA after lead-in (chances of achieving SVR being 13–25% only [33]).
  • Stop all therapy if HCV RNA ≥100 IU/ml at week 12.
  • Stop all therapy if HCV RNA detectable at week 24.
  • Stop all therapy if previously negative HCV RNA becomes confirmed positive again under treatment.


Key points are summarised in table 3.

Funding / potential competing interests: SASL or the SASL Council Members have not received any financial support in relation with the writing of this article. DM and BM as corresponding authors assume responsibility for the integrity of this article. Both have received research support from MSD and Roche and have acted as advisors to Janssen, MSD and Roche.

Correspondence: Professor Darius Moradpour, MD, Division of Gastroenterology and Hepatology, Centre Hospitalier Universitaire Vaudois, University of Lausanne, Rue du Bugnon 44, CH-1011 Lausanne, Switzerland, darius.moradpour[at]
Professor Beat Müllhaupt, MD, Division of Gastroenterology and Hepatology, University Hospital Zürich, Rämistrasse 100, CH-8091 Zürich, Switzerland,


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Medicyte and PRIMACYT Receive Grant to Develop Human Liver Cells for Cell-based Therapies



Monday, 05 March 2012 11:15 (UTC + 1)

Heidelberg and Schwerin, Germany, March 5, 2012 / B3C newswire / - Medicyte, specializing in the generation of human primary cells based on the upcyte® technology, and PRIMACYT, specializing in long-term culturing of primary human hepatocytes, have received a 300k Euro grant from the BMBF to develop culturing methods of human hepatocytes for use in cell-based therapies.

Cell-based therapies and the development of transplantable bioartificial livers to treat severe liver diseases still fail due to the limited availability of appropriate cells in large numbers and clinical quality. These failures are often related to the complex and difficult culturing of liver cells.

Medicyte’s upcyte® technology enables the expansion of human primary liver cells to large amounts and with consistent quality. Upcyte® hepatocytes are functionally equivalent to human primary liver cells and therefore suitable for use in cell-based bioartificial liver systems. PRIMACYT’s main expertise lies in the serum-free, long-term culturing of primary human hepatocytes and the development of cell culture media. Both companies now combine their knowledge to develop modified liver cells in large amounts for use in cell-based therapies.

Dr. Braspenning, Managing Director and CSO of Medicyte stated: “We are enthusiastic about working together with well-known German experts. I am sure that this collaboration will result in a vast pool of scientific data that support upcyte® as enabling technology of great value.”

Dr. Runge, Managing Director of PRIMACYT added: “The application and development of improved in-vitro systems for the treatment of severe liver disease is a key area of focus of our research and we believe the partnership with Medicyte and the University of Tübingen creates an ideal opportunity for our two companies to improve bioartificial liver devices.”

The three-year project is supported by a team from the University of Tübingen lead by Prof. Andreas Nüssler, a well-known liver cell expert. The Federal Ministry of Education and Research (BMBF) is supporting the joint effort out of the grant program “KMU-innovativ”.

Chronic liver disease is the fifth common cause of death in Europe. In Germany approximately 70.000 patients suffer from an inpatient treated severe liver disease e.g. fatty liver, cirrhosis or acute liver failure. These diseases can result in temporary to permanent liver failure. At present liver transplant is the only hope for patients with end stage liver diseases. The Number of patients waiting for a donor liver is many times higher than available organs.

About Medicyte
Medicyte is specialised in the controlled generation and standardisation of human primary cell products in virtually unlimited quantities and of highest quality for cell therapy and cell- based R&D. Medicytes proprietary technologies upcyte® and vericyte® enable to expand human hepatocytes from different donors and other cells in a standardized way, thereby making these cells for the first time commercially available in high numbers and consistent quality. Increasingly pharmaceutical companies consider using upcyte® hepatocytes for in vitro ADMET testing.

PRIMACYT Cell Culture Technology GmbH (, located in the technology- and business park in Schwerin, is a GLP certified company that provides services in the area of in vitro technologies for pharmaceutical and biotech industry. Human and animal hepatocytes are offered as biosensoric assay systems for pharmacologic-toxicological analyses of drugs and for analysis of chemicals and environmental substances.
With HEPAC2, the human hepatocyte cell culture system developed by PRIMACYT, clinical functional liver parameters in patients should be better predetermined than by animal studies.


Medicyte GmbH
Stefan Holder
Im Neuenheimer Feld 581
69120 Heidelberg
Tel.: +49-6221-72925-30 This e-mail address is being protected from spambots. You need JavaScript enabled to view it

PRIMACYT Cell Culture Technology Gmbh
Dieter Runge
Hagenower Str. 73
D-19061 Schwerin
Tel.: +49-385-3993-600


Nuron Biotech Expands Portfolio With License of Therapeutic and Prophylactic Hepatitis Vaccine Candidates



March 5, 2012, 8:05 a.m. EST

EXTON, Pa., Mar 05, 2012 (BUSINESS WIRE) -- Nuron Biotech Inc. today announced it has acquired an exclusive license of technology and product rights relating to Chimigen(R) multi-antigen vaccines from Akshaya Bio Inc., of Edmonton, Alberta, Canada, for the hepatitis B virus (HBV). Nuron Biotech has also acquired an exclusive option to license prophylactic and therapeutic products for the hepatitis C virus (HCV). Currently, no therapeutic vaccine for HBV and no prophylactic vaccine for HCV exist on the market. Financial terms were not disclosed.

"These licenses and options fit incredibly well with Nuron Biotech's strategy of identifying and in-licensing life-saving and life extending product candidates in the areas of vaccines and biologics," said Shankar Musunuri, Ph.D., MBA, Chief Executive Officer of Nuron Biotech. "This chimeric vaccine platform (Chimigen(R) technology), which is used in generating both therapeutic and prophylactic vaccines, is advanced to the point where we can expect to transition our first candidate into a Phase 1 clinical trial in 2013."

"This unique technology provides Nuron Biotech with the capability to develop a highly efficient vaccine for the treatment and prevention of HBV and HCV by inducing both cellular (T cell) and humoral (B cell, antibody) immune responses to clear disease," said Robert G. Gish, M.D., Chief of Clinical Hepatology and Professor of Clinical Medicine, University of California, San Diego. Dr. Gish is also a member of the Scientific Advisory Board for Nuron Biotech. "HBV and HCV are life-altering and potentially fatal diseases, and this technology may offer a break-through for a new generation of novel therapies and preventative vaccines for patients around the world."

Currently, 380 million people worldwide are infected with chronic HBV, which is not curable by any known therapy. More than 170 million people are infected by HCV, which is one of the leading causes of chronic liver disease, cirrhosis, liver transplantation and hepatocellular carcinoma.

About Chimigen(R) Vaccine Technology

The bifunctional nature of the chimeric multi-antigen vaccine technology represents a unique and direct approach in the therapy of chronic infectious diseases by specifically targeting antigen-presenting cell receptors with the most effective combination of viral antigen(s) and novel antibody tail fragment, the chimeric antigen. This technology offers to induce a balanced cellular as well as humoral immune response to attack chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) and may offer protection from infection.

About Nuron Biotech

Nuron Biotech is developing novel biologics and vaccines for the prevention and treatment of chronic neurodegenerative and infectious diseases. Our team of industry veterans is advancing products to meet unmet medical needs in the areas of multiple sclerosis, Alzheimer's, hepatitis B and hepatitis C for patients across the globe. Our lead drug candidate, NU100 (interferon beta-1b), is a new chemical entity currently in Phase 3 for patients with multiple sclerosis. .

SOURCE: Nuron Biotech Inc.