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Pegylated interferons: a nurses' review of a novel multiple sclerosis therapy.


Most multiple sclerosis (MS) therapies are injectable drugs, and the frequency of injections has been shown to be inversely proportional to overall compliance. One method of improving therapeutic compliance and thus clinical outcomes is to develop medications that require less frequent dosing. One of the most promising modification techniques to extend the bioavailability of a drug is poly(ethylene glycol) conjugation (pegylation), which increases the size of a molecule by attaching polyethylene glycol moieties to the parent compound, resulting in slower clearance and metabolism. This approach has been used to improve the efficacy of a number of therapeutic molecules, including interferons. Peginterferon beta-1a, a pegylated form of interferon beta-1a, is currently in phase III clinical trials for relapsing MS and has the potential to improve patient compliance by reducing the number of injections while maintaining clinical efficacy. The role of nurses in educating patients about the effective use of this new MS therapy is discussed.

Keywords: adherence, novel therapeutics, polyethylene glycol


Multiple sclerosis (MS) is a chronic disease characterized by central nervous system demyelination, axonal injury, and neuronal death (Compston & Coles, 2002; Noseworthy, Lucchinetti, Rodriguez, & Weinshenker, 2000). It most often presents in young adults aged 20-40 years and is more common among women than men. The disease is associated with a significant societal cost, estimated to exceed $500,000 annually per patient when both patient care and lost productivity are taken into account (Naci, Fleurence, Birt, & Duhig, 2010; Orlewska et al., 2005; Reese et al., 2011).

The majority (80%-90%) of patients with MS first present with relapsing MS (RMS; Kremenchutzky, Rice, Baskerville, Wingerchuk, & Ebers, 2006). This form of the disease is characterized by episodic exacerbations of neurological symptoms that develop over several days, followed by symptom stabilization, and then improvement over the following days or weeks. Magnetic resonance imaging (MRI) is increasingly used in the diagnosis of RMS and in the subsequent monitoring of the appearance and location of MS lesions. The clinical presentation of RMS, including the frequency and severity of relapses, the number of MRI-identified lesions, and the progression of disability, varies considerably between patients. It is estimated that 50% of patients with untreated RMS eventually transition to secondary progressive MS, characterized by a steady progression of clinical neurological damage with or without concurrent relapses and minor remissions (Hauser & Oksenberg, 2006; Reynolds et al., 2011).

Approximately 10%-20% of patients with MS experience primary progressive MS rather than RMS (Kremenchutzky et al., 2006). This form of MS is characterized by progressive deterioration in gait and progressive spastic paraparesis in the absence of relapses. Many patients with primary progressive MS show evidence of spinal atrophy, a hallmark of axon and oligodendrocyte cell loss, and progressive spastic paraplegia.

Given the chronic nature of MS and the highly variable spectrum of disability seen in this patient population, medical care for these patients requires a multidisciplinary approach, in which nurses play a critical role. In addition to helping patients cope with troubling symptoms and adapt to living with specific disabilities, nurses provide significant patient education about the effective use of disease-modifying therapies (DMTs; Webb, 2008).

Current MS Therapies

High-quality class I evidence shows the clinical efficacy of DMTs for the treatment of patients with RMS or who have had a single demyelinating event (clinically isolated syndrome); however, these drugs have not been shown to be effective for patients with progressive forms of MS (La Mantia et al., 2012; Pemmal & Khan, 2012). The DMTs can reduce the frequency and severity of relapses and slow disability progression associated with RMS. They can also reduce the number of lesions identified on MRI and improve scores on various cognitive measures. Although none of the currently approved therapies completely prevent relapses and disability progression (Goodin et al., 2012), these therapies are able to significantly limit the activity of the disease in most patients with RMS.

Ten MS therapies are currently approved in the United States (Table 1). Most of the U.S. Food and Drug Administration (FDA)-approved first-line therapies for RMS are interferon beta preparations, including intramuscular (im) interferon beta-1a (Avonex, B iogen Idec, 2008), subcutaneous (SC) interferon beta-1a (Rebif, EMD Serono, 2009), SC interferon beta-1b (Betaseron, Bayer HealthCare Pharmaceuticals, 2010), and SC interferon beta-1b (Extavia, Novartis Pharmaceutical Company, 2012). Interferon beta is a widely used recombinant polypeptide that exerts antiviral, antiproliferative, and immunomodulatory effects through interferon beta receptor-mediated reductions in antigen presentation and changes in protein expression, although its precise mechanism of action remains unclear (Kieseier, 2011). Whereas im interferon beta-1a is given weekly, SC interferon beta preparations require injection either every other

day (SC interferon beta-lb) or three times per week (SC interferon beta-1a). In contrast to these interferon beta therapies, glatiramer acetate (Copaxone, Teva Neuroscience, 2009) is a mix of amino acid polymers that requires daily SC administration. Glatiramer acetate's mechanism of action is believed to be mediated by competition with various myelin antigens for presentation to T-cells. It may also induce specific suppressor [T.sub.H]2 cells that migrate to the brain, leading to in situ bystander suppression (Arnon & Aharoni, 2004; Schrempf & Ziemssen, 2007). Although these therapies are generally well tolerated, they all exhibit at most moderate clinical efficacy and require self-injection on a variety of schedules (Table 1).

Other therapies for the treatment of RMS that act at different points along the inflammatory cascade have also been developed. Therapies with different mechanisms of action that have been approved by the FDA include mitoxantrone (Novantrone, EMD Serono, 2012), natalizumab (Tysabri, Biogen Idec, 2011), dimethyl fumarate (Tecfidera, Biogen Idec, 2013), fingolimod (Gilenya, Novartis Pharmaceuticals Corporation, 2011), and teriflunomide (Aubagio, Genzyme Corp., 2012). Mitoxantrone and natalizumab are given by infusion, whereas dimethyl fumarate, fingolimod, and teriflunomide are oral drugs. With the exception of dimethyl fumarate, which is classified as an immunomodulator, each of these therapies induces selective immunosuppression and thus poses a risk for reduced central nervous system immunosurveillance. In addition, cardiovascular side effects have been noted for fingolimod (U.S. FDA, 2012), and teriflunomide can be hepatotoxic and teratogenic.

There are also a number of potential new RMS therapies that are in clinical trials or have been submitted for FDA approval. These compounds include alemtuzumab and laquinimod, among others (Saidha, Eckstein, & Calabresi, 2012). All of these compounds in development achieve clinical efficacy through different mechanisms of action than currently approved therapies (Saidha et al., 2012). As with the established DMTs, these newer compounds may be associated with varying degrees of patient risk, although long-term safety data are not yet available for these newer therapies.

An Unmet Need in MS Therapy

In spite of the positive safety profile of both interferon beta and glatiramer acetate, the need for frequent dosing and patients' difficulty in adhering to prescribed dosing schedules may limit the therapeutic efficacy of these drugs (Reynolds, Stephen, Seaman, & Rajagopalan, 2010; Wong, Gomes, Mamdani, Manno, & O'Connor, 2011). Given the therapeutic requirement for frequent self-injection, issues such as needle phobia, injection-site reactions, and needle fatigue may reduce adherence. In addition, adherence to a therapeutic regimen is particularly challenging for patients with chronic diseases, such as MS that is characterized by infrequent episodes (Osterberg, Boivie, & Yhuomas, 2005; Treadaway et al., 2009). Several well-controlled studies have shown that, in developed countries, adherence to prescribed therapy across many different chronic diseases averages only 50% (Sabate, 2003). Low adherence rates have been a primary reason for suboptimal clinical outcomes. Among patients with MS, higher dosing frequency and greater treatment regimen complexity have been associated with poorer adherence and a significantly increased risk of relapse (Giovannoni, Southam, & Waubant, 2012; Ingersoll & Cohen, 2008; Steinberg, Fails, Chang, Chan, & Tankersley, 2010; Tan, Cai, Agarwal, Stephenson, & Kamat, 2011). The lowest compliance rates are associated with those therapies that require the most frequent injections (Devonshire et al., 2011). Given these findings, MS therapeutics with more convenient dosing regimens could improve medication compliance and adherence and thus clinical outcomes.


One approach currently being used to optimize drug properties is poly(ethylene glycol; PEG) conjugation (pegylation), a modification that can substantially improve a drug's pharmacokinetic profile and prolong its bioavailability after dosing. In addition to slowing clearance, pegylation may also attenuate protease degradation (Fishburn, 2008). Other potential benefits of pegylation include molecular stabilization, improved solubility, and reduced immunogenicity, which may be critically important in treating diseases with a strong immune component like MS (Baker et al., 2010). The successful development of a pegylated interferon therapy for MS has the potential to significantly increase patient compliance without sacrificing clinical efficacy (Hu et al., 2012).

Depending on the desired end product, PEG moieties composed of different numbers of repeating units of PEG may be arranged in a variety of sizes and structures (straight-chain or branched structures). In addition, specific conjugation sites on the parent molecule can be targeted, allowing for substantial sophistication in the design of the final macromolecule (Bailon et al., 2001; Wang et al., 2002). A number of different strategies have been used to attach PEG moieties to target molecules (Baker et al., 2010; Pasut & Veronese, 2009, 2012). Technical advances in targeted protein modification now allow PEG molecule attachment to specific molecular sites using the appropriate reactive linker molecules (Figure 1A).


Currently Approved Pegylated Pharmaceuticals

Pegylation has been used widely to increase the therapeutic benefit of existing pharmaceuticals, primarily by reducing the clearance of drugs and thus prolonging their bioavailability. There are currently at least nine FDA-approved pegylated compounds and a number of others in development. These pegylated molecules include enzymes, cytokines, antibodies, and growth factors and have been approved to treat a variety of diseases, including specific cancers, hepatitis C, and rheumatoid arthritis (Table 2).

Pegylated interferon alpha compounds are the most widely used pegylated human therapeutics. Although they have now been approved for several clinical indications, the most extensive clinical experience has been with chronic hepatitis C infection. These drugs have proved highly effective at reducing viral titers and have also been shown to improve patient compliance (Hoofnagle & Seeff, 2006). On the basis of this experience, pegylated interferon alphas have been the worldwide standard of care for symptomatic hepatitis C since the mid-1990s. Two pegylated interferon alphas have been used extensively in this patient population: peginterferon alpha-2a (Pegasys, The Roche Group) and peginterferon alpha-2b (Peglntron, Merck & Co, Inc.), both of which are administered by SC injection (Table 2; Aghemo, Rumi, & Colombo, 2010). These compounds differ substantially in terms of their pharmacokinetics, but an analysis of four head-to-head clinical trials found no substantial differences in the sustained virological response, with a slight advantage to peginterferon alpha-2a because of its somewhat better pharmacokinetic profile (Aghemo et al., 2010). The two drugs show similar tolerability, with comparable frequencies and types of adverse events (Rumi, Aghemo, & Prati, 2012).

Safety and Other Considerations With Pegylated Drugs

PEG has an established history as a nontoxic, minimally immunogenic, slowly biodegraded polymer and is classified as "generally regarded to be safe" by the FDA (Jevsevar, Kunstelj, & Porekar, 2010; Pasut & Veronese, 2012). However, it is also associated with a number of possible safety and efficacy issues pertaining to immunogenic reactions. For example, although pegylated compounds may be less immunogenic than native molecules, anti-PEG antibodies that can limit the efficacy of the pegylated drug have been reported (Pasut & Veronese, 2012); however, there are no data from controlled clinical trials suggesting that anti-PEG antibodies alter clinical efficacy. Additional biological responses to exposure, such as changes in immune cell profiles and/or function, metabolic changes, and liver enzyme abnormalities, have also been reported as part of the hepatitis C clinical experience with pegylated interferon alpha compounds (Aghemo et al., 2010).

Another consideration, related to the slowed clearance of pegylated compounds, is the possibility of toxicity associated with the accumulation of PEG. As with other polymers, PEG is excreted in either the urine or feces, with the specific route depending on the size of the PEG molecule. PEG moieties smaller than 30 kDa are excreted primarily via the kidneys. Although bioaccumulation of very large pegylated compounds has been reported (Pasut & Veronese, 2009), there is no published evidence documenting the bioaccumulation of currently prescribed pegylated interferon alphas. As a rule, however, drugs with a molecular weight greater than 30 kDa are excreted mainly through the feces via hepatic metabolism, and this route is believed to be the primary means of excretion for pegylated interferon alphas (Knop, Hoogenboom, Fischer, & Schubert, 2010; Pasut & Veronese, 2009). Finally, dosing calculations for a pegylated drug will be different from those for the parent compound because of differences in pharmacokinetics and the pharmacokinetic-pharmacodynamic relationship (Pasut & Veronese, 2012). In summary, the pegylated interferon alphas are well tolerated and have a good safety profile, although variations in the specific arrangement of the PEG moieties may affect a number of pharmacokinetic and pharmacodynamic properties (Alconcel et al., 2011).

Rationale for and Clinical Development of Peginterferon Beta-1a for MS

Although there have been major advances in MS therapeutics over the past 20 years, there remains an unmet medical need for safe, effective, and convenient therapies for people living with MS. Current MS therapies can reduce annual relapse rates and slow disability progression but have also been associated with a range of side effects related to the route and frequency of administration, including injection-site reactions and flu-like symptoms. Pegylated interferon beta preparations have the potential to offer patients with RMS a more convenient alternative to conventional first-line therapies, allowing less frequent dosing while maintaining the proven efficacy, safety, and tolerability of the unmodified parent molecules.

Clinical Development of Peginterferon Beta-1a for RMS

Pegylated interferon beta compounds in development as therapies for RMS include peginterferon beta-1a (Biogen Idec, Inc.), AZ01 (Allozyne, Inc.), ARX424 (Merck Serono, Inc.), and NU400 (Nuron Biotech). These compounds differ in terms of the initial interferon that is modified (interferon beta-1a or beta-1 b); the number, molecular weight, and structure (single or branched) of the attached PEG moieties; the effective molecular volume of the circulating pegylated interferon; and the degree to which pegylation shields the interferon molecule from interacting with the type I interferon receptor. Each of these variables is expected to contribute to the overall kinetics, metabolism, and efficacy of the drug and to the homogeneity of the final compound.

Peginterferon beta-1a has completed both preclinical testing (Hu et al., 2011) and phase I clinical testing (Hu et al., 2012), and a phase III trial evaluating the drug's efficacy and safety in patients with relapsing RMS has recently been completed, the results of which were reported in early 2013 (Biogen Idec, 2013). Peginterferon beta-1a is a homogeneous formulation, with pegylation of interferon beta-1a on a site that does not substantially affect the biological activity of the parent molecule (Figure 1B; Baker et al., 2006). In preclinical studies, peginterferon beta-1a showed improved pharmacokinetics and pharmacological activity in rhesus monkeys compared with interferon beta-1a (Hu et al., 2011). In addition, the toxicology profile of peginterferon beta-1a in rhesus monkeys was generally consistent with that of interferon beta-1a, and there were no other potential safety concerns (Hu et al., 2011).

Two phase I clinical studies of peginterferon beta-1a have been reported: a single-dose study (n = 60) comparing SC and im injections of peginterferon beta-1a (63, 125, and 188 [micro]g) with unmodified im interferon beta-1a of 30 [micro]g and a multiple-dose study (n = 69) comparing SC peginterferon beta-1a injected every 2 or 4 weeks with placebo (Hu et al., 2012). Changes in the expression of several biomarkers of the interferon beta response were greater and more sustained after dosing with peginterferon beta-1a than with interferon beta-1a (Hu et al., 2012). With peginterferon beta-1a dosing every 2 or 4 weeks, there were no unexpected adverse events and no reported evidence for either drug accumulation or marked loss of pharmacological response with repeated dosing. In summary, phase I evaluation of peginterferon beta-1a indicated that optimal exposure may be achieved using a reduced dosing schedule, suggesting that expanded dosing intervals are feasible with peginterferon beta-1a.

On the basis of these positive phase I study results, Biogen Idec initiated ADVANCE, a global, 2-year, randomized, double-blind, placebo-controlled phase III study evaluating the drug's efficacy and safety in patients with RMS. In ADVANCE, patients with RMS are administered with 125-[micro]g peginterferon beta-1a SC once every 2 or 4 weeks. The dose of peginterferon beta-1a (125 [micro]g) selected for evaluation in the ADVANCE study was chosen on the basis of its pharmacokinetic, pharmacodynamic, and tolerability profile, as determined in the phase I studies. The patient population for this trial includes individuals between ages 18 and 65 years who have a baseline Expanded Disability Status Scale score of <5.0 and who have had at least two relapses within the last 3 years and at least one relapse in the 12 months before randomization. For all subjects randomized to peginterferon beta-1a, initial dosing incorporates a titration schedule, with an initial dose of 63 [micro]g followed by a 94-[micro]g dose 2 weeks later and the target 125-[micro]g dose 2 weeks after that. Placebo-dosed subjects are rerandomized after 1 year on study to receive peginterferon beta-1a either every 2 or 4 weeks in a dose-blinded fashion, whereas subjects on active drug continue their original dosing schedule.

The phase III trial was designed to determine whether peginterferon beta-1a is able to reduce the patient annualized relapse rate at 1 year relative to placebo (primary study end point). Secondary objectives include determining the efficacy of peginterferon beta-1a in reducing the total number of new or newly enlarging T2-hyperintense lesions on brain MRI, reducing the proportion of subjects who relapse, and slowing the progression of disability. After completing 2 years in the ADVANCE study, subjects will have the option of enrolling in ATTAIN, an open-label extension study. In addition, an ADVANCE substudy includes an investigation of the reliability of biomarkers for interferon activity relative to MRI variables.

The results of these clinical evaluations will provide needed information about the potential benefits of peginterferon beta-1a for treating RMS, including reduced dosing frequency and improved patient convenience and satisfaction, in addition to potential validation that peginterferon beta-1a maintains the proven efficacy, safety, and tolerability of interferon beta-1a.

Potential Role of Nurses in Peginterferon beta-1a Therapy

The recent literature indicates that treatment adherence and early therapeutic intervention are both associated with reduced longer-term disability in patients with RMS (Tan et al., 2011). Nurses play a critical role with respect to both of these factors, as they are often patients' primary clinical contact and source of disease- and therapy-related information. Specifically, nurses provide education on how to properly self-administer injectable therapies and on ways to mitigate injection-site reactions as well as any therapy-related adverse events, including flu-like symptoms. The quality of the nurse-patient relationship can, therefore, play an important role in patient compliance with therapy (Rifion, Buch, Holley & Verdun, 2011; Tan et al., 2011; Tremlett et al., 2008).

To effectively educate patients about the need for early therapeutic intervention and good adherence to prescribed therapy, MS nurses need to be able to recognize the many factors that may lead to poor compliance. As shown by Rinon et al. (2011), physicians and patients differed substantially in the causes to which they attributed lapses in compliance with injectable DMTs. For example, physicians felt that treatment side effects, such as flu-like symptoms, were responsible for over 80% of lapses, although only 42% of patients linked nonadherence to these side effects. By contrast, 13% of patients reported emotional fatigue as a major factor prompting a break in treatment, although this factor was not mentioned by clinicians. Thus, nurses need to work closely with their patients to fully understand the factors that might lead to poor therapeutic adherence and to intervene on their behalf accordingly.

Because the frequency of injections may contribute to the emotional fatigue that patients cite as a reason for noncompliance, adherence to therapy may be improved with therapies that need to be injected less frequently. In this regard, peginterferon beta-1a may be an appealing treatment option for patients whose disease is well controlled with interferon beta therapy, and nurses may be well positioned to identify those patients who would benefit most from the reduced dosing frequency allowed by peginterferon beta-1a.


Pegylation is a well-established technique for improving the pharmacokinetic and pharmacodynamic properties of biological drugs. Pegylated forms of interferon beta-1 are being developed to offer patients with RMS effective and more convenient alternatives to the current injectable therapies. If clinical evaluations such as the ADVANCE trial of peginterferon beta-1a yield positive results, these new interferon drug therapies may provide patients with RMS an effective treatment option that requires significantly fewer injections than currently approved parenterally administered first-line therapies. Nurses will play a vital role in ensuring the optimal use of this new interferon.


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Questions or comments about this article may be directed to Anne Howley, RN, at She is a Research Coordinator at the Multiple Sclerosis Clinic, London Health Sciences Centre, London, Ontario, Canada.

Marcelo Kremenchutzky, MD, is the Director of the Multiple Sclerosis Clinic and a Consultant Neurologist at London Health Sciences Centre and an Associate Professor of Neurology at Western University, London, Ontario, Canada.

Anne Howley has no funding sources or conflicts of interest to report. Marcelo Kremenchutzky has received consultant fees and/ or grant funding from Bayer, Biogen Idec, EMD Serono, Novartis, Sanofi, and Teva.

Biogen Idec provided funding for editorial support in the development of this article, Anne Williamson from Infusion Communications wrote the first draft of the manuscript based on input from authors, and Joshua Safran from Infusion Communications copyedited and styled the manuscript per journal requirements. Biogen Idec reviewed and provided feedback on the article to the authors. The authors had full editorial control of the article and provided their final approval of all content.

TABLE 1. Current DMTs for the Treatment of MS

Generic (Brand)   Indication(s)

Glatiramer        To reduce relapse frequency in patients with
acetate           RMS and patients who have experienced
(Copaxone)        a first clinical episode and have MRI
                  features consistent with MS

Interferon        To slow accumulation of physical disability
beta-1a           and decrease frequency of clinical
(Avonex)          exacerbations in patients with RMS and
                  patients who have experienced a first
                  clinical episode and have MRI features
                  consistent with MS

Interferon        To slow accumulation of physical disability
beta-1a (Rebif)   and decrease frequency of clinical
                  exacerbations in RMS

Interferon        To reduce the frequency of clinical
beta-1b           exacerbations in patients with RMS and
(Betaseron)       patients who have experienced a first
                  clinical episode and have
                  MRI features consistent with MS

Interferon        To reduce the frequency of clinical
beta-1b           exacerbations in patients with RMS and
(Extavia)         patients who have experienced a first
                  clinical episode and have
                  MRI features consistent with MS

Dimethyl          Indicated for patients with relapsing
fumarate          forms of MS

Fingolimod        To reduce frequency of clinical
(Gilenya)         exacerbations and delay accumulation of
                  physical disability in patients with RMS

Natalizumab       As monotherapy for RMS; to delay
(Tysabri)         accumulation of physical disability and
                  reduce frequency of clinical exacerbations

Mitoxantrone      To reduce neurological disability and/or
(Novantrone)      the frequency of clinical relapses in
                  secondary-(chronic) progressive,
                  progressive-relapsing, or worsening
                  relapsing-remitting MS

Teriflunomide     Indicated for patients with relapsing
(Aubagio)         forms of MS

                  Dosing       Elimination
Generic (Brand)   Route and    Half-life
Name              Frequency

Glatiramer        SC, daily    [approximately
acetate                        equal to]
(Copaxone)                     20 hours

Interferon        im, once     [approximately
beta-1a           weekly       equal to]
(Avonex)                       10 hours

Interferon        SC, three    69 [+ or -] 37
beta-1a (Rebif)   times per    hours

Interferon        SC, every    8 minutes-
beta-1b           other day    4.3 hours

Interferon        SC, every    8 minutes-
beta-1b           other day    4.3 hours

Dimethyl          Oral,        1 hour
fumarate          twice
(Tecfidera)       daily

Fingolimod        Oral, once   6-9 days
(Gilenya)         daily

Natalizumab       Infusion,    11 [+ or-] 4
(Tysabri)         once         days

Mitoxantrone      Infusion,    23-215
(Novantrone)      four times   hours
                  per year

Teriflunomide     Oral, once   >3 weeks
(Aubagio)         daily

Note. Information from Copaxone prescribing information
(Teva Neuroscience, 2009), Avonex prescribing information
(Biogen Idec, 2008), Rebif prescribing information (EMD
Serono, 2009), Betaseron prescribing information (Bayer
HealthCare Pharmaceuticals, 2010), Extavia prescribing
information (Novartis Pharmaceuticals Corporation, 2012),
Tecfidera prescribing information (Biogen Idec, 2013),
Gilenya prescribing information (Novartis Pharmaceuticals
Corporation, 2011), Tysabri prescribing information (Biogen
Idec, 2011), Novantrone prescribing information (EMD Serono,
2012), and Aubagio prescribing information (Genzyme Corp.,
2012). DMT = disease-modifying therapy; MS = multiple
sclerosis; RMS = relapsing multiple sclerosis; MRI =
magnetic resonance imaging; SC = subcutaneous; im =
intramuscular. (a) Elimination half-life of active
metabolite, monomethyl fumarate.

TABLE 2. FDA--Approved Pegylated Therapeutics

Name         Drug Name        Native Compound

PegIntron    Peginterferon    Interferon alpha-2b

Pegasys      Peginterferon    Interferon alpha-2a

Adagen       Pegadamase       Adenosine deaminase

Oncaspar     Pegaspargase     Asparaginase

Krystexxa    Pegloticase      Mammalian urate

Neulasta     Pegfilgrastim    Granulocyte

Cimzia       Certolizumab     Therapeutic
             pegol            monoclonal antibody

Mircera      Polyethylene     Epoetin beta

Somavert     Pegvisomant      Growth hormone
                              receptor antagonist

                                     Half-       Half-
                                    life of     life of
                                     Native    Pegylated
Commercial   Clinical               Compound   Compound
Name         Indication             (hours)     (hours)

PegIntron    Hepatitis C, gliomas      9          28

Pegasys      Hepatitis C               8          65

Adagen       Severe combined          0.5       72-144

Oncaspar     Leukemias (acute          20         357
             lymphoblastic and

Krystexxa    Gout                      4          331

Neulasta     Febrile neutropenia      3.5         42

Cimzia       Crohn disease,            NA         336

Mircera      Renal anemia              20         139

Somavert     Acromegaly                NA         144

Note. Adapted with permission from Alconcel, Baas, and
Maynard (2011), copyright 2011 Royal Society of Chemistry.
FDA = U.S. Food and Drug Administration; NA = not
COPYRIGHT 2014 American Association of Neuroscience Nurses
No portion of this article can be reproduced without the express written permission from the copyright holder.
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Author:Howley, Anne; Kremenchutzky, Marcelo
Publication:Journal of Neuroscience Nursing
Article Type:Report
Date:Mar 22, 2014
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