Plegridy (peginterferon beta-1a) is a subcutaneous injectable therapy, in which interferon beta-1a is pegylated to extend its half-life to permit a less frequent dosing schedule.
Plegridy is specifically indicated for relapsing forms of multiple sclerosis.
Plegridy is supplied as a solution for subcutaneous administration. The recommended dosage of Plegridy is 125 micrograms injected subcutaneously every 14 days. Patients should start treatment with 63 micrograms on day 1. On day 15 (14 days later), the dose is increased to 94 micrograms, reaching the full dose of 125 micrograms on day 29 (after another 14 days). Patients should continue with the full dose (125 micrograms) every 14 days thereafter.
The FDA approval of Plegridy was based on a randomized, double-blind, and placebo controlled, one-year study. The trial compared clinical and MRI outcomes at 48 weeks in patients who received Plegridy 125 micrograms (n=512) or placebo (n=500) subcutaneously once every 14 days. All subjects had a baseline Expanded Disability Status Scale (EDSS) score from 0 to 5, had experienced at least 2 relapses within the previous three years, and had experienced at least 1 relapse in the previous year. None of the subjects had progressive MS. Neurological evaluations were scheduled at baseline, every 12 weeks, and at the time of a suspected relapse. Brain MRI evaluations were scheduled at baseline, week 24, and week 48. The primary outcome was the annualized relapse rate over 1 year. The annualized relapse rate was 0.26 in the Plegridy arm and 0.40 in the placebo arm; relative reduction 36% (p=0.0007).
Adverse effects associated with the use of Plegridy may include, but are not limited to, the following:
Plegridy (peginterferon beta-1a) is a subcutaneous injectable therapy, in which interferon beta-1a is pegylated to extend its half-life to permit a less frequent dosing schedule. Interferon-beta (IFN-beta) is a polypeptide, normally produced by fibroblasts, that has antiviral and antiproliferative effects. Binding of IFN-beta to its receptor induces a complex transcriptional response. In immune cells (the most likely target of IFN-beta's therapeutic effect in MS), IFN-beta reduces antigen presentation and T-cell proliferation, alters cytokine and matrix metalloproteinase (MMP) expression, and restores suppressor function. Therapeutic forms of IFN-beta can be produced in bacterial expression systems (IFN-beta1b) or in mammalian cells (IFN-beta1a). The exact mechanism by which Plegridy exerts its effects in patients with multiple sclerosis is unknown.
For additional information regarding Plegridy or relapsing multiple sclerosis, please visit www.plegridy.com