Düsseldorf, Germany, September 10, 2009 –
The multiple sclerosis drug Betaferon® (interferon beta-1b) of Bayer Schering Pharma AG, Germany, may play a role in the protection of brain tissue in patients with multiple sclerosis (MS). This emerged from the results of two new studies presented today at the 25th Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS).
“These novel findings suggest that Betaferon, in addition to its well-established anti-inflammatory properties, could also play a role in controlling oxidative cell damage,” said Ed Croze, Ph.D., Bayer HealthCare, Richmond, CA, the principal investigator of the studies. “It is well known that, in part, neuronal damage can be caused by elevated levels of oxidative stress and free radical formation, suggesting a possible role for Betaferon in neuroprotection. While significant further research needs to be conducted, this is a first indication that Betaferon may regulate important antioxidative pathways.”
Accumulating data indicates that oxidative stress plays a major role in the pathogenesis of MS. These reactive oxygen species are produced during the inflammatory process and may overwhelm the antioxidant defenses, as well as initiate and promote neuronal damage.
The first study in RRMS patients (ECTRIMS, poster topic 16) shows that treatment with Betaferon consistently induced the production of proteins called metallothioneins (MT). MTs have anti-inflammatory properties, which have been shown to protect against oxidative stress and have been demonstrated to act as agents in numerous neuroprotective models.(1)
The second study showed that Betaferon treatment in MS patients induced the expression of a unique form of a protein called NCOA7 (ECTRIMS, poster topic 16). This form of NCOA7 has been shown, like the MTs, to be capable of protecting against oxidative DNA damage.(2)
In patients with MS, the evolution of lesions to chronic black holes has been stipulated to represent a surrogate marker for neuroprotective properties. Chronic black holes are believed to represent permanent brain damage in multiple sclerosis. Thus, the aforementioned anti-oxidative mechanisms may in part explain the results of a recent study published in the August online issue of Journal of Neurology, Neurosurgery & Psychiatry. The BECOME study analyzed the formation of chronic back holes in patients treated with Copaxone® (glatiramer acetate) or Betaferon.
“The results of the BECOME study revealed that the majority of new brain lesions that occur in patients with relapsing MS randomized to treatment with glatiramer acetate or interferon beta-1b when studied by frequent, advanced MRI techniques did not result in chronic black holes, which are thought to represent irreversible damage in multiple sclerosis,” said Stuart D. Cook, M.D., Professor of Neurosciences, Neurology Department, The University of Medicine & Dentistry of New Jersey (UMDNJ). “However, there were significantly fewer black holes that evolved from the inflammatory lesions with interferon beta -1b versus glatiramer acetate.”
BECOME was the first head-to-head trial comparing Betaferon and Copaxone using sensitive monthly MRI parameters to evaluate their potential role in reducing inflammation, decreasing the evolution of inflammatory-enhancing lesions to chronic black holes and limiting loss of axons, neurons and myelin.(3)
About the Study: “Betaferon Increases Expression of Metallothioneins in Relapsing-Remitting Multiple Sclerosis (RRMS) Patients Suggesting a Role for Betaferon in Neuroprotection”
The study used Affymetrix GeneChip® methodologies to test both healthy individuals and RRMS patients after two months of treatment with Betaferon. Betaferon-dependent induction of MT gene expression was confirmed and validated analyzing RNA isolated from blood cells obtained from the subjects.(1)
About the Study: “Betaferon Induces a Novel Alternate Start Transcript in Cells Obtained from Relapsing-Remitting Multiple Sclerosis Patients and Human Brain that is Associated with Control of Oxidative Resistance”
This study used ALL Exon™ GeneChip methodologies to study the effects of a single dose of Betaferon in RRMS patients.(2)