Latest research on Betaseron

Human interferon beta (165 residues), cysteine 17 is substituted with serine. Produced in E. coli, no carbohydrates, MW=18.5kD

Latest findings

Patients with a diagnosis of RRMS were eligible if they had been continuously treated with an approved DMT—interferon (IFN) (Avonex, Betaferon, Extavia, or Rebif) or GA (Copaxone)—for at least 30 days, and if informed consent was given prior to study inclusion. [source, 2016]
Of the thirty-three RR-MS patients, fourteen patients were on interferon-β1a (Avonex, Biogen Idec, Cambridge, MA USA), ten patients were on interferon-β1a (Rebif, Merck Serono, Rockland, MA, USA), seven patients were on interferon-β1a (Betaseron, Bayer HealthCare Pharmaceuticals, Montville, NJ, USA), ten patients were on glatiramer acetate (Copaxone, Teva pharmaceuticals, North Wales, PA, USA) and one patient was on natalizumab (Tysabri, Biogen Idec, Cambridge, MA USA). [source, 2015]
Of the twelve PP-MS patients, four were on interferon-β1a (Avonex, Biogen Idec, Cambridge, MA USA), two patients were on interferon-β1a (Rebif, Merck Serono, Rockland, MA, USA), four patients were on interferon-β1a (Betaseron, Bayer HealthCare Pharmaceuticals, Montville, NJ, USA) and two patients were on glatiramer acetate (Copaxone, Teva pharmaceuticals, North Wales, PA, USA). [source, 2015]
Thus, we compared these subjects to RRMS on stable Betaseron therapy. [source, 2015]
We found that levels of TROVE2, SSB, poly(A) + Y1 RNA and poly(A) + U1 snRNA were close to CTRL levels in RRMS subjects on Betaseron therapy compared to RRMS subjects on either Copaxone or no immunomodulatory therapy (Figure 6A, B). [source, 2015]
We examined responses of three individuals in longitudinal studies who initiated Betaseron and found that correction of levels of TROVE2, SSB, poly(A) + Y1 RNA and poly(A) + U1 RNA was very rapid. [source, 2015]
We hypothesize that signaling pathways either directly or indirectly activated by Betaseron interfere with signaling pathways driving defects in polyadenylation of structural RNAs in and expression of TROVE2 and SSB in RRMS and that Betaseron will be a useful tool to identify underlying mechanisms. [source, 2015]
Further, measurement of polyadenylated species of ncRNAs may provide a useful means to monitor responses to Betaseron or other immunomodulatory therapies in RRMS. [source, 2015]
Finally, IFN-β1b or Betaseron, a common therapy for RRMS, but not other autoimmune diseases, restores the balance of polyadenylated structural RNAs to normal and reverses the loss of Ro60 and La that is seen in RRMS. [source, 2015]
It is also noteworthy that therapy IFN-β1b (Betaseron), a common treatment for RRMS, restores levels of Ro60 and La proteins and polyadenylated structural RNA substrates to near normal. [source, 2015]