Research Groups
Biotechnology Development
Research Interests and Description
Research Interests
Development of biogenerics.Description of Research
The Biotechnology Development Group (BDG) focuses on the development of simple and innovative technologies for the production of biosimilars. The aim is to increase the know-how and capabilities of the pharmaceutical industries in ICGEB Member States by transferring technologies for the production and quality control of pharmaceutical recombinants: erythropoietin (EPO), interferon alpha 2a and b (IFN alpha 2), interferon beta 1b, granulocyte colony stimulating factor (G-CSF) and Insulin. The labs procedures can be adapted to the conditions existing in Member States with only minimal financial investments necessary to set-up the production facilities.The transfer of these technologies involves the training of scientists from pharmaceutical companies for periods of one to two months. During this time they learn the manipulation of recombinant strains, practice the downstream process and perform quality control procedures in accordance with the guidelines of the European Pharmacopoeia.
Over the past few years, the Group has trained more than 70 scientists from 17 pharmaceutical companies operating in different ICGEB Member States. Most of these companies are now producing biosimilars using our technologies. These products are not only sold on the local markets but also successfully compete on the international market.
Collaborations
PEG-IFN and PEG-G-CSF: The Protein Structure Group (PSG) at the Trieste Component has developed a new technology for the production of Interferon peguilated (IFN-PEG). The PSG is also developing the technology for the peguilation of G-CSF and new methods for the activation of PEG. Presently, we are working on an innovative EPO-PEG technology.
Recent Publications
Zago, P., Baralle, M., Ayala, Y.M., Skoko, N., Zacchigna, S., Buratti, E., Tisminetzky, S. 2009. Improving human interferon-beta production in mammalian cell lines by insertion of an intronic sequence within its naturally uninterrupted gene. Biotechnol. Appl. Biochem. 52, 191-198 [Pubmed link]
Skoko, N., Baralle, M., Buratti, E., Baralle, F.E. 2008. The pathological splicing mutation c.6792C>G in NF1 exon 37 causes a change of tenancy between antagonistic splicing factors. FEBS Lett. 582, 2231–2236 [Pubmed link]
Goina, E., Skoko, N., Pagani, F. 2008. Binding of DAZAP1 and hnRNPA1/A2 to an exonic splicing silencer in a natural BRCA1 exon 18 mutant. Mol. Cell Biol. 28, 3850-3860 [Pubmed link]
Baralle, M., Baralle, F.E. 2008. Genetics and molecular biology: variations in alternative spliced pre-mRNA-protein isoforms and their role in disease. Curr. Opin. Lipidol. 19, 429-430
Baralle, M., Pastor, T., Bussani, E., Pagani, F. 2008. Influence of Friedreich ataxia GAA noncoding repeat expansions on pre-mRNA processing. Am. J. Hum. Genet. 83, 77-88
