MUBODINA® is a new recombinant human monoclonal antibody against the Complement component C5. The molecule antibody has an anti-inflammatory action. This minibody prevents the cleavage of C5 and inhibits the generation of inflammatory molecule C5a and of TCC lytic complex. The inhibition of component C5 preserves the immunoprotection and immunoregulation of upstream components critical functions that brings to the opsonization of pathogen-mediated C3b and immune complexes cleaning.

MUBODINA® has been approved as Orphan Drug by FDA in 2009 for the indication: "Treatment of primary membranoproliferative glomerulonephritis. MUBODINA® has been approved as Orphan Drug by EMA in 2008 for the indication "Treatment of atypical Haemolitic Uremic Syndrome (aHUS) associated with an inherited abnormality of the complement system" and by FDA in 2009 for the indication "Treatment of primary membranoproliferative glomerulonephritis" and in 2011 for the indication "Treatment of atypical Hemolitic Uremic Syndrome associated with an inherited abnormality of the complement system".

MUBODINA® has been developed through the SAND5 Project together with another interesting antibody molecule: ERGIDINA®.


Learn more about atypical Hemolytic-Uremic Syndrome (aHUS)



Hemolytic-Uremic Syndrome (HUS) combines pathological conditions affecting the blood and kidneys, such as hemolytic anemia, thrombocytopenia and acute renal failure. Affects predominantly, but not exclusively, the children. In most cases (80-90%) is preceded by episodes of diarrhea caused by a strain of Escherichia coli, the enterohemorrhagic (O157: H7). This typical form of HUS has a mortality rate that is between 5 and 10% of cases.

The atypical or non-enteropathic hemolytic-uremic syndrome (aHUS) is associated with a less favorable prognosis than the classic form. Missing an onset of symptoms affecting the gastro-intestinal tract, the atypical HUS usually has an etiology due to genetic factors and therefore can affect, even after some time, members of the same family group. Finally, there are rare cases in which the hemolytic-uremic syndrome develops as a sequela of systemic infection by Streptococcus pneumoniae.


Learn more about Membranoproliferative-glomerulonephritis (MPGN)

Membranoproliferative-glomerulonephritis (MPGN) is a renal disease, resulting in inflammation of the glomerular lesions caused by membrane filtration and glomerular cell proliferation. In its primary type, the MPGN is an immune complex disease. The clinical picture is characterized by severe proteinuria and nephrotic syndrome related to door within about 10 years to the development of ESRD.    

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