Technology FAQ

GlycoMAb technology is specifically designed for increasing the potency of therapeutic antibodies. For products blocked at any stage of development due to poor efficacy, GlycoMAb may be able to return them back into development.

Yes, GlycoMAb operates in the constant region of therapeutic antibodies and is therefore applicable to chimeric, humanized or fully human antibodies, independent of their variable regions.

Yes, we have successfully implemented our GlycoMAb in a wide variety of standard antibody producing cell lines commonly used in the biotechnology and pharmaceutical industries. We are regularly able to generate stable clones that maintain their specific antibody productivity and growth rate.

GlycoMAb leads to robust and highly stable production cell lines. GlycoMAb offers the flexibility to choose the pathway for its implementation; i.e. to apply GlycoMAb to an antibody producing cell line or to incorporate the antibody genes in an “empty” GlycoMAb cell line. It is rapidly implemented via standard procedures widely used in industry. It does not affect the specific antibody productivity or the growth rate of the parent cell line. GlycoMAb is a natural and cost efficient technology that does not use toxic, immunogenic, or radioactive moieties that can lead to complex logistics from production to administration to patients. Implementation of GlycoMAb does not add new unit operations to the production process.

Recent scientific work for some target-cell killing antibodies shows a correlation between objective patient response rates and increased binding affinity of the constant region of the antibody to CD16 (Fc-receptor expressed in immune effector cells). Such binding is largely increased with GlycoMAb.

GlycoMAb can deliver the maximal increase in binding affinity to FcgRIIIa that can be achieved by Fc de-fucosylation. The efficient and robust method to achieve high levels of non-fucosylated complex oligosaccharides in antibodies produced in any cell line was taught in US patent 6,602,684 (priority date April 1998).

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