Thromb Haemost 1990; 63(03): 386-391
DOI: 10.1055/s-0038-1645053
Original Article
Schattauer GmbH Stuttgart

Lack of Immune Response to Mouse IgG in Hemophilia A Patients Treated Chronically with Monoclate®, a Monoclonal Antibody Affinity Purified Factor VIII Preparation

Hugh M Davis
Rorer Central Research, King of Prussia, PA, USA
,
Susan K Brown
Rorer Central Research, King of Prussia, PA, USA
,
David W Nash
Rorer Central Research, King of Prussia, PA, USA
,
Aniello M Pennetti
Rorer Central Research, King of Prussia, PA, USA
,
Phyllis M Salzman
Rorer Central Research, King of Prussia, PA, USA
,
Alian B Schreiber
Rorer Central Research, King of Prussia, PA, USA
,
Joseph Haimovich
Rorer Central Research, King of Prussia, PA, USA
› Institutsangaben
Weitere Informationen

Publikationsverlauf

Received 15. November 1989

Accepted after revision 06. März 1990

Publikationsdatum:
30. Juni 2018 (online)

Summary

Hemophilia A is caused by factor VIII deficiency that historically has been treated with either a cryoprecipitate fraction of serum or factor VIII concentrate. Recently, the availability of affinity isolated factor VIII (Monoclate®) has allowed for a highly purified preparation for the chronic therapy of hemophilia A. This factor VIII preparation contains a trace quantity (<50 ng/ 100 I. U.) of mouse IgG. Immunoassays for the measurement of human IgG, IgJVl and IgE anti-mouse TgG antihody (HAMA) were developed and used to measure HAMA levels in hemophilia A patients undergoing chronic therapy with Monoclate® in three different clinical studies. Natural antibodies to mouse IgG were observed in patient sera prior to Monoclate® infusion. Data is presented demonstrating that induction of HAMA upon Monoclate® treatment does not occur. The low level of mouse IgG contained in Monoclate® appears to be below the threshold of immunogenicity. Most importantly, clinical symptoms related to hypersensitivity or anaphylaxis were never observed in any patient undergoing chronic therapy with Monoclate® in these clinical studies.