Valziflocept (BAX1810) is a recombinant soluble human FcγRIIb receptor that targets Fc and FcγR. FcγRs bind to and neutralize pathogenic IgG, thereby acting as a "decoy" or "scavenger" receptor that reduces the severity of autoimmune diseases. Valziflocept is used in research on autoimmune diseases such as systemic lupus erythematosus (SLE) [1] [2] [3].
In Vivo, Valziflocept (200 μg per dose; i.v.; 5 occasions with 3-day intervals) significantly ameliorates collagen-induced arthritis in male DBA/1 mice, reducing mean arthritic scores, pathogenic antibody levels, and inflammatory cytokine mRNA expression[1]. Valziflocept (50-150 μg/week; s.c.; weekly; 4 weeks) delays onset of lupus pathology and improves survival in NZB/NZW F1 mice, while valziflocept (100 μg/week; s.c.; weekly; until death or study end (therapeutic)) significantly prolongs survival despite established kidney damage[2].
In Vitro, Valziflocept significantly inhibits phagocytosis of IgG-opsonised murine red blood cells by thioglycolate-elicited peritoneal macrophages from female NZB/NZW F1 mice[2].
References:
[1]. Magnusson SE, et al. Amelioration of collagen-induced arthritis by human recombinant soluble FcgammaRIIb. Clin Immunol. 2008;127(2):225-233.
[2]. Werwitzke S, et al. Treatment of lupus-prone NZB/NZW F1 mice with recombinant soluble Fc gamma receptor II (CD32). Ann Rheum Dis. 2008 Feb;67(2):154-61.
[3]. Zuercher AW, et al. Next-generation Fc receptor-targeting biologics for autoimmune diseases. Autoimmun Rev. 2019;18(10):102366.
In Vivo, Valziflocept (200 μg per dose; i.v.; 5 occasions with 3-day intervals) significantly ameliorates collagen-induced arthritis in male DBA/1 mice, reducing mean arthritic scores, pathogenic antibody levels, and inflammatory cytokine mRNA expression[1]. Valziflocept (50-150 μg/week; s.c.; weekly; 4 weeks) delays onset of lupus pathology and improves survival in NZB/NZW F1 mice, while valziflocept (100 μg/week; s.c.; weekly; until death or study end (therapeutic)) significantly prolongs survival despite established kidney damage[2].
In Vitro, Valziflocept significantly inhibits phagocytosis of IgG-opsonised murine red blood cells by thioglycolate-elicited peritoneal macrophages from female NZB/NZW F1 mice[2].
References:
[1]. Magnusson SE, et al. Amelioration of collagen-induced arthritis by human recombinant soluble FcgammaRIIb. Clin Immunol. 2008;127(2):225-233.
[2]. Werwitzke S, et al. Treatment of lupus-prone NZB/NZW F1 mice with recombinant soluble Fc gamma receptor II (CD32). Ann Rheum Dis. 2008 Feb;67(2):154-61.
[3]. Zuercher AW, et al. Next-generation Fc receptor-targeting biologics for autoimmune diseases. Autoimmun Rev. 2019;18(10):102366.