ATGAM is composed of antibodies that bind a wide variety of proteins on the surface of lymphocytes. In addition, ATGAM binds to granulocytes, platelets, bone marrow cells, and other cell types. The mechanism of ATGAM-induced immunosuppression has not been determined. Published data indicate that the primary mechanism is the depletion of circulating lymphocytes, with greatest effect on T lymphocytes. Lymphocyte depletion may be caused by complement dependent lysis and/or activation-induced apoptosis. In addition, immunosuppression may be mediated by the binding of antibodies to lymphocytes which results in partial activation and induction of T lymphocyte anergy.
The mechanism of ATGAM therapy for aplastic anemia is attributed to its immunosuppressive actions. In addition, ATGAM directly stimulates the growth of hematopoietic stem cells and release of hematopoietic growth factors such as interleukin-3 and granulocyte/macrophage colony stimulating factor.
Standard pharmacodynamic studies were not performed. Key efficacy endpoints in the ATGAM pivotal studies were clinical responses rather than pharmacodynamic endpoints [see Clinical Studies (14)].
Distribution
In a multicenter study, ATGAM pharmacokinetics were evaluated in 27 renal transplant patients. During infusion of 10 to 15 mg/kg/day, the mean peak value was found to be 727 ± 310 μg/mL.
Metabolism and Elimination
The half-life of equine immunoglobulin after ATGAM infusion was found to be 5.7 ± 3.0 days in renal transplant patients (n=27). The range for half-life was 1.5 to 13 days.
Specific Populations
Ethnicity
ATGAM pharmacokinetics were evaluated in a study of 6 Japanese adult patients with moderate or severe aplastic anemia. When administered via intravenous infusion at a dose of 10 mg/kg/day (n=3) or 20 mg/kg/day (n=3) for 8 days, the mean concentration was 1,180 ± 240 µg/mL and 2,060 ± 340 µg/mL, respectively at 1 hour after completion of infusion on Day 8. The apparent elimination half-life after the last dose varied from 1.3 to 6 days in these patients.
ATGAM is composed of antibodies that bind a wide variety of proteins on the surface of lymphocytes. In addition, ATGAM binds to granulocytes, platelets, bone marrow cells, and other cell types. The mechanism of ATGAM-induced immunosuppression has not been determined. Published data indicate that the primary mechanism is the depletion of circulating lymphocytes, with greatest effect on T lymphocytes. Lymphocyte depletion may be caused by complement dependent lysis and/or activation-induced apoptosis. In addition, immunosuppression may be mediated by the binding of antibodies to lymphocytes which results in partial activation and induction of T lymphocyte anergy.
The mechanism of ATGAM therapy for aplastic anemia is attributed to its immunosuppressive actions. In addition, ATGAM directly stimulates the growth of hematopoietic stem cells and release of hematopoietic growth factors such as interleukin-3 and granulocyte/macrophage colony stimulating factor.
Standard pharmacodynamic studies were not performed. Key efficacy endpoints in the ATGAM pivotal studies were clinical responses rather than pharmacodynamic endpoints [see Clinical Studies (14)].
Distribution
In a multicenter study, ATGAM pharmacokinetics were evaluated in 27 renal transplant patients. During infusion of 10 to 15 mg/kg/day, the mean peak value was found to be 727 ± 310 μg/mL.
Metabolism and Elimination
The half-life of equine immunoglobulin after ATGAM infusion was found to be 5.7 ± 3.0 days in renal transplant patients (n=27). The range for half-life was 1.5 to 13 days.
Specific Populations
Ethnicity
ATGAM pharmacokinetics were evaluated in a study of 6 Japanese adult patients with moderate or severe aplastic anemia. When administered via intravenous infusion at a dose of 10 mg/kg/day (n=3) or 20 mg/kg/day (n=3) for 8 days, the mean concentration was 1,180 ± 240 µg/mL and 2,060 ± 340 µg/mL, respectively at 1 hour after completion of infusion on Day 8. The apparent elimination half-life after the last dose varied from 1.3 to 6 days in these patients.
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