Felzartamab's Potential in Reducing Antibody-Mediated Kidney Allograft Rejection
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Reviewed & Translated by Dat Tien Nguyen, B.A, ScM.
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Posted on August 9th, 2024
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Currently, no approved treatment exists for antibody-mediated rejection of kidney allografts. CD38, a glycoprotein abundantly expressed on plasma cells and natural killer cells, presents a promising therapeutic target. Inhibiting CD38 can neutralize these immune cells and reduce inflammation. Felzartamab, an antibody targeting CD38, was studied in a trial sponsored by MorphoSys to evaluate its effectiveness in reducing the risk of kidney allograft rejection.
The phase 2 clinical trial involved 22 participants diagnosed with antibody-mediated rejection within 180 days of kidney transplantation, with a median estimated glomerular filtration rate (eGFR) of 37 mL/min/1.73 square meters. Participants were randomly assigned to receive either a placebo or felzartamab at a dose of 16 mg per kilogram of body weight, administered intravenously once per week for the first four weeks, and then once a month for the next five months. After 24 weeks, 82% of those treated with felzartamab showed little or no antibody-mediated rejection, compared to 20% in the placebo group. Additionally, those treated with felzartamab experienced less microvascular inflammation. Felzartamab did not cause significant adverse reactions. However, due to the small sample size, a larger phase 3 clinical trial with a longer observation period is necessary to draw definitive conclusions about the effectiveness and safety profile of felzartamab.
The phase 2 clinical trial involved 22 participants diagnosed with antibody-mediated rejection within 180 days of kidney transplantation, with a median estimated glomerular filtration rate (eGFR) of 37 mL/min/1.73 square meters. Participants were randomly assigned to receive either a placebo or felzartamab at a dose of 16 mg per kilogram of body weight, administered intravenously once per week for the first four weeks, and then once a month for the next five months. After 24 weeks, 82% of those treated with felzartamab showed little or no antibody-mediated rejection, compared to 20% in the placebo group. Additionally, those treated with felzartamab experienced less microvascular inflammation. Felzartamab did not cause significant adverse reactions. However, due to the small sample size, a larger phase 3 clinical trial with a longer observation period is necessary to draw definitive conclusions about the effectiveness and safety profile of felzartamab.