HOT OFF THE PRESS! NEJM Felzartamab paper

We are excited to report the publication of our recent collaborative study with Vienna and Berlin, published Saturday in N Engl J Medicine (https://www.nejm.org/doi/full/10.1056/NEJMoa2400763). We studied the problem of antibody-mediated rejection (ABMR), a microcirculation disease mediated by NK cells that damages the kidney microcirculation in thousands of kidney and heart transplant recipients.

We analyzed the molecular effects of Felzartamab (FELZ) anti CD38 antibody on antibody-mediated rejection in kidney transplant recipients, in addition to changes in histology and circulating donor-derived cell-free DNA.  The FELZ treatment suppressed ABMR molecular and histologic ABMR activity, particularly the NK cell genes, and suppressed dd-cfDNA. This is historic: since we first described ABMR as a microcirculation disease 34 years ago (1), this is the first controlled trial to show an agent that can suppress the microcirculation inflammation.  It also suggests that dd-cfDNA could be used to help manage these patients during treatment. We are committed to seeing how this agent can benefit kidney transplants with ABMR in a controlled phase 3 trial, hopefully led by our collaborators in Vienna and Berlin.

(1) Halloran, P. F., et al. (1990). "The significance of the anti-class I antibody response. I. Clinical and pathologic features of anti-class I-mediated rejection." Transplantation 49(1): 85-91.