We're proud to share this concise overview of our work showcased at @ATCMeeting. The team has been driven over decades to provide improved diagnostic methods that will ultimately change patient care, & we're excited to share this glimpse into our work.
youtube.com/watch?v=lWsDFtY4…
ALT Panel A: Sankey plots of the dynamics of morphologic antibody-mediated rejection (active or chronic active) as compared with no activity (chronic inactive or no rejection) in the felzartamab and placebo groups across biopsy samples obtained at baseline, week 24, and week 52.
Panel B: The microvascular inflammation score (a sum score of glomerulitis and peritubular capillaritis)
in biopsy samples according to the Banff classification at baseline, week 24, and week 52.
Panel C: Molecular score reflecting the probability of antibody-mediated rejection in biopsy samples obtained at baseline, week 24, and week 52.
ALT Panel A: Graph with line plots and I bars showing the percent change in the mean fluorescence intensity of donor-specific antibody in the two trial groups.
Panel B: Box plot of peripheral-blood CD16bright NK-cell counts.
Panel C: Box plot of the fraction of donor-derived cell-free DNA.
Panel D: Box plot of the number of copies of torque teno virus (TTV).
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.
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 microcirculation inflammation.