FB102 is an anti-human CD122 (IL-2Rβ) monoclonal antibody with selective activity. FB102 blocks the proliferation and activation of pathogenic NK cells and specific T cell subsets induced by IL-2 and IL-15, without affecting the proliferation of regulatory T cells. FB102 inhibits IL-2/IL-15-induced activation of CD4+ and CD8+ T cells in in vitro disease models. FB102 is applicable to research related to celiac disease [1].
In Vitro, FB102 selectively blocks medium affinity IL-2, low affinity IL-15, and medium affinity IL-15/IL-15Rα binding to CD122/CD132 on effector T or NK cells, while sparing high affinity IL-2 binding to Treg CD25/CD122/CD132 receptors, with measured dissociation constants of ~1 nM, ~10 nM, ~0.01 nM, and ~1 nM respectively for each interaction[1]. FB102 (100 nM) potently inhibits IL-2- and IL-15-induced CD4+ and CD8+ T cell proliferation by 4.1-fold and 4.6-fold respectively, reducing signaling to unstimulated baseline levels with statistically significant effects[1]. FB102 (100 nM) potently inhibits IL-2- and IL-15-induced NK cell proliferation by 15.8-fold and 21.8-fold respectively, reducing signaling to unstimulated baseline levels with statistically significant effects[1]. FB102 does not inhibit IL-2/CD3-induced regulatory T cell proliferation or impact Treg viability in the absence of IL-2 stimulation[1]. FB102 potently inhibits IL-2- and IL-15-induced secretion of IL-6, TNF-α, IFN-γ, and CSF-1 in T cells from three independent human donors[1]. FB102 provides nearly complete inhibition of IL-2/IL-15-induced activation of CD4+ and CD8+ T cells in an in vitro celiac disease model, reducing CD25 expression to near-baseline levels with statistically significant effects[1].
References:
[1]. A. JAMES DAVESON, et al. FB102 prevents histological damage and mitigates glutenchallenge-induced symptoms in a celiac disease Phase 1b study. FORTE BIOSCIENCES. September 15, 2025.
In Vitro, FB102 selectively blocks medium affinity IL-2, low affinity IL-15, and medium affinity IL-15/IL-15Rα binding to CD122/CD132 on effector T or NK cells, while sparing high affinity IL-2 binding to Treg CD25/CD122/CD132 receptors, with measured dissociation constants of ~1 nM, ~10 nM, ~0.01 nM, and ~1 nM respectively for each interaction[1]. FB102 (100 nM) potently inhibits IL-2- and IL-15-induced CD4+ and CD8+ T cell proliferation by 4.1-fold and 4.6-fold respectively, reducing signaling to unstimulated baseline levels with statistically significant effects[1]. FB102 (100 nM) potently inhibits IL-2- and IL-15-induced NK cell proliferation by 15.8-fold and 21.8-fold respectively, reducing signaling to unstimulated baseline levels with statistically significant effects[1]. FB102 does not inhibit IL-2/CD3-induced regulatory T cell proliferation or impact Treg viability in the absence of IL-2 stimulation[1]. FB102 potently inhibits IL-2- and IL-15-induced secretion of IL-6, TNF-α, IFN-γ, and CSF-1 in T cells from three independent human donors[1]. FB102 provides nearly complete inhibition of IL-2/IL-15-induced activation of CD4+ and CD8+ T cells in an in vitro celiac disease model, reducing CD25 expression to near-baseline levels with statistically significant effects[1].
References:
[1]. A. JAMES DAVESON, et al. FB102 prevents histological damage and mitigates glutenchallenge-induced symptoms in a celiac disease Phase 1b study. FORTE BIOSCIENCES. September 15, 2025.