Ramantamig (JNJ-79635322) is a humanized monoclonal antibody targeting human CD3ε, GPRC5D, and TNFRSF17 (BCMA). Ramantamig binds to BCMA and GPRC5D on multiple myeloma cells, binds to CD3ε on T cells, forms immunological synapses, and enables T-cell-mediated cytotoxicity. Ramantamig activates T cells concomitantly with inducing myeloma cell cytotoxicity, with no nonspecific T-cell activation in the absence of target myeloma cells. Ramantamig carries mutations to reduce interaction with Fc receptors and disrupt protein A binding of monomeric and homodimerized chains. Ramantamig can be used for the research of multiple myeloma [1].
In Vivo, Ramantamig (JNJ-79635322) (0.1-2.5 mg/kg; i.p.; twice weekly; 8 doses) induces dose-dependent tumor growth inhibition and complete regression in RPMI 8226 multiple myeloma xenografts, with the 2.5 mg/kg dose achieving 111.2% ΔTGI and 95.2% tumor regression by day 38, and 100% complete regression by day 60[1]. Ramantamig (0.025-1 mg/kg; i.p.; twice weekly; 7 doses) induces dose-dependent tumor growth inhibition and complete regression in MM.1S multiple myeloma xenografts, with the 1 mg/kg dose achieving 109% ΔTGI and 100% tumor regression by day 34, and sustaining 100% complete regression by day 51[1].
In Vitro, Ramantamig (72 h) potently induces T-cell-mediated cytotoxicity and activation in BCMA-GPRC5D dual-positive human multiple myeloma cell lines (MM.1S, H929, JIM-3, OPM-2) with sub-nanomolar to low nanomolar EC50 values, but has no effect on dual-negative myeloid cell lines[1]. Ramantamig (72 h) induces potent T-cell-mediated cytotoxicity and activation in H929-WT, H929-BCMA-KO, and H929-GPRC5D-KO human multiple myeloma cell lines, with significantly higher potency against dual-target-expressing H929-WT cells[1]. Ramantamig (48 h) potently induces T-cell-mediated cytotoxicity, T-cell activation, and proinflammatory cytokine production in H929 human multiple myeloma cells spiked into healthy human whole blood, with low nanomolar EC50 values[1]. Ramantamig (48 h) does not induce nonspecific T-cell activation or immune cell cytotoxicity in healthy human purified T cells or whole blood, except at very high concentrations (>10 nM)[1].
References:
[1]. Pillarisetti K, et al. Ramantamig (JNJ-79635322), a novel T-cell-engaging trispecific antibody targeting BCMA, GPRC5D, and CD3, in multiple myeloma models. Blood. 2026;147(8):834-847.
In Vivo, Ramantamig (JNJ-79635322) (0.1-2.5 mg/kg; i.p.; twice weekly; 8 doses) induces dose-dependent tumor growth inhibition and complete regression in RPMI 8226 multiple myeloma xenografts, with the 2.5 mg/kg dose achieving 111.2% ΔTGI and 95.2% tumor regression by day 38, and 100% complete regression by day 60[1]. Ramantamig (0.025-1 mg/kg; i.p.; twice weekly; 7 doses) induces dose-dependent tumor growth inhibition and complete regression in MM.1S multiple myeloma xenografts, with the 1 mg/kg dose achieving 109% ΔTGI and 100% tumor regression by day 34, and sustaining 100% complete regression by day 51[1].
In Vitro, Ramantamig (72 h) potently induces T-cell-mediated cytotoxicity and activation in BCMA-GPRC5D dual-positive human multiple myeloma cell lines (MM.1S, H929, JIM-3, OPM-2) with sub-nanomolar to low nanomolar EC50 values, but has no effect on dual-negative myeloid cell lines[1]. Ramantamig (72 h) induces potent T-cell-mediated cytotoxicity and activation in H929-WT, H929-BCMA-KO, and H929-GPRC5D-KO human multiple myeloma cell lines, with significantly higher potency against dual-target-expressing H929-WT cells[1]. Ramantamig (48 h) potently induces T-cell-mediated cytotoxicity, T-cell activation, and proinflammatory cytokine production in H929 human multiple myeloma cells spiked into healthy human whole blood, with low nanomolar EC50 values[1]. Ramantamig (48 h) does not induce nonspecific T-cell activation or immune cell cytotoxicity in healthy human purified T cells or whole blood, except at very high concentrations (>10 nM)[1].
References:
[1]. Pillarisetti K, et al. Ramantamig (JNJ-79635322), a novel T-cell-engaging trispecific antibody targeting BCMA, GPRC5D, and CD3, in multiple myeloma models. Blood. 2026;147(8):834-847.