Fig. 5
EDO-S101 is active in four xenograft models of human plasmacytoma. a CB17-SCID mice (n = 5/group) were treated with vehicle (control group) and EDO-S101 (60 mg/kg iv, weekly) for 21 days, and tumor growth evolution was evaluated. b Survival of mice in experiment a analyzed with a Kaplan–Meier curve. c Four CB17-SCID mice (n = 2/group) with large plasmacytomas (median of 4000 mm3) were administered two consecutive doses of EDO-S101 (60 mg/kg) in two consecutive days, and tumors were then excised to analyze the mechanism of action of EDO-S101. Representative immunohistochemical stainings of big plasmacytomas are shown. d Tumor volume evolution of mice with large plasmacytomas (n = 2/group), different from experiment c, were treated for 21 days at 60 mg/kg. e Two de novo Vk*MYC mice with established MM (M-spike >10 g/L) received two weekly doses of 40 mg/kg EDO-S101 by intra-cardiac injection. M-spike levels were measured at day 14 and plotted as percentage of day 0. The response to standard of care agents is shown as a comparison. f Four C57BL/6 wild type mice engrafted with Vk12653 MM tumor cells received two weekly doses of 40 mg/kg EDO-S101 by intra-cardiac injection. M-spike levels were measured at day 14 and plotted as percentage of day 0. The response to standard of care agents is shown as a comparison. g Kaplan–Meier survival curve of 18 C57BL/6 WT mice transplanted with Vk12653 MM tumor cells and randomized to receive vehicle or two weekly doses of 40 mg/kg EDO-S101 by intra-cardiac injection upon tumor engraftment (M-spike >10 g/L)