Journal: Frontiers in Immunology
Article Title: Maplirpacept: a CD47 decoy receptor with minimal red blood cell binding and robust anti-tumor efficacy
doi: 10.3389/fimmu.2025.1518787
Figure Lengend Snippet: Maplirpacept controls tumor burden in in vivo models of hematological malignancy. Tumor growth of (A) DLBCL models (DOHH2 [n=10], SUDHL8 [n=10], Toledo [n=9]), (B) Karpas 299 (n=8) and (C) OCI-AML2 (n=10) implanted subcutaneously in immune deficient mice and dosed with maplirpacept at 3 mg/kg (Karpas 299), 10 mg/kg (DOHH2, Toledo, OCI-AML2) or, 50 mg/kg (SU-DHL-8). Dosing was initiated when initial tumor volumes reached 100-150 mm 3 . Toledo study had 5/9 unmeasurable tumors at the beginning of dosing. (D) Tumor growth of luciferase expressing MOLP-8 tumors implanted intravenously and treated with 10 mg/kg maplirpacept subcutaneously. Tumor growth was measured by bioluminescent imaging (BLI), (n=8). (E) NOD.SCID mice were preconditioned with sublethal irradiation and anti-CD122 antibody and then transplanted with AML patient derived mononuclear cells by intrafemoral injection. Treatment with maplirpacept (1 or 5 mg/kg i.p. 3×/week for 4 weeks) or equimolar Fc Control was initiated 14 days post-transplantation. The percent AML engraftment (% cells expressing human CD45 and CD33) was assessed by flow cytometry. Each symbol represents one mouse (Fc Control, n =7; Maplirpacept. n=8). Error bars represent SEM. Statistical significance was determined by one-way ANCOVA (A–D) or one-way ANOVA (E) (*P <0.05, **P<0.01, ****P<0.0001). CR=complete responder (defined as unmeasurable tumor at study end for subcutaneous models (not necessarily TGI endpoint in some studies) and BLI equivalent to baseline in IV models).
Article Snippet: All cell lines were obtained from ATCC except DOHH2 (DSMZ), MOLP-8 (DSMZ), OCI-AML2 (DSMZ) and Karpas 299 (Sigma-Aldrich).
Techniques: In Vivo, Luciferase, Expressing, Imaging, Irradiation, Derivative Assay, Injection, Control, Transplantation Assay, Flow Cytometry
DSMZ is a verified supplier 
![Maplirpacept controls tumor burden in in vivo models of hematological malignancy. Tumor growth of (A) DLBCL models <t>(DOHH2</t> [n=10], SUDHL8 [n=10], Toledo [n=9]), (B) Karpas 299 (n=8) and (C) OCI-AML2 (n=10) implanted subcutaneously in immune deficient mice and dosed with maplirpacept at 3 mg/kg (Karpas 299), 10 mg/kg (DOHH2, Toledo, OCI-AML2) or, 50 mg/kg (SU-DHL-8). Dosing was initiated when initial tumor volumes reached 100-150 mm 3 . Toledo study had 5/9 unmeasurable tumors at the beginning of dosing. (D) Tumor growth of luciferase expressing MOLP-8 tumors implanted intravenously and treated with 10 mg/kg maplirpacept subcutaneously. Tumor growth was measured by bioluminescent imaging (BLI), (n=8). (E) NOD.SCID mice were preconditioned with sublethal irradiation and anti-CD122 antibody and then transplanted with AML patient derived mononuclear cells by intrafemoral injection. Treatment with maplirpacept (1 or 5 mg/kg i.p. 3×/week for 4 weeks) or equimolar Fc Control was initiated 14 days post-transplantation. The percent AML engraftment (% cells expressing human CD45 and CD33) was assessed by flow cytometry. Each symbol represents one mouse (Fc Control, n =7; Maplirpacept. n=8). Error bars represent SEM. Statistical significance was determined by one-way ANCOVA (A–D) or one-way ANOVA (E) (*P <0.05, **P<0.01, ****P<0.0001). CR=complete responder (defined as unmeasurable tumor at study end for subcutaneous models (not necessarily TGI endpoint in some studies) and BLI equivalent to baseline in IV models).](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_7230/pmc11897230/pmc11897230__fimmu-16-1518787-g004.jpg)