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. 2023 Jul-Aug;64(7):1335-1339.
doi: 10.1080/10428194.2023.2210710. Epub 2023 May 11.

[211At]astatine-based anti-CD22 radioimmunotherapy for B-cell malignancies

George S Laszlo  1 , Brenda M Sandmaier  1   2 , Allie R Kehret  1 , Johnnie J Orozco  1   2 , Donald K Hamlin  3 , Shannon L Dexter  1 , Sheryl Y T Lim  1 , Frances M Cole  1 , Jenny Huo  1 , D Scott Wilbur  3 , Roland B Walter  1   4   5   6
Affiliations

[211At]astatine-based anti-CD22 radioimmunotherapy for B-cell malignancies

George S Laszlo et al. Leuk Lymphoma. 2023 Jul-Aug.
No abstract available

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Conflict of interest statement

COMPETING INTERESTS

All authors declare no competing conflict of interest.

Figures

Figure 1
Figure 1. In vitro characteristics of anti-CD22 mAbs.
FPLC traces and SDS-PAGE Western blot analyses under non-reducing and reducing conditions for (A) epratuzumab and (B) G5/44. CD22+ Raji and Ramos cells were used for flow cytometric phenotyping of unconjugated anti-CD22 mAs (epratuzumab (C) and G5/44 (D)) or anti-CD22 mAbs that were reacted with 5, 10, or 15 equivalents of B10. A secondary mAb-only control is also shown.
Figure 2
Figure 2. In vivo characteristics of 211At-labeled anti-CD22 mAbs.
(A) For assessment of in vivo CD22+ cell targeting with 211At-CD22 RIT, 106 parental (CD22+) Ramos cells were implanted into the flanks of NRG mice. One week later, animals (5/group) received 10 or 50 μg of either B10-conjugated epratuzumab, B10-conjugated G5/44, or B10-conjugated human IgG1 negative control mAb dual-labeled with 10 μCi 211At and 5 μCi of 125I. 24 hours later mice were euthanized, organs harvested, and tissues analyzed on a gamma counter for activity accumulated in tissues, and again at ~96 hours for 125I activity once 211At had completely decayed. Data are presented as mean±SD. For 211At (unpaired t test): P=0.0012 (Ctrl vs. G5/44 at 10 μg), P=0.12 (Ctrl vs. epratuzumab at 10 μg), P=0.0006 (Ctrl vs. G5/44 at 50 μg), P=0.006 (Ctrl vs. epratuzumab at 50 μg). For 125I: P=0.0004 (Ctrl vs. G5/44 at 10 μg), P=0.90 (Ctrl vs. epratuzumab at 10 μg), P=0.0009 (Ctrl vs. G5/44 at 50 μg), P=0.008 (Ctrl vs. epratuzumab at 50 μg). (B) For assessment of in vivo efficacy of 211At-CD22 RIT, 0.2×106 Ramos cells were injected into the tail veins of NRG mice. 2 days later, groups of 8 animals were treated with radiolabeled mAbs as indicated; one group did not receive any mAb and served as no-treatment control. Shown are Kaplan-Meier survival estimates. All deaths were attributed to progressive lymphoma except 1 mouse that was sacrificed at day +100 without evidence of lymphoma. P=0.0248 (Hu-IgG1 ctrl vs. epratuzumab at 10 μg; log-rank test), P=0.0036 (Hu-IgG1 ctrl vs. epratuzumab at 50 μg). (C) In a repeat efficacy assessment, 0.2×106 Ramos cells were injected into the tail veins of 8 NRG mice/group followed by treatment with radiolabeled mAbs 2 days later (lower disease burden) or 4 days later (higher disease burden) as indicated; one group served as no-treatment control and did not receive any mAb. For lower disease burden: P=0.0121 (Hu-IgG1 ctrl vs. epratuzumab), P=0.0026 (Hu-IgG4 ctrl vs. G5/44). For higher disease burden: P=0.51 (Hu-IgG1 ctrl vs. epratuzumab), P=0.0002 (Hu-IgG4 ctrl vs. G5/44).
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