Dual targeting of ROR1 and ROR2 with glycoengineered antibodies elicits potent and selective immunotherapy in hairy cell leukemia

Abstract Receptor tyrosine kinase-like orphan receptors 1 and 2 (ROR1 and ROR2) are oncoembryonic antigens aberrantly expressed on hairy cell leukemia (HCL) B cells and various other cancers, but absent from healthy B cells and postpartum tissues. We generated novel, glycoengineered monoclonal antibodies—GE-zilovertamab (anti-ROR1) and GE-6E6 (anti-ROR2)—by removing core fucose residues from the Fc regions of their parental humanized IgG1 antibodies, zilovertamab (UC-961/cirmtuzumab) and 6E6, respectively. To assess their immunotherapeutic potential, we engineered the CD20+ B cell leukemia MEC1 cell line to stably express either ROR1 or ROR2, generating MEC1-ROR1 and MEC1-ROR2 cell lines. Co-culture of these targets with Jurkat-Lucia™ NFAT-CD16A (V158) reporter cells and antibody treatments revealed that glycoengineered antibodies (GE-zilovertamab and GE-6E6), but not their parental antibodies, robustly triggered luminescence activity in NFAT-CD16 cells in an antigen-specific manner. Chromium-51 (Cr51) release assays further demonstrated that GE-zilovertamab or GE-6E6, in the presence of human peripheral blood mononuclear cells (PBMCs), respectively induced potent and selective lysis of ROR1+ or ROR2+ MEC1 variants that was comparable to that of rituximab against CD20+ parental MEC1 cells, and consistently superior to the non-glycoengineered parental antibodies. These findings were extended to primary HCL cells, which express CD20, ROR1, and ROR2. GE-zilovertamab and GE-6E6 induced greater cytotoxicity against Cr51-labeled HCL cells than their parental antibodies and equaled or surpassed the efficacy of rituximab. Combination treatment with glycoengineered anti-ROR1 and anti-ROR2 antibodies mediated significantly higher killing of Cr51-labeled HCL cells than either agent alone, or rituximab, or the combination of the two parental antibodies. Importantly, in contrast to rituximab, GE-zilovertamab and GE-6E6 spared normal B cells, which lack expression of ROR1 and ROR2. In summary, our findings show that dual targeting with glycoengineered anti-ROR1 and anti-ROR2 antibodies achieves superior, selective ADCC against ROR1/2+ hairy cell leukemia, sparing normal B cells. This approach offers a promising and potentially safer immunotherapeutic strategy for patients with HCL or other ROR-expressing B-cell malignancy.

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Journal
Blood
Published
2025-11-03
DOI
https://doi.org/10.1182/blood-2025-2359
Primary Topic
Monoclonal and Polyclonal Antibodies Research
Type
article
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article

Dual targeting of ROR1 and ROR2 with glycoengineered antibodies elicits potent and selective immunotherapy in hairy cell leukemia

George F. Widhopf, Thomas J. Kipps, Md Kamrul Hasan
Blood
Monoclonal and Polyclonal Antibodies Research
article

Dual targeting of ROR1 and ROR2 with glycoengineered antibodies elicits potent and selective immunotherapy in hairy cell leukemia

George F. Widhopf, Thomas J. Kipps, Md Kamrul Hasan
article en

Abstract

Abstract Receptor tyrosine kinase-like orphan receptors 1 and 2 (ROR1 and ROR2) are oncoembryonic antigens aberrantly expressed on hairy cell leukemia (HCL) B cells and various other cancers, but absent from healthy B cells and postpartum tissues. We generated novel, glycoengineered monoclonal antibodies—GE-zilovertamab (anti-ROR1) and GE-6E6 (anti-ROR2)—by removing core fucose residues from the Fc regions of their parental humanized IgG1 antibodies, zilovertamab (UC-961/cirmtuzumab) and 6E6, respectively. To assess their immunotherapeutic potential, we engineered the CD20+ B cell leukemia MEC1 cell line to stably express either ROR1 or ROR2, generating MEC1-ROR1 and MEC1-ROR2 cell lines. Co-culture of these targets with Jurkat-Lucia™ NFAT-CD16A (V158) reporter cells and antibody treatments revealed that glycoengineered antibodies (GE-zilovertamab and GE-6E6), but not their parental antibodies, robustly triggered luminescence activity in NFAT-CD16 cells in an antigen-specific manner. Chromium-51 (Cr51) release assays further demonstrated that GE-zilovertamab or GE-6E6, in the presence of human peripheral blood mononuclear cells (PBMCs), respectively induced potent and selective lysis of ROR1+ or ROR2+ MEC1 variants that was comparable to that of rituximab against CD20+ parental MEC1 cells, and consistently superior to the non-glycoengineered parental antibodies. These findings were extended to primary HCL cells, which express CD20, ROR1, and ROR2. GE-zilovertamab and GE-6E6 induced greater cytotoxicity against Cr51-labeled HCL cells than their parental antibodies and equaled or surpassed the efficacy of rituximab. Combination treatment with glycoengineered anti-ROR1 and anti-ROR2 antibodies mediated significantly higher killing of Cr51-labeled HCL cells than either agent alone, or rituximab, or the combination of the two parental antibodies. Importantly, in contrast to rituximab, GE-zilovertamab and GE-6E6 spared normal B cells, which lack expression of ROR1 and ROR2. In summary, our findings show that dual targeting with glycoengineered anti-ROR1 and anti-ROR2 antibodies achieves superior, selective ADCC against ROR1/2+ hairy cell leukemia, sparing normal B cells. This approach offers a promising and potentially safer immunotherapeutic strategy for patients with HCL or other ROR-expressing B-cell malignancy.

BloodVol. 146(Supplement 1)
Molina Center for Energy and the Environment (US)
Openalex Percentile: Top 47%
Monoclonal and Polyclonal Antibodies Research
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