Chugai’s SAIL66, under Development for CLDN6 Positive Solid Tumors, Non-Clinical Research Results Published in the Journal for ImmunoTherapy of Cancer
2024-10-24 · Chugai Pharmaceutical · original chugai-pharm.co.jp ↗
A renowned academic journal in the field of cancer immunotherapy has accepted the non-clinical research results of SAIL66, which applies Dual-Ig technology, Chugai’s proprietary antibody engineering technology Non-clinical studies suggest that SAIL66 has high selectivity for CLDN6 and may demonstrate superior anti-tumor effects compared to conventional T-cell engagers through CD3 and CD137 co-stimulation A Phase I clinical study to investigate SAIL66 in CLDN6-positive solid tumors is ongoing TOKYO, October 24, 2024 -- Chugai Pharmaceutical Co., Ltd. (TOKYO: 4519) announced that the results of non-clinical research on SAIL66, a Chugai’s in-house project under Phase I clinical development for CLDN6 positive solid tumors, have been published in the Journal for ImmunoTherapy of Cancer. The journal is a renowned academic journal in the field of cancer immunotherapy, published by the Society for Immunotherapy of Cancer (SITC) in the United States. “SAIL66, a next generation CLDN6-targeting T-cell engager, demonstrates potent antitumor efficacy through dual binding to CD3/CD137” ( https://doi.org/10.1136/jitc-2024-009563 ) The following findings were demonstrated in this research, which suggest that SAIL66 may be useful as a treatment for CLDN6 positive solid tumors. Creation of SAIL66, which is a novel tri-specific T-cell engager* (TCE) for Claudin-6 (CLDN6), CD3, and CD137, applying Dual-Ig ® technology, Chugai’s proprietary antibody engineering technology *T-cell engager: A therapeutic agent that exerts anti-tumor effects by bringing T cells, which are immune cells, closer to tumor cells SAIL66 binds to CLDN6, which is specifically expressed on tumor tissue, and does not bind to other CLDN family proteins (CLDN3, 4, or 9) with similar amino sequences in vitro , SAIL66 was shown to strongly activate T cells and exert cancer cell cytotoxicity by not only triggering CD3 signaling like conventional TCEs, but also by providing CD137 co-stimulation In experiments using mice, SAIL66 was shown to increase intratumor T-cells and decrease the number of exhausted T cells, leading to enhanced antitumor efficacy compared to conventional TCEs About SAIL66 SAIL66 is an anti-CLDN6/CD3/CD137 trispecific antibody and one of the next-generation T-cell engagers (TCEs) applying Chugai’s proprietary Dual-Ig ® technology. Conventional TCEs are designed to guide T cells to the target cancer cells by activating and engaging T cells through its binding to CD3 on T cells. Dual-Ig technology is a novel technology providing antibodies with the ability to induce CD137 signaling, a co-stimulating molecule, in addition to CD3 signaling. This property enables to maintain T cell activity, potentially inducing more potent antitumor effects than conventional T-cell engagers. 1 Trademarks used or mentioned in this release are protected by laws. Sources Hirofumi Mikami et al. Engineering CD3/CD137 Dual Specificity into a DLL3-Targeted T-Cell Engager Enhances T-Cell Infiltration and Efficacy against Small-Cell Lung Cancer. Cancer Immunol Res June 2024; 12 (6): 719–730.
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