B6-H11-hCLEC4C mice are humanized models generated by gene editing technology, in which the human CLEC4C genomic DNA was inserted at the H11 safe harbor. This modification does not affect the expression of the mouse homologous gene Clec4b1. This model can be used to study the pathological mechanisms and therapeutic methods of autoimmune disorders and hematological malignancies, as well as the screening and development of CLEC4C-targeted drugs, and preclinical efficacy and safety evaluations.

The B6-h4-1BB (TNFRSF9) mouse is a humanized model. The sequence encoding the endogenous extracellular domain of the mouse Tnfrsf9 is replaced in situ with the sequence encoding the human TNFRSF9 extracellular domain. This model can be used for studies on cancer immunology and autoimmune diseases, as well as for the development, screening, and evaluation of 4-1BB agonists in preclinical research.

The B6-h4-1BB-L (hTNFSF9) mouse is a humanized model constructed by in situ replacement of the coding sequence of the murine endogenous Tnfsf9 gene with that of the human TNFSF9 gene. This model can be used in studies of cancer immunotherapy and autoimmune diseases, as well as in the screening, development, and safety evaluation of 4-1BB-L-targeted drugs.

B6-h4-1BB/hPDL1 mice are TNFRSF9 and CD274 double humanized mouse models obtained by mating TNFRSF9 humanized mouse models (Catalog No. C001604) with CD274 humanized mouse models (Catalog No. C001235). They express human TNFRSF9 and CD274 genomic sequences under the control of mouse promoters. This model is a valuable tool for studying cancer immunotherapy. In addition, this model also provides a powerful preclinical research platform for evaluating the efficacy and mechanism of therapeutic drugs targeting TNFRSF9 and CD274.

The B6-hB7-H3 (hCD276) mouse is a humanized model constructed by replacing the sequence of the mouse Cd276 endogenous extracellular domain (aa.29~248) in situ with the corresponding extracellular domain from the human CD276. The murine signal peptide (aa.1~28) and aa.249~316 were preserved. The B6-hB7-H3 (hCD276) mice can be used for the study of the pathogenesis of various cancers such as breast cancer, glioblastoma, and non-small cell lung cancer, as well as for CD276-targeted drug development.

The B6-hB7-H4 (hVTCN1) mouse is a humanized model, constructed by replacing the partial extracellular domain (aa.35~255) of the endogenous mouse Vtcn1 gene with the partial extracellular domain (aa.35~255) of the human VTCN1 gene. B6-hB7-H4 (hVTCN1) mice can be used for research into the pathogenesis of various cancers, as well as autoimmune and inflammatory diseases. They are also useful for the screening, development, and safety evaluation of VTCN1-targeted drugs.

The B6-hBAFF (TNFSF13B) mouse is a humanized model generated using gene editing technology, in which the protein-coding sequence (CDS) encoding the extracellular domain of the human TNFSF13B protein is integrated into a specific site within the mouse Tnfsf13b gene, while retaining the endogenous gene sequence encoding the mouse cytoplasmic and transmembrane domains (aa.1-68). Homozygous B6-hBAFF (TNFSF13B) mice are viable and fertile. This model can be used for studying the pathological mechanisms and therapeutic approaches of autoimmune diseases and specific B cell malignancies and for the development of BAFF-targeted drugs.

The B6-hBAFFR (hTNFRSF13C) mouse is a humanized model constructed by replacing the sequence of the mouse Tnfrsf13c endogenous extracellular domain (aa.1~71) in situ with the corresponding extracellular domain (aa.1~78) from the human TNFRSF13C. The B6-hBAFFR (hTNFRSF13C) mice can be used for the study of the pathogenesis of immune-mediated disorders such as common variable immunodeficiency (CVID), systemic lupus erythematosus (SLE), and Sjögren's syndrome, and certain B cell malignancies, as well as for TNFRSF13C-targeted drug development.

The B6-hBCMA (TNFRSF17) mouse is a humanized model constructed using gene editing technology, where the mouse BCMA endogenous extracellular domain (aa.1~49) was replaced with the human BCMA extracellular domain (aa.1~54). Homozygous B6-hBCMA (TNFRSF17) mice are viable and fertile. This model can be used for studying the pathological mechanisms and therapeutic approaches of multiple myeloma, systemic lupus erythematosus and various B cell-related diseases and for the development of BCMA-targeted drugs.

B6-hCD19 mice are a humanized model generated by replacing the mouse endogenous Cd19 gene sequence from the ATG start codon to part of intron 4 with the corresponding human CD19 gene sequence using gene editing technology. This model is applicable for studying B cell development and function, as well as therapeutic research on autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), and B cell malignancies. It is an ideal research platform for preclinical efficacy evaluation of anti-human CD19 CAR-T cell therapy, and the development of bispecific antibodies and combination therapies.