B6-3*hSMN2 mice are a humanized disease model carrying three copies of the human SMN2 gene, which can be used to mimic SMA patients with three SMN2 gene copies. Since the SMN2 gene primarily produces SMNΔ7 protein lacking exon 7, rather than full-length SMN protein, the humanized SMN2 gene cannot fully compensate for the abnormalities caused by Smn1 deficiency, resulting in the manifestation of SMA-like phenotypes in this model.

B6-4*hSMN2 mice are a humanized disease model carrying four copies of the human SMN2 gene, which can be used to mimic SMA patients with four SMN2 gene copies. Since the SMN2 gene primarily produces SMNΔ7 protein lacking exon 7, rather than full-length SMN protein, the humanized SMN2 gene cannot fully compensate for the abnormalities caused by Smn1 deficiency, resulting in the manifestation of SMA-like phenotypes in this model.

The B6-APOE4/htau mouse is a model generated by crossing B6-APOE4 mice (Catalog No.: C001079) with B6-htau mice (Catalog No.: C001410). It can be used to study the pathogenic mechanisms and therapeutic approaches of neurodegenerative diseases such as Alzheimer’s disease (AD), frontotemporal dementia (FTD), and cerebral amyloid angiopathy (CAA), as well as cardiovascular diseases such as atherosclerosis.

The B6-APOE4/htau*P301L mouse is a model generated by crossing B6-APOE4 mice with B6-htau*P301L mice. It can be used to study the pathogenic mechanisms and therapeutic approaches of neurodegenerative diseases such as Alzheimer’s disease (AD), frontotemporal dementia (FTD), and cerebral amyloid angiopathy (CAA), as well as cardiovascular diseases such as atherosclerosis.

The B6-APOE4/htau*P301S mice are a model obtained by crossing B6-APOE4 mice with B6-htau*P301S mice. This model can be used for the research on the pathogenic mechanisms and treatment methods of neurodegenerative diseases such as Alzheimer's disease (AD) and progressive cerebral amyloid angiopathy (CAA), as well as cardiovascular diseases such as atherosclerosis.

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-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.

This strain is a mouse Abca4 gene humanized model and can be used to research STGD, CRD, and RP. The homozygous B6-hABCA4 mice are viable and fertile. In addition, based on the independently developed TurboKnockout fusion BAC recombination technology, Cyagen can also generate hot mutation (ABCA4 c.5461-10 T to C) models based on this strain and provide customized services for specific mutations to meet the experimental needs in pharmacology and other fields.

The B6-hABCA4*c.5461-10T>C mouse is a humanized model of the Abca4 gene, where the mouse Abca4 gene has been replaced with the human ABCA4 gene carrying the c.5461-10T>C mutation using gene editing technology. This model can be used for research on various retinal degeneration diseases such as Stargardt disease (STGD), cone-rod dystrophy (CRD), and retinitis pigmentosa (RP).

This strain is a humanized mouse model of the Alb gene, obtained by in situ replacement of the entire mouse Alb gene sequence, including the UTR region, with the human ALB gene sequence. This model can be used for the development of ALB-targeted drugs, as well as for the research and development of drugs using HSA as a carrier, and for in vivo pharmacodynamics and pharmacokinetics studies, including albumin-drug conjugates or albumin-binding prodrugs.