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.

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.

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.

B6-hANG2 (ANGPT2) mouse model was generated using gene editing technology to replace the entire sequence of the mouse Angpt2 gene with the human ANGPT2 gene sequence, achieving stable expression of human ANGPT2 protein. This model is suitable for studying tumorigenesis, vascular hyperproliferative diseases (e.g., diabetic retinopathy, age-related macular degeneration), autoimmune disorders, and preclinical evaluation of human ANGPT2-targeted therapeutics.

The B6-hANGPTL7 mouse is a humanized model, constructed by replacing the sequences from 5'UTR to 3'UTR of the endogenous mouse Angptl7 gene with the corresponding human ANGPTL7 gene sequence. B6-hANGPTL7 mice can be used for research into the pathogenesis of glaucoma, type 2 diabetes mellitus (T2DM), and obstructive sleep apnea (OSA). They are also useful for the screening, development, and safety evaluation of ANGPTL7-targeted drugs.

This strain is a mouse Atp7b gene humanized model and can be used for HLD. The homozygous B6-hATP7B mice are viable and fertile.

This strain is a humanized point mutation model constructed by introducing the common pathogenic mutation p.H1069Q (CAC>CAA) into the humanized ATP7B gene of B6-hATP7B mice (Catalog No.: I001130). This model is suitable for studying the pathogenic mechanisms of Wilson's disease, and homozygous animals are viable and fertile.