The Agxt KO mouse is a gene knockout model created using gene-editing techniques to knock out the coding sequence of the Agxt gene (the homolog of the human AGXT gene) in mice. This model is used to research the pathogenic mechanisms of primary hyperoxaluria and develop related therapeutic strategies.

This strain is an Atp7b deletion mouse model, which uses gene editing technology to knock out Atp7b, the homolog of the human ATP7B gene in mice that lack the expression of ATP7B protein and can be used in the study of disorders related to copper metabolisms such as Wilson's disease, acute liver failure, and steatohepatitis. The heterozygous Atp7b KO mice are viable and fertile, and homozygous mice have a reduced life expectancy.

B6-Pnpla3*I148M mice are obtained by introducing the I148M mutation into the mouse Pnpla3 gene using gene editing technology. Homozygous B6-Pnpla3*I148M mice are viable and fertile. This model can be used for research on the disease mechanisms and treatment methods of metabolism-associated fatty liver disease (MASLD), alcoholic liver disease, and liver fibrosis.

The B6-RCL-hLPA/Alb-cre/TG (APOB) mice express human LP(a) and ApoB, two risk factors for cardiovascular disease. It can be used in the study of hyperlipidemia, stroke, coronary heart disease, familial hypercholesterolemia (FH), and other atherosclerotic cardiovascular diseases (ASCVD). Internal data (not shown) indicates that, compared to the Cyagen strain B6-LPA (CKI) /Alb-Cre & Tg (APOB) mice (Catalog No. C001494), this model exhibits a more stable expression of human LPA protein at different ages. Please choose the model based on the experimental need for continuous stability of human LPA protein expression.

The B6-hALK7 (hACVR1C) mouse is a humanized model constructed using gene editing technology, where the region from aa.27 in exon 2 to partial intron 2 of mouse Acvr1c was replaced with "ACVR1C chimeric CDS-WPRE-BGH pA" cassette. The murine signal peptide (aa.1~25) of Acvr1c was preserved. This model can be used for studying the pathological mechanisms and therapeutic approaches of metabolic disorders such as obesity and type 2 diabetes, and certain cancers like retinoblastoma, and for the development of ACVR1C-targeted drugs.

The B6-hDPP4 (line 2) mouse is a humanized model constructed by gene editing technology to replace a partial region of the mouse Dpp4 gene with the human DPP4 gene CDS sequence. This model can be used to study the infection mechanisms of viruses such as MERS-CoV and COVID-19, as well as to develop related virus vaccines. Additionally, this model can be utilized to develop DPP4 inhibitor therapies. Similar models include the B6-hDPP4(line 1) mouse (Catalog ID: I001187), constructed on the C57BL/6NCya background strain, which replaces the sequence encoding aa.29~aa.760 of the mouse Dpp4 gene with the human DPP4 gene CDS sequence (aa.29-766), and the BALB/c-hDPP4 (line 2) mouse (Catalog ID: I001189), constructed on the BALB/cAnCya background strain. These models meet the experimental needs of different strain backgrounds.

The B6-hDPP4 (line 1) mouse is a humanized model constructed by gene editing technology to replace a partial region of the mouse Dpp4 gene with the human DPP4 gene CDS sequence. This model can be used to study the infection mechanisms of viruses such as MERS-CoV and COVID-19, as well as to develop related virus vaccines. Additionally, this model can be utilized to develop DPP4 inhibitor therapies. Additionally, Cyagen Biosciences has developed B6-hDPP4(line 2) mice (Catalog ID: I001188) on the C57BL/6JCya background strain and BALB/c-hDPP4 (line 2) mice (Catalog ID: I001189) on the BALB/cAnCya background strain. These two models replace the mouse Dpp4 gene p.S29 to part of intron 2 with the Human DPP4 CDS (aa.29-766)-rBG pA expression cassette, meeting the experimental needs for different strain backgrounds.

B6-hFGF21 mice are humanized models generated by replacing the sequence of the mouse Fgf21 gene in situ with the corresponding sequence from the human FGF21 gene. This model can be used to study the pathological mechanisms and therapeutic methods of metabolic diseases such as obesity, diabetes, and metabolic associated steatohepatitis (MASH), cardiovascular diseases, cancers, as well as the screening and development of FGF21-targeted drugs, and preclinical efficacy and safety evaluations.

B6-hFGFR1c mice are humanized models generated by gene editing technology, in which the p.22R to partial intron 2 of the mouse Fgfr1 gene was replaced in situ with p.22R to 376E from the coding sequence of the human FGFR1 gene, p.377I to 823X from the coding sequence of the mouse Fgfr1 gene, and the 3'UTR of the mouse Fgfr1 gene. This model can be used to study the pathological mechanisms and therapeutic methods of cancers, metabolic diseases such as obesity, diabetes, and metabolic-associated steatohepatitis (MASH), as well as the screening and development of FGFR1c-targeted drugs, and preclinical efficacy and safety evaluations.

The B6-hGCGR mouse is a humanized model constructed by replacing the sequence of the mouse Gcgr gene in situ with the corresponding sequence from the human GCGR gene. The B6-hGCGR mice can be used for studies on obesity, type 2 diabetes, metabolic dysfunction-associated steatohepatitis, and other glucose-related metabolic disorders, as well as for GCGR-targeted drug development.