Preclinical Kidney Disease R&D Solutions

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Project Description

All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.

Customized Animal Models of IgA Nephropathy

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Introduction to Animal Models of IgA Nephropathy

IgA nephropathy (IgAN) is a primary glomerular disease characterized by the abnormal deposition of IgA1 immune complexes within the glomeruli. IgAN has complex pathophysiological mechanisms. The development of reliable animal models for IgA nephropathy can improve the understanding of IgAN pathogenesis and explore potential therapeutic avenues.

The most commonly used animal models of IgA nephropathy are induced animal models, spontaneous animal models and genetically engineered animal models. Genetically engineered animal models are more commonly used to study the pathophysiology of IgAN, while spontaneous animal models of IgAN are often used to assess the efficacy of new drugs.

Fig. 1. IgAN mouse models developed between 2004 and 2020. (Wehbi B, et al., 2021)

R&D Services Using Animal Models of IgAN

Pathogenic Mechanisms

At Ace Therapeutics, we provide services to explore the pathogenic mechanisms of IgA nephropathy, including the formation and deposition of immune complexes and the renal inflammatory response.

Targets Discovery

Ace Therapeutics can offer solutions for identifying targets such as blood pressure targets (e.g., ETAR) and immunomodulatory targets (e.g., BAFF, APRIL, MASP-2, C3, C5).

Preclinical Research

We can utilize animal models of IgA nephropathy to provide preclinical research services, including drug metabolism, pharmacokinetic and pharmacodynamic studies, safety assessment, and toxicology.

Custom Animal Models of IgA Nephropathy

IgA nephropathy is a complex kidney disease whose pathogenic mechanisms are not yet fully understood. To improve the understanding of IgAN pathogenesis and accelerate drug development, Ace Therapeutics is dedicated to providing clients with customized animal models of IgAN.

Animal Selection

Ace Therapeutics provides expert guidance to help clients choose the most appropriate animal species and strains for their research needs. By considering factors such as genetic background and study objectives, we ensure optimal model selection for the development of therapeutic approaches.

BALB/c Mice
C57BL/6 Mice
C57BL/6J Mice

C57BL/6N Mice
ddY Mice
HIGA Mice

FVB/N Mice
SD Rat

Animal Modeling Services

Types of Animal Models	Modeling Methods	Services Details
Induced Animal Models	BSA+LPS+CCl₄	Intragastric administration of BSA and injection of LPS and CCl4.
Genetically Engineered Animal Models	CD89 Tg mice	Expression of human CD89 in mice using transgenic technology to develop IgA1 deposition.
	α1KI-CD89Tg mice	The α1KI mice (expressing human IgA1) are backcrossed with CD89 Tg mice to generate the α1KI-CD89Tg mice.
	CD37 Tg mice	Knockout of CD37 in mice results in increased serum IgA levels.
	BAFF-Tg mice	We overexpression of human BAFF in mice to elevate serum IgA levels.
	β4GalT-I KO mice	Knockout of the β4GalT-I gene using Cre-LoxP technology to induce aberrant glycosylation of IgA1.
	Uteroglobin Tg mice	We knock out the uteroglobin gene in mice to develop IgAN, characterized by albuminuria and glomerular deposits of IgA.
	Bcl-2 Tg mice	We are able to enhance the systemic IgA immune response by overexpressing Bcl-2 in mice using transgenic technology.
	FDC-SP KO mice	Knockout of the FDC-SP gene using Cre-LoxP technology to significantly increase levels of IgA.
	hα1+/+AID−/− mice	The α1KI mice, which express the heavy chain of human IgA1, in an AID-deficient background has been constructed.
Spontaneous Animal Models	ddY mice	The development of IgA deposits and elevated serum levels of IgA have been observed in ddY mice.
Spontaneous Animal Models	HIGA mice	HIGA mice will spontaneously develop IgA1 deposits in the glomeruli.

Validation of Animal Models

We provide a series of detailed assessment services to validate the accuracy and reliability of animal models of IgA nephropathy, including but not limited to:

Biochemical assessment (e.g., urinary glucose, 24-hour urinary protein, and RBC counts)
Kidney function (e.g., serum BUN and creatinine levels)
Renal pathology (e.g., glomerular changes, tubulointerstitial changes, vascular changes, and deposition of immune complexes)

References

Wehbi B., et al. (2021). History of IgA nephropathy mouse models. Journal of Clinical Medicine, 10(14):3142.
Monteiro R.C.; Suzuki Y. (2021). Are there animal models of IgA nephropathy? Semin Immunopathol, 43(5):639-648.