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Systemic lupus erythematosus (SLE) animal model

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Model Introduction

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Systemic lupus erythematosus

Introduction to SLE Animal Models

Clinically, systemic lupus erythematosus has a complex etiology, poor treatment outcomes, a tendency for frequent relapses, and a certain mortality rate. It is generally believed that disease onset results from the interplay of genetic, environmental, sex‑hormonal, and infectious factors. Establishing SLE animal models is an essential approach for investigating the pathogenesis, underlying mechanisms, and clinical management of systemic lupus erythematosus.

Advantages of Aniphe BioLab’s SLE Animal Model Platform Services

Our platform has established a well‑established animal model of systemic lupus erythematosus (SLE) with rigorous quality control, enabling us to comprehensively support a wide range of research and new‑drug development projects.

	Typical pathological features Animals exhibit elevated autoantibodies, renal damage, and lesions in the skin and immune organs; the model demonstrates a stable phenotype and high reproducibility.
	End-to-end compliance management Animals were housed under SPF‑grade conditions, with regular monitoring of clinical signs, serological parameters, and organ status; all data are complete and traceable.
	Comprehensive test coverage Supports multi-dimensional detection and analysis, including autoantibodies, inflammatory cytokines, imaging, histopathology, and molecular immunology.
	Flexible, customized solutions The intervention cycle and dosing regimen can be tailored to experimental requirements, enabling alignment with diverse pharmacodynamic profiles and mechanistic research designs.
	One-stop closed-loop service From model establishment and animal husbandry to sample collection and biomarker analysis, the entire workflow is fully implemented, providing robust support for both basic research and IND submissions.

Modeling cycle	4–32 weeks
Laboratory animals	BALB/c mice, spontaneous systemic lupus erythematosus MRL/Lpr mice
Positive drug	Prednisone, cyclophosphamide, and dexamethasone are the most widely used and well‑established classic positive control drugs in animal models of SLE and lupus nephritis.
Application areas	This model is primarily used to investigate the pathogenic mechanisms underlying systemic lupus erythematosus, including autoimmune dysregulation, aberrant antibody expression, and multi-organ damage. It facilitates the screening of pharmacological efficacy, the elucidation of mechanisms of action, and the safety evaluation of immunosuppressive, anti-inflammatory, and target‑organ–protective drugs and biologics. Additionally, it can be employed for drug target validation and the development of innovative therapies, providing broad support for basic immunology research as well as preclinical programs such as Investigational New Drug (IND) submissions.

Construction of an SLE animal model

The pristane‑induced SLE animal model is typically established by intraperitoneal injection of pristane, which continuously activates the host immune response and induces animals to develop typical SLE phenotypes, such as lupus nephritis.

Model features:

This model is easy to establish, with well‑controlled experimental conditions, low animal mortality, and a prolonged disease course. Its pathological features are pronounced and most characteristic compared with other chemically induced SLE animal models. Moreover, it closely mimics human SLE in clinical manifestations, immunological parameters, and histopathology, making it one of the most ideal SLE animal models available today.

Data on the combination therapy of the novel drug Ganetespib with cyclophosphamide (CTX)

This study investigated mice with lupus nephritis, comparing the therapeutic effects of a vehicle control group, conventional-dose cyclophosphamide (CTX), half-dose CTX (CTX/2), Ganetespib (Gpib) monotherapy, and a combination therapy group (Comb). The results showed that the combination of Ganetespib and cyclophosphamide was more effective than either agent alone in alleviating glomerular pathological damage, inhibiting the progression of proteinuria, and ameliorating lupus nephritis. Moreover, this combination regimen reduced the effective dose of CTX, mitigated its weight‑loss–inducing toxicity, thereby achieving enhanced efficacy with reduced adverse effects.

The combination of ganetespib and cyclophosphamide significantly suppresses the pathological lymph node and splenic hyperplasia and enlargement in lupus‑prone mice, ameliorating the features of excessive proliferation in the peripheral lymphatic system. The therapeutic effect of this combination is superior to that of either agent administered alone, further demonstrating that this dual‑agent regimen can systematically modulate the systemic autoimmune proliferative lesions characteristic of lupus.