Preclinical Evaluation Of Novel Drug Candidates Against SLE In NZB/W F1 Mouse Models

Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease and the most common form of lupus, affecting multiple organ systems with varying severity. SLE symptoms range from skin rashes, joint pain, and swelling to persistent low-grade fevers and extreme fatigue. In more severe cases, the disease leads to complications such as lymph node enlargement, proteinuria, and kidney failure, significantly impacting patients’ quality of life. Despite advancements in autoimmune research, effective treatment options for SLE remain limited, necessitating the development of reliable preclinical models for evaluating novel therapeutics.

The NZB/W F1 mouse model is one of the most well-established and widely used models for studying the pathophysiology of SLE. This female crossbred (NZB x NZW) F1 mouse spontaneously develops lupus-like symptoms, including progressive kidney disease, autoantibody production, and immune system dysregulation, closely resembling human SLE. However, the severity and onset of disease can vary between individual models, making precise evaluation of therapeutic candidates crucial for translational success.

Preclinical efficacy studies using the NZB/W F1 model have provided valuable insights into the disease mechanisms and the effectiveness of potential treatments. In this article, we explore the efficacy of Cyclophosphamide—a standard treatment for SLE—within this model, demonstrating its impact on disease progression and immune regulation. By leveraging this well-characterized mouse model, researchers can accelerate the development of novel anti-SLE therapies, ultimately contributing to more effective treatment strategies for patients living with this complex autoimmune disorder.