• Modeling Mechanism：

  As a C3aR-specific small molecule ligand, BR103 can specifically bind to the C3a receptor (C3aR) on the surface of foot tissue and immune cells, activate downstream signaling pathways (such as the Wnt/β-catenin pathway), induce the release of pro-inflammatory factors and immune cell infiltration, trigger local inflammatory responses, and lead to foot tissue edema and swelling, mimicking the pathological process of complement activation-related inflammatory damage.

• Related Products：

  BR103 (T70659)

• Modeling Method：

  Experimental Subject：

  Mice, C57BL/6 or Sprague-Dawley rats, 6–8 weeks old, body weight 20–25 g

  Dosage and Administration Route：

  1–10 mg/kg BR103 (dissolved in physiological saline or physiological saline containing 0.1% DMSO), Subplantar injection, Unilateral or bilateral foot administration permissible

  Dosing Frequency and Duration Model：

  Single dose

• Validation：

  Clinical phenotype: Significant foot swelling occurred 6-24 hours after administration. Foot thickness/circumference measured with calipers increased by ≥20% compared with the control group (injected with physiological saline or 0.1% DMSO); Histological indicators: HE staining of foot tissue sections showed congestion and edema in the dermis and subcutaneous tissue, with increased infiltration of neutrophils and macrophages; Molecular indicators: C3aR expression was upregulated in foot tissue homogenate, and the levels of pro-inflammatory factors (such as IL-6, TNF-α) and Wnt3/β-catenin protein were increased, while the anti-inflammatory factor IL-10 showed no significant change; Specificity verification: The combined use of C3aR antagonists (such as SB290157, JR14a) can significantly inhibit BR103-induced foot swelling and the release of inflammatory factors.

*Precautions： All mice /Rats at specified time points after modeling (e.g. 6,12,twenty four, 48(Hours) were used to euthanize the animal and collect foot tissue for testing.

*References：Gao S,et,al. Complement C3a and C3a Receptor Activation Mediates Podocyte Injuries in the Mechanism of Primary Membranous Nephropathy. J Am Soc Nephrol. 2022 Sep;33(9):1742-1756.