Acute Kidney Injury Models in C57BL6 mice
Detailed methodology for inducing bilateral renal ischemia (30 min) followed by reperfusion in C57BL/6 mice, ensuring consistent injury and high reproducibility.
Serum creatinine (CREA) and blood urea nitrogen (BUN) data demonstrating marked renal dysfunction, quantitative endpoints that directly reflect glomerular filtration impairment.
H&E staining reveals classic features of AKI: tubular dilation, epithelial degeneration, brush border loss, and necrosis, providing a morphological foundation for injury grading.
Evidence of renoprotection with dexamethasone treatment, showing significant attenuation of pathological changes and preservation of renal architecture, proof of concept for intervention screening.
A full spectrum of available readouts and analyses, biochemical, histological, and beyond, tailored to meet the specific endpoints of your nephrology drug discovery programs.
Download the full case study today and empower your AKI research with Ace Therapeutics' expertly characterized IRI model, your gateway to reliable, translatable results in kidney disease therapeutics.
Robust ischemia-reperfusion and cisplatin-induced AKI in C57BL/6 mice with validated injury biomarkers.
Translational AKI platforms covering ischemic, nephrotoxic, and sepsis-induced injury across multiple species.
Transgenic human CD89/hIGHA1 mice recapitulating spontaneous mesangial IgA deposition and podocyte injury.
Comprehensive IgA nephropathy panel including humanized, active immunization, and lectin-induced models for therapeutic evaluation.
Ace Therapeutics has a group of highly committed and skilled researchers with the objective to provide innovative preclinical contract research solutions to cope with kidney diseases.
We strives to accelerate the development of innovative therapies that address unmet medical needs.
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