Ace Therapeutics, we provide comprehensive preclinical research solutions tailored to advance drug development and mechanistic understanding of acute kidney injury. Our expertise lies in designing and executing robust AKI models that replicate human pathophysiology, ensuring reliable data for translational applications.
Acute kidney injury can arise from ischemic events, exposure to nephrotoxic agents or systemic inflammation. Accurate modeling of these diverse etiologies enables:
Ace Therapeutics delivers a full spectrum of acute kidney injury (AKI) model-based services to support translational preclinical research. Our platform covers model selection, induction protocol development, multi-timepoint assessments, and comprehensive data delivery. Each project is supported by dedicated scientific advisors and technical specialists to ensure methodological rigor and relevance to client goals.
To support evaluation of therapeutic timing and renal recovery, we provide models simulating transient or moderate AKI. These include short-duration ischemia–reperfusion injury or low-dose nephrotoxins that enable monitoring of functional restoration over time. Non-invasive renal function tests and urinary biomarker panels (e.g., NGAL, KIM-1, cystatin C) offer dynamic insight into injury resolution.
For assessing compounds targeting severe renal damage, our platforms include prolonged ischemia, high-dose cisplatin, and sepsis-induced injury with hemodynamic collapse. These models are validated through histological analysis of tubular necrosis, interstitial inflammation, and fibrosis. They are ideal for testing agents intended to interrupt irreversible injury cascades or promote tissue regeneration.
Recognizing the clinical complexity of AKI, Ace Therapeutics offers models integrating comorbid factors such as aging, obesity, or diabetic conditions. These systems reflect heightened susceptibility and altered repair responses seen in human populations. By using tailored induction protocols and extended evaluation windows, we support in-depth investigation of compound performance under clinically relevant stressors.
Robust validation ensures reproducibility and translational fidelity:
Model | Species/Strain | Key Validation Endpoints |
Ischemia–reperfusion ± uninephrectomy | C57BL/6 mouse | GFR (transdermal), histology, tubular necrosis |
Cisplatin AKI | C57BL/6 mouse | Serum creatinine, histopathology, fibrosis scoring |
Gentamicin nephrotoxicity | Sprague–Dawley rat | Tubular apoptosis, urinary biomarkers, histology |
CLP-induced sepsis AKI | Sprague–Dawley rat | Cytokine panels, hemodynamics, renal histology |
Ascending pyelonephritis | Wistar rat | Bacterial count, lesion grade, inflammatory markers |
Validation techniques include multispectral optoacoustic tomography (MSOT), transdermal GFR monitoring and immunohistochemistry for injury markers (e.g. NGAL, KIM-1).
Our AKI platform integrates with:
Our AKI models support:
How do I select the most suitable AKI model for my study?
Our team will guide you based on your research goals. For example, cisplatin models suit nephrotoxicity studies, while CLP models are ideal for sepsis-related AKI.
Can you customize models to include comorbidities like diabetes or hypertension?
Yes. We integrate comorbidities (e.g., uninephrectomy for chronic kidney disease) to mimic clinical complexity.
What endpoints are typically measured in your AKI studies?
Standard endpoints include functional biomarkers (sCr, BUN), histopathology, and molecular pathways (e.g., SIRT1/NF-κB, Nrf2/HO-1).
Do you provide pharmacokinetic (PK) or efficacy testing alongside AKI models?
Yes. We offer integrated PK/PD studies to evaluate drug distribution and renoprotective effects.
How are your models validated for consistency?
Each model undergoes strict quality control, including baseline biomarker profiling and reproducibility checks across multiple cohorts.
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