Immune-mediated nephropathies represent complex disorders driven by dysregulated immune responses, leading to renal inflammation and progressive dysfunction. At Ace Therapeutics, we specialize in preclinical research services utilizing rigorously validated disease models to support drug discovery and mechanistic investigations. Our platforms are designed to replicate key immunological pathways and renal injury patterns observed in human immune-mediated kidney diseases.
Immune-mediated nephropathies encompass a spectrum of glomerular diseases driven by autoantibody formation, immune complex deposition or autoreactive T cell infiltration. Precise modeling of these conditions underpins:
By recapitulating hallmark features such as proteinuria, complement activation and histological lesions, our models facilitate mechanistic studies and support preclinical candidate selection.
We maintain an array of validated models to address diverse immune-mediated kidney pathologies:
Model name and acronym | Species/Strain | Key features |
Anti-glomerular basement membrane (NTN) | C57BL/6 mouse, Wistar rat | Rapid onset proteinuria, crescent formation |
Lupus nephritis | NZB/W F1 and MRL/lpr mice | Autoantibody-driven glomerulonephritis |
IgA nephropathy | ddY mouse, gd-IgA1 challenge | Mesangial IgA deposition, hematuria |
Passive Heymann nephritis (PHN) | Sprague–Dawley rat | Membranous injury, subepithelial deposits |
ANCA-associated vasculitis | C57BL/6 mouse | Pauci-immune glomerulonephritis, necrosis |
Beyond these core systems, Ace Therapeutics can develop or adapt models such as cytokine-induced interstitial nephritis or transgenic systems expressing human autoantigens to mirror cutting-edge therapeutic targets.
Reproducibility and translational fidelity are ensured through standardized validation pipelines:
Validation Parameter | Methodology |
Functional kidney assessment | Transdermal GFR monitoring, serum creatinine |
Histological scoring | Semi-quantitative analysis of glomerular lesions |
Immunohistochemistry | Staining for complement (C3, C5b-9) and CD3 |
Biomarker profiling | Urinary proteinuria, NGAL, KIM-1 panels |
Molecular readouts | RT-qPCR for pro-inflammatory cytokines |
Routine batch controls, blinded histopathology reads and inter-cohort comparisons safeguard data integrity and cross-study consistency.
At Ace Therapeutics, each project benefits from a coordinated workflow that includes:
Collaborating with Ace Therapeutics accelerates your preclinical program, reduces rework and enhances confidence in candidate selection.
How do I select the most appropriate model for my compound?
Our scientific advisors review your target, mechanism and therapeutic modality to recommend models that best align with your study objective, whether that involves autoantibody blockade, complement inhibition or T cell modulation.
Can comorbidities be integrated into these immune-mediated models?
Yes. We can incorporate factors such as hypertension, diabetes or aging to reflect clinical complexity and evaluate compound performance under multifactorial stress.
What endpoints are typically measured?
Standard readouts include proteinuria, serum creatinine, histopathological scoring, complement deposition, cytokine panels and, where relevant, imaging biomarkers of renal structure and perfusion.
Do you offer PK/PD studies alongside nephropathy models?
We provide integrated pharmacokinetic assessments and link exposure metrics to efficacy endpoints, supporting informed dose selection for translational studies.
How do you ensure reproducibility across cohorts?
Quality control measures include standardized induction protocols, blinded pathology assessments, batch controls for reagents and regular inter-cohort comparisons to monitor consistency.
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