In Vitro Efficacy Testing Services for Iga Nephropathy

We provide robust and sensitive in vitro screening and characterization platforms for accelerating the discovery and screening of potential therapies for IgA Nephropathy. Our services are tailored to evaluate candidate compounds for their effects on key molecular targets involved in IgA deposition, inflammation, and immune complex-mediated kidney injury. We focus on critical proteins and pathways such as complement components, angiotensin II receptors, and inflammatory mediators implicated in the pathogenesis of IgA Nephropathy. Our assays enable detailed analysis of cellular activation, protein-protein interactions, and signaling pathways associated with glomerular damage and immune dysregulation.

Our comprehensive testing portfolio includes cell-based assays, biochemical binding assays, reporter gene assays, and advanced biophysical interaction analyses. These methods enable evaluation of compound efficacy, mechanism of action, and target engagement, supporting informed decision-making during therapeutic development. Each assay is designed to model relevant aspects of IgA Nephropathy pathology and pharmacology.

Arrestin protease recruitment assay: Measures receptor activation and downstream signaling by assessing the recruitment of arrestin proteins, critical for GPCR-targeted drug evaluation.

Biolayer interferometry assay: Provides real-time analysis of biomolecular interactions, allowing quantification of binding affinities between candidate drugs and their targets.

Boyden chamber assay: Assesses cell migration and chemotaxis, relevant for studying inflammatory cell infiltration in nephropathy.

Chemiluminescent assay: Detects and quantifies proteins or enzyme activity via light emission, offering sensitive readouts for immune and signaling proteins.

Competitive binding assay: Evaluates the ability of compounds to displace labeled ligands from their targets, informing on binding affinity and specificity.

Displacement of [125I]-[Sar1,Ile8]-angiotensin II: Measures the competition between test compounds and radiolabeled angiotensin II analogs for receptor binding, relevant to renin-angiotensin system modulation.

Displacement of [125I]-[Tyr4]-angiotensin II: Similar to above, utilizes a different radiolabeled angiotensin II analog for receptor binding studies.

Displacement of [125I]-angiotensin II: Assesses competitive inhibition at angiotensin II receptors, key in hypertension and renal pathology.

Displacement of [125I]-complement component 5a: Quantifies compound binding to C5a, central to complement-mediated inflammation.

Displacement of [125I]-endothelin-1: Measures inhibition at endothelin-1 receptors, important for vascular and inflammatory responses.

Displacement of [3H]-rosiglitazone: Evaluates binding to PPARγ, relevant for metabolic and anti-inflammatory effects.

Displacement of [3H]-valsartan: Measures binding to angiotensin II type 1 receptors, important in renal and cardiovascular diseases.

ELISA assay: Quantifies proteins, cytokines, or antibodies in biological samples, facilitating immune and inflammatory marker analysis.

Flow cytometry assay: Enables multiparametric analysis of cell populations, including immune cell activation and surface marker expression.

Fluorescence resonance energy transfer (FRET) assay: Detects molecular proximity and interactions, useful for signaling and binding studies.

Fluorescent assay: Employs fluorescence-based detection for sensitive quantification of biomolecules or cellular events.

Fluorescent-activated cell sorting (FACS) assay: Sorts and analyzes individual cells based on fluorescent markers, aiding detailed immune cell profiling.

Luciferine/luciferase assay: Measures gene expression or enzymatic activity using luminescence, often applied in reporter gene studies.

RNA assay: Quantifies gene expression changes to assess compound effects on target gene regulation.

Radioactivity assay: Utilizes radiolabeled compounds to precisely quantify binding or metabolic activity, providing high sensitivity.

Surface plasmon resonance assay: Real-time, label-free analysis of molecular interactions and binding kinetics, supporting high-resolution affinity measurements.

We measure a comprehensive set of pharmacological parameters to characterize compound potency, efficacy, and binding properties. These metrics, including IC-50, Kd, and Ki, enable quantitative comparison of candidate drugs and inform lead optimization. Accurate parameter determination is essential for advancing promising therapies into clinical development.

ED-50: The effective dose at which 50% of the maximal response is achieved, indicating in vitro potency.

IC-50: The concentration of a compound required to inhibit a specific biological function by 50%, widely used for comparing inhibitor strengths.

Kd: The equilibrium dissociation constant, reflecting the affinity between a ligand and its target; lower Kd values indicate stronger binding.

Ki: The inhibition constant, representing the binding affinity of an inhibitor for its target, critical for assessing selectivity and potency.

MEC: Minimum effective concentration, the lowest concentration at which a compound elicits a measurable effect.

MED: Minimum effective dose, the smallest amount of a compound producing a desired biological response.

MIC: Minimum inhibitory concentration, the lowest concentration that prevents visible biological activity, relevant for anti-infective or anti-inflammatory screening.

pA-2: The negative logarithm of the antagonist concentration required to double the agonist concentration for a given response; used to assess antagonist potency.

pIC-50: The negative logarithm of the IC-50 value, facilitating easy comparison of compound potencies on a logarithmic scale.

pKi: The negative logarithm of the Ki value, commonly used to express inhibitor binding affinity in a standardized form.

Recommended In Vitro Efficacy Tests

Angiotensin Ii Receptor Type 1

The Angiotensin II Receptor Type 1 (AT1R) plays a key role in IgA Nephropathy by mediating hypertension and renal inflammation. AT1R testing is crucial for evaluating drug candidates targeting this pathway. We employ competitive binding, fluorescent, and radioactivity assays—including displacement of radiolabeled ligands and arrestin recruitment—to assess binding affinity and receptor activity. Main parameters measured include pA-2, pKi, pIC-50, IC-50, and Ki, providing robust pharmacological profiling.

Cd38 Molecule

The CD38 molecule plays a crucial role in immune regulation and inflammation in IgA Nephropathy. CD38 testing is vital for identifying therapeutic targets and monitoring drug efficacy. Our service utilizes flow cytometry, ELISA, fluorescent assays, surface plasmon resonance, and FACS to characterize CD38 activity. Key parameters measured include ED-50, IC-50, and Kd, providing essential data for drug development and optimization in IgA Nephropathy therapy.

Complement C3

Complement C3 plays a pivotal role in the pathogenesis of IgA Nephropathy by mediating inflammatory responses and contributing to glomerular injury. Accurate C3 testing is essential for evaluating drug efficacy in modulating complement activity. Our service utilizes flow cytometry, ELISA, and fluorescent assays to quantify C3 activation and inhibition, providing key readouts such as IC-50 and MED for robust pharmacodynamic assessment in drug development.

Complement C5

Complement C5 plays a pivotal role in the inflammatory response and progression of IgA Nephropathy. Testing C5 activity is crucial for evaluating therapeutic candidates targeting complement-mediated injury. Our service utilizes ELISA assays to quantitatively measure C5 and its inhibition. The main parameter assessed is IC-50, indicating the concentration required to inhibit 50% of C5 activity, providing essential data for drug efficacy assessment.

Complement C5A Receptor 1

Complement C5A Receptor 1 (C5aR1) mediates inflammatory responses implicated in IgA Nephropathy pathogenesis. Testing C5aR1 is vital for assessing drug efficacy and safety targeting this pathway. Our service employs fluorescent and chemiluminescent assays, arrestin protease recruitment, [125I]-C5a displacement, and Boyden chamber assays to measure receptor activity and inhibition. Key parameters reported include pIC-50, IC-50, and MIC, enabling robust evaluation of candidate therapeutics.

Complement Factor B

Complement Factor B plays a critical role in the alternative complement pathway, contributing to kidney inflammation in IgA Nephropathy. Testing its activity is essential for evaluating drug candidates targeting this pathway. Our services utilize ELISA, surface plasmon resonance, and FRET assays to assess drug effects. Key parameters measured include IC-50 for inhibitory potency and Kd for binding affinity, providing robust data to guide IgA Nephropathy drug development.

Endothelin Receptor Type A

Endothelin Receptor Type A (ETA) plays a crucial role in IgA Nephropathy by mediating vasoconstriction and promoting kidney inflammation. Testing ETA is vital for developing targeted therapies. Our service utilizes competitive binding and fluorescent assays, including displacement of [125I]-endothelin-1, to evaluate candidate drugs. Key parameters measured are IC50 and Ki, providing essential data on compound affinity and potency for advancing IgA Nephropathy drug development.

Heme Oxygenase 1

Heme Oxygenase 1 (HO-1) modulates oxidative stress and inflammation in IgA Nephropathy, influencing disease progression. HO-1 testing is crucial for assessing therapeutic impact and guiding drug development. Our service uses sensitive RNA assays to quantify HO-1 expression, with Minimum Effective Concentration (MEC) determination as a primary parameter. This enables precise evaluation of candidate compounds’ efficacy in modulating HO-1 for optimal therapeutic strategies.

Mbl Associated Serine Protease 2

Our MBL-Associated Serine Protease 2 testing service supports IgA Nephropathy drug development by measuring MASP-2 activity, a key player in complement-mediated renal injury. Accurate MASP-2 quantification and interaction profiling are conducted using ELISA, biolayer interferometry, surface plasmon resonance, and RNA assays. Main readouts include IC-50 for inhibitor potency and Kd for binding affinity, providing essential data for therapeutic candidate evaluation.

Peroxisome Proliferator Activated Receptor Gamma

Peroxisome Proliferator Activated Receptor Gamma (PPARγ) modulates inflammation and fibrosis in IgA Nephropathy, influencing disease progression. Testing PPARγ activity is vital for evaluating potential therapeutics targeting this pathway. Our service utilizes [3H]-rosiglitazone displacement assays to assess compound binding affinity, providing precise Ki values. These key parameters enable informed decision-making in drug development for effective IgA Nephropathy treatments.

Spleen Associated Tyrosine Kinase

Spleen Associated Tyrosine Kinase (SYK) plays a crucial role in the inflammatory signaling pathways implicated in IgA Nephropathy. Accurate SYK testing is essential for evaluating potential drug candidates targeting this pathway. Using a chemiluminescent assay, our service quantifies SYK inhibition, providing precise IC-50 values to assess compound potency. This enables informed decision-making in IgA Nephropathy drug development by identifying promising SYK inhibitors.

Tnf Superfamily Member 13B

The Tnf Superfamily Member 13B (also known as BAFF) plays a crucial role in B-cell activation and IgA production, contributing to IgA Nephropathy pathogenesis. Testing its modulation is vital for IgA Nephropathy drug development. Our service employs luciferin/luciferase, surface plasmon resonance, and ELISA assays to evaluate compound efficacy and binding. Main parameters measured include IC-50, minimal effective dose (MED), and binding affinity (Kd), ensuring robust therapeutic candidate assessment.