In Vitro Efficacy Testing Services for Complement-Mediated Disease

We provide robust and sensitive in vitro screening and characterization platforms for accelerating the discovery and screening of potential therapies for Complement-Mediated Disease. Our services enable precise evaluation of candidate molecules targeting the complement cascade, a key mediator in various autoimmune and inflammatory disorders. We focus on critical targets such as complement proteins C3, C5, C5b9, and pathways including the classical and alternative complement pathways. Our assays are designed to assess pathological processes like complement activation, membrane attack complex formation, and complement-dependent cell lysis.

Our comprehensive suite of testing methods includes biochemical, biophysical, and functional assays to evaluate the efficacy and mechanism of complement-targeted therapeutics. These approaches allow for detailed profiling of compound activity, binding properties, and pathway specificity, ensuring actionable insights for drug development.

5,5'-dithiobis(2-nitrobenzoic) acid (DTNB) reduction assay: Measures the reduction of DTNB to quantify enzyme or protein activity involved in the complement pathway, providing insights into mechanism of action.

Biolayer interferometry assay: A label-free technique for real-time analysis of biomolecular interactions, useful for determining binding kinetics and affinities between compounds and complement proteins.

Complement component C5b9 formation assay: Detects the generation of the membrane attack complex (C5b9), indicating the extent of terminal complement pathway activation and therapeutic efficacy.

ELISA assay: Quantifies specific complement components, activation products, or therapeutic antibodies, allowing for sensitive detection of pathway modulation.

Hemolysis assay: Assesses complement-mediated lysis of erythrocytes, serving as a functional readout of complement activity and inhibitor potency.

Hemolysis assay (alternative pathway-specific): Selectively evaluates the activity and inhibition of the alternative complement pathway using pathway-specific conditions.

Hemolysis assay (classical pathway-specific): Selectively measures the function and inhibition of the classical complement pathway, facilitating pathway-targeted drug evaluation.

Surface plasmon resonance assay: Enables real-time, label-free analysis of biomolecular interactions to determine binding kinetics and affinities.

Surface plasmon resonance assay (At 25 degree Celsius): Conducts SPR binding studies at 25°C to assess temperature-dependent binding profiles.

Surface plasmon resonance assay (At 30 degree Celsius): Conducts SPR analyses at 30°C, allowing for evaluation of interactions under physiological-like conditions.

Surface plasmon resonance assay (At 37 degree Celsius): Assesses binding kinetics and affinities at human body temperature, providing physiologically relevant data.

With 5% human serum: Incorporates human serum into assays to closely mimic in vivo conditions and evaluate compound efficacy and stability in a biologically relevant matrix.

We measure key pharmacological parameters including potency, inhibition, and binding affinity to comprehensively characterize candidate therapeutics. These parameters are critical for ranking compounds, understanding mechanism, and predicting clinical efficacy. Accurate measurement ensures informed decisions throughout the drug development process.

EC-50: The concentration of a compound that produces 50% of its maximal effect, used to assess potency and efficacy.

IC-50: The concentration of an inhibitor required to reduce a specific biological or biochemical function by 50%, essential for determining inhibitor strength.

Kd: The equilibrium dissociation constant, reflecting the binding affinity between a drug and its target; lower values indicate stronger binding, informing optimization and selection of lead compounds.

Recommended In Vitro Efficacy Tests

Complement C1S

Complement C1S is a serine protease crucial in initiating the classical complement pathway, implicated in complement-mediated diseases. Accurate C1S testing is vital for drug development targeting dysregulated complement activity. Our service uses surface plasmon resonance and ELISA assays to assess drug-C1S interactions and inhibition. Key parameters measured include IC-50, indicating inhibitory potency, and Kd, reflecting binding affinity, providing essential data for candidate evaluation.

Complement C2

Complement C2 is a critical component of the classical complement pathway, and its dysfunction is implicated in complement-mediated diseases. Accurate measurement of C2 interactions is essential for drug development targeting these pathways. Our Complement C2 testing service utilizes surface plasmon resonance assays to determine binding kinetics, with a focus on calculating the equilibrium dissociation constant (Kd), providing precise insights into therapeutic candidate efficacy.

Complement C3

Complement C3 is central to complement-mediated diseases, driving inflammation and tissue damage. Accurate C3 testing is vital for drug development, enabling assessment of drug efficacy and mechanism. Our service employs ELISA, biolayer interferometry, surface plasmon resonance, and hemolysis assays to quantify C3 activity and drug interactions. Key parameters measured include EC-50, IC-50, and Kd, providing essential data for optimizing complement-targeted therapeutics.

Complement C4B (Chido/Rodgers Blood Group)

Complement C4B (Chido/Rodgers Blood Group) plays a vital role in complement-mediated diseases by influencing immune complex clearance and inflammatory responses. Testing C4B is crucial for identifying genetic variants and functional deficiencies that impact disease susceptibility and therapeutic response. Key methods include genotyping, immunoassays, and functional assays. Main parameters assessed are C4B gene copy number, protein levels, and functional activity, supporting drug development and patient stratification.

Complement C5

Complement C5 is pivotal in the pathogenesis of complement-mediated diseases, making it a key therapeutic target. Our testing service evaluates drug candidates using hemolysis assays (classical and alternative pathways), ELISA, C5b9 formation, biolayer interferometry, and surface plasmon resonance at multiple temperatures, with 5% human serum to ensure physiological relevance. Critical parameters measured include IC50 and Kd, supporting robust drug development and efficacy assessment.

Complement C5A Receptor 1

Complement C5A Receptor 1 (C5aR1) mediates inflammatory responses in complement-mediated diseases, making it a critical drug target. Our C5aR1 testing service supports drug development by assessing receptor binding, signaling, and inhibition. Key methods include ligand-binding assays, cell-based functional assays, and flow cytometry. Main parameters measured are binding affinity, receptor expression levels, and downstream signaling activity, enabling precise evaluation of therapeutic candidates targeting C5aR1.

Complement C7

Complement C7 plays a vital role in forming the membrane attack complex, contributing to tissue damage in complement-mediated diseases. Testing C7 is crucial for evaluating drug efficacy and safety during development. Our service employs ELISA and functional hemolytic assays to assess C7 concentration and activity. Main parameters include C7 protein levels, functional activity, and complement pathway integrity, providing essential data for therapeutic intervention strategies.

Complement Factor D

Complement Factor D is a key protease in the alternative complement pathway, implicated in complement-mediated diseases. Accurate measurement is vital for drug development targeting this pathway. Our service offers robust quantification of Factor D activity and inhibition using the DTNB reduction assay and Factor D-specific ELISA. Key parameters, including IC-50 values, enable precise evaluation of candidate inhibitors, supporting effective therapeutic development.