In Vitro Efficacy Testing Services for Food Allergy
Drug R&D Solutions

In Vitro Efficacy Testing Services for Food Allergy

Inquiry

We provide robust and sensitive in vitro screening and characterization platforms for accelerating the discovery and screening of potential therapies for Food Allergy. Our services enable the evaluation of compound efficacy, allergen-antibody interactions, and mechanism of action studies specific to food allergy pathways. Key targets include IgE, FcεRI, mast cells, basophils, and associated signaling molecules involved in hypersensitivity reactions. We assess processes such as allergen-induced immune activation, mediator release, and inhibition of allergic pathways to support therapeutic development.

Our platform offers a comprehensive suite of biochemical, cell-based, and molecular assays to measure compound efficacy and mechanism of action in food allergy models. These methods enable detailed investigation of binding affinities, functional activity, cellular responses, and pathway modulation. The diversity of assays ensures that both upstream molecular events and downstream functional outcomes can be systematically evaluated.

ATP assay: Measures cellular viability and metabolic activity, useful for assessing cytotoxicity and immune cell activation.

Chemiluminescent assay: Detects enzyme activities or analyte concentrations via light emission, enabling sensitive readouts for mediator release or immune response.

Competitive binding assay: Quantifies the ability of test compounds to inhibit allergen or antibody binding, critical for evaluating therapeutic candidates.

Competitive binding assay (qPCR): Combines binding measurement with quantitative PCR for precise detection of nucleic acid-associated targets.

Displacement of [3H]-desloratadine: Assesses binding interactions at histamine receptors, important for allergy medication targeting.

Displacement of [3H]-mepyramine: Evaluates compound competition for histamine H1 receptor binding, relevant in anti-allergy drug screening.

Displacement of [3H]-pyrilamine: Measures inhibition of pyrilamine binding to histamine receptors, indicating potential anti-allergic activity.

ELISA assay: Quantifies specific proteins, antibodies, or cytokines, widely used for allergen-specific IgE or mediator detection.

Flow cytometry assay: Analyzes cell surface markers and activation states, allowing profiling of immune cell populations.

Fluorescence resonance energy transfer (FRET) assay: Detects proximity-dependent molecular interactions, suitable for signaling pathway analysis.

Fluorescent assay: Utilizes fluorescence to monitor cellular or biochemical events, facilitating high-throughput screening.

Fluorescent-activated cell sorting (FACS) assay: Sorts and analyzes cell populations based on fluorescent labeling, enabling detailed immune cell characterization.

Gene reporter assay: Measures gene expression changes in response to stimuli, often used to study pathway activation or inhibition.

Homogeneous Time Resolved Fluorescence (HTRF) assay: Enables sensitive quantification of proteins or interactions in a no-wash format, ideal for high-throughput studies.

Occupancy assay: Determines the proportion of target molecules occupied by test compounds, critical for understanding drug-target engagement.

Peptide as substrate: Uses synthetic peptides to study enzyme activity or epitope recognition relevant to allergen processing.

Poly(L-glutamate/L-tyrosine) [Poly(E,Y)1-4] as substrate: Assesses enzyme-mediated modifications on synthetic substrates, useful for mechanistic studies.

Poly(glutamine/tyrosine) peptide as substrate: Evaluates enzyme activity on defined peptide sequences, aiding in pathway elucidation.

Radioactivity assay: Employs radiolabeled compounds for high-sensitivity detection of binding or enzymatic activity.

Surface plasmon resonance assay: Measures real-time biomolecular interactions without labeling, providing kinetic and affinity data.

beta-Galactosidase assay: Detects reporter gene activity or substrate cleavage, commonly used for monitoring gene expression.

We measure a range of quantitative pharmacological parameters, including potency, efficacy, and binding affinity, to thoroughly characterize candidate compounds. These parameters are essential for comparing therapeutic profiles and optimizing lead selection. Accurate parameter assessment supports rational drug design and regulatory decision-making.

ED-50: The effective dose at which 50% of the maximal response is observed, indicating compound potency.

IC-50: The concentration required to inhibit a biological process by 50%, used to assess inhibitory strength.

Kd: The dissociation constant reflecting the affinity between a ligand and its target, critical for binding studies.

Ki: The inhibition constant representing the binding affinity of an inhibitor, important for competitive assays.

MED: The minimum effective dose that produces a measurable biological effect, useful for dose optimization.

MIC: The minimum inhibitory concentration needed to prevent visible growth of a microorganism or biological process, relevant in antimicrobial and allergen suppression studies.

pKi: The negative logarithm of the Ki value, providing a standardized measure of inhibitor potency.

Recommended In Vitro Efficacy Tests

Bruton Tyrosine Kinase

Bruton Tyrosine Kinase (BTK) plays a crucial role in B cell activation and allergic immune responses, making it a key target in Food Allergy drug development. BTK testing assesses drug efficacy and selectivity using advanced methods including occupancy, flow cytometry, competitive binding (qPCR), ATP, FRET, fluorescent, ELISA, chemiluminescent, HTRF, FACS, and radioactivity assays. Key parameters measured are Ki, IC₅₀, and MED, ensuring robust evaluation of candidate therapeutics.

Pharmacological Activity Material Method Parameter
Calcium mobilization, inhibition Cells transfected with enzyme Fluorescent assay IC-50
Integrin CD69 expression (anti-IgM/IgG-induced), inhibition Blood, human Fluorescent-activated cell sorting (FACS) assay IC-50
Integrin CD86 expression (anti-IgM-induced), inhibition Blood, rat (heparinized) (interleukin-4-stimulated) Flow cytometry assay IC-50
Protein-tyrosine kinase (BTK) (C481S-mutated), inhibition Recombinant enzyme ATP assay IC-50
Protein-tyrosine kinase (BTK) (C481S-mutated), inhibition Recombinant human enzyme ATP assay IC-50
Protein-tyrosine kinase (BTK) (C481S-mutated), inhibition Recombinant human enzyme Peptide as substrate IC-50
Protein-tyrosine kinase (BTK) (C481S-mutated), inhibition Recombinant human enzyme Radioactivity assay IC-50
Protein-tyrosine kinase (BTK) (L528M-mutated), inhibition Recombinant enzyme ATP assay IC-50
Protein-tyrosine kinase (BTK) (L528V-mutated), inhibition Recombinant enzyme ATP assay IC-50
Protein-tyrosine kinase (BTK) (L528W-mutated), inhibition Recombinant enzyme Homogeneous Time Resolved Fluorescence (HTRF) assay IC-50
Protein-tyrosine kinase (BTK) (L528W-mutated), inhibition IC-50
Protein-tyrosine kinase (BTK) (T474I-mutated), inhibition Recombinant enzyme ATP assay IC-50
Protein-tyrosine kinase (BTK) (T474I-mutated), inhibition IC-50
Protein-tyrosine kinase (BTK) (T474I/C481S-mutated), inhibition Recombinant enzyme ATP assay IC-50
Protein-tyrosine kinase (BTK) (T474I/C481S-mutated), inhibition IC-50
Protein-tyrosine kinase (BTK) (T474L-mutated), inhibition Recombinant enzyme ATP assay IC-50
Protein-tyrosine kinase (BTK) (T474M-mutated), inhibition Recombinant enzyme ATP assay IC-50
Protein-tyrosine kinase (BTK) (T474M/C481S-mutated), inhibition Recombinant enzyme ATP assay IC-50
Protein-tyrosine kinase (BTK) (T474M/C481T-mutated), inhibition Recombinant enzyme ATP assay IC-50
Protein-tyrosine kinase (BTK) (V416L-mutated) inhibition IC-50
Protein-tyrosine kinase (BTK) (Y223-mutated) phosphorylation, inhibition Recombinant human enzyme Homogeneous Time Resolved Fluorescence (HTRF) assay IC-50
Protein-tyrosine kinase (BTK) (mutated), inhibition Recombinant human enzyme Fluorescence resonance energy transfer (FRET) assay IC-50
Protein-tyrosine kinase (BTK) (mutated), inhibition Recombinant human enzyme Peptide as substrate IC-50
Protein-tyrosine kinase (BTK) affinity Blood, human IC-50
Protein-tyrosine kinase (BTK) affinity Mononuclear cells (blood), human (chronic lymphocytic leukemia) Chemiluminescent assay IC-50
Protein-tyrosine kinase (BTK) affinity Spleen, rat Occupancy assay MED
Protein-tyrosine kinase (BTK) affinity Competitive binding assay Ki
Protein-tyrosine kinase (BTK) affinity Competitive binding assay (qPCR) Ki
Protein-tyrosine kinase (BTK) affinity IC-50
Protein-tyrosine kinase (BTK) phosphorylation, inhibition Ramos human Burkitt's lymphoma B-lymphocytes Homogeneous Time Resolved Fluorescence (HTRF) assay IC-50
Protein-tyrosine kinase (BTK) phosphorylation, inhibition Ramos human Burkitt's lymphoma B-lymphocytes IC-50
Protein-tyrosine kinase (BTK), inhibition B-Lymphocytes (CD19+), human (anti-IgM/interleukin-4-activated) Flow cytometry assay IC-50
Protein-tyrosine kinase (BTK), inhibition Blood, human IC-50
Protein-tyrosine kinase (BTK), inhibition Mononuclear cells (blood), human IC-50
Protein-tyrosine kinase (BTK), inhibition Ramos human Burkitt's lymphoma B-lymphocytes ELISA assay IC-50
Protein-tyrosine kinase (BTK), inhibition Recombinant enzyme ATP assay IC-50
Protein-tyrosine kinase (BTK), inhibition Recombinant enzyme Fluorescence resonance energy transfer (FRET) assay IC-50
Protein-tyrosine kinase (BTK), inhibition Recombinant enzyme Peptide as substrate IC-50
Protein-tyrosine kinase (BTK), inhibition Recombinant human enzyme ATP assay IC-50
Protein-tyrosine kinase (BTK), inhibition Recombinant human enzyme ELISA assay IC-50
Protein-tyrosine kinase (BTK), inhibition Recombinant human enzyme Fluorescence resonance energy transfer (FRET) assay IC-50
Protein-tyrosine kinase (BTK), inhibition Recombinant human enzyme Peptide as substrate IC-50
Protein-tyrosine kinase (BTK), inhibition Recombinant human enzyme Poly(glutamine/tyrosine) peptide as substrate IC-50
Protein-tyrosine kinase (BTK), inhibition Recombinant human enzyme Radioactivity assay IC-50
Protein-tyrosine kinase (BTK), inhibition Recombinant human enzyme IC-50
Protein-tyrosine kinase (BTK), inhibition Chemiluminescent assay IC-50
Protein-tyrosine kinase (BTK), inhibition ELISA assay IC-50
Protein-tyrosine kinase (BTK), inhibition Fluorescence resonance energy transfer (FRET) assay IC-50
Protein-tyrosine kinase (BTK), inhibition Fluorescent assay IC-50
Protein-tyrosine kinase (BTK), inhibition Homogeneous Time Resolved Fluorescence (HTRF) assay IC-50
Protein-tyrosine kinase (BTK), inhibition Poly(L-glutamate/L-tyrosine) [Poly(E,Y)1-4] as substrate IC-50
Protein-tyrosine kinase (BTK), inhibition Poly(glutamine/tyrosine) peptide as substrate IC-50
Protein-tyrosine kinase (BTK), inhibition IC-50

C-C Motif Chemokine Receptor 9

C-C Motif Chemokine Receptor 9 (CCR9) plays a crucial role in T cell recruitment and gut inflammation during food allergy responses. Testing CCR9 activity is essential for evaluating drug candidates targeting allergic pathways. Our service utilizes a sensitive fluorescent assay to assess compound efficacy, with IC-50 determination as the main parameter, providing precise quantification of inhibitor potency for effective food allergy drug development.

Pharmacological Activity Material Method Parameter
Chemotaxis (chemokine (C-C motif) ligand 25 [CCL25]-induced), inhibition MOLT4 human acute T-lymphoblastoid leukemia cells Fluorescent assay IC-50

Histamine Receptor H1

Histamine Receptor H1 mediates allergic responses, making it a vital target in food allergy drug development. Our testing service evaluates compound interactions with H1 using assays such as [3H]-mepyramine, [3H]-pyrilamine, [3H]-desloratadine displacement, fluorescent and beta-galactosidase assays, and radioactivity analyses. Key parameters determined include ED-50, IC-50, Ki, and pKi, enabling precise assessment of drug efficacy and receptor affinity for optimal candidate selection.

Pharmacological Activity Material Method Parameter
Bronchoconstriction (histamine-induced), inhibition Guinea pigs ED-50
Bronchoconstriction (histamine-induced), inhibition Trachea, guinea pig IC-50
Calcium mobilization (serotonin-induced), inhibition CHO Chinese hamster ovary cells transfected with human H1 receptor Fluorescent assay pKi
Gene (cAMP response element) transcription (histamine-induced), inhibition SK-N-MC human neuroblastoma cells transfected with human H1 receptor beta-Galactosidase assay IC-50
Histamine H1 receptor affinity Brain, guinea pig Displacement of [3H]-pyrilamine IC-50
Histamine H1 receptor affinity Brain, mouse Radioactivity assay ED-50
Histamine H1 receptor affinity Brain, rat Displacement of [3H]-mepyramine Ki
Histamine H1 receptor affinity Brain, rat Displacement of [3H]-pyrilamine Ki
Histamine H1 receptor affinity CHO Chinese hamster ovary cells transfected with human receptor Displacement of [3H]-desloratadine Ki
Histamine H1 receptor affinity CHO Chinese hamster ovary cells transfected with human receptor Displacement of [3H]-mepyramine Ki
Histamine H1 receptor affinity CHO Chinese hamster ovary cells transfected with human receptor Displacement of [3H]-pyrilamine IC-50
Histamine H1 receptor affinity Cells transfected with human receptor pKi
Histamine H1 receptor affinity Cerebellum, guinea pig Displacement of [3H]-mepyramine IC-50
Histamine H1 receptor affinity Cerebellum, guinea pig Displacement of [3H]-pyrilamine Ki
Histamine H1 receptor affinity Cortex, guinea pig Displacement of [3H]-mepyramine pKi
Histamine H1 receptor affinity Cortex, guinea pig Radioactivity assay ED-50
Histamine H1 receptor affinity Cortex, rat Displacement of [3H]-pyrilamine IC-50
Histamine H1 receptor affinity Cortex, rat Radioactivity assay ED-50
Histamine H1 receptor affinity Forebrain, guinea pig Displacement of [3H]-pyrilamine pKi
Histamine H1 receptor affinity Human receptor Radioactivity assay IC-50
Histamine H1 receptor affinity Human receptor IC-50
Histamine H1 receptor affinity Lung, guinea pig Displacement of [3H]-mepyramine Ki
Histamine H1 receptor affinity Lung, guinea pig Radioactivity assay ED-50

Interleukin 13

Interleukin 13 (IL-13) is a key cytokine in the pathogenesis of food allergy, promoting IgE synthesis and inflammatory responses. Testing IL-13 is essential for evaluating drug efficacy and mechanism. Our service utilizes chemiluminescent, surface plasmon resonance, ELISA, and fluorescent assays to measure IL-13 activity and interactions. Main parameters assessed include IC-50 (inhibitory concentration) and Kd (binding affinity), providing critical data for food allergy drug development.

Pharmacological Activity Material Method Parameter
Interleukin-13 affinity Recombinant cynomolgus monkey protein Surface plasmon resonance assay Kd
Interleukin-13 affinity Recombinant human protein Surface plasmon resonance assay Kd
Interleukin-13 production, inhibition B9 mouse hybridoma cells IC-50
Interleukin-13/Interleukin-13 receptor subunit alpha-2 interaction, inhibition Recombinant human receptor ELISA assay IC-50
Mitogenesis (interleukin-13-induced), inhibition TF1 human erythroleukemia cells Chemiluminescent assay IC-50
Mitogenesis (interleukin-13-induced), inhibition TF1 human erythroleukemia cells Fluorescent assay IC-50
Signal transducer and activator of transcription-6 (STAT6) phosphorylation (interleukin-13-induced), inhibition HT29 human colon adenocarcinoma cells IC-50

Interleukin 17A

Interleukin 17A (IL-17A) is a pro-inflammatory cytokine implicated in food allergy pathogenesis. Testing IL-17A interactions is vital for developing targeted allergy therapeutics. Our service utilizes surface plasmon resonance assays to quantitatively assess IL-17A binding with candidate drugs, providing accurate affinity data. Key parameters measured include the dissociation constant (Kd), enabling precise evaluation of drug efficacy and guiding optimal compound selection in food allergy drug development.

Pharmacological Activity Material Method Parameter
Interleukin-17A affinity Cynomolgus monkey protein Surface plasmon resonance assay Kd
Interleukin-17A affinity Human protein Surface plasmon resonance assay Kd
Interleukin-17A/F affinity Cynomolgus monkey protein Surface plasmon resonance assay Kd
Interleukin-17A/F affinity Human protein Surface plasmon resonance assay Kd

Interleukin 17F

Interleukin 17F is implicated in food allergy pathogenesis by promoting inflammatory responses. Accurate testing of IL-17F interactions is vital for developing targeted food allergy therapies. Our service utilizes surface plasmon resonance assays to quantitatively assess binding kinetics, with a primary focus on determining the equilibrium dissociation constant (Kd). This enables precise evaluation of candidate drugs' efficacy in modulating IL-17F activity, accelerating the development of effective food allergy treatments.

Pharmacological Activity Material Method Parameter
Interleukin-17F affinity Cynomolgus monkey protein Surface plasmon resonance assay Kd
Interleukin-17F affinity Human protein Surface plasmon resonance assay Kd

Tnf Receptor Superfamily Member 17

Tnf Receptor Superfamily Member 17 (TNFRSF17) is implicated in immune regulation relevant to food allergy pathogenesis. Testing its ligand-binding properties aids in evaluating drug candidates targeting allergic responses. Surface plasmon resonance (SPR) assays are employed to quantitatively assess interactions, with the equilibrium dissociation constant (Kd) as the principal parameter, providing crucial insights into drug-receptor affinity and potential therapeutic efficacy.

Pharmacological Activity Material Method Parameter
Tumor necrosis factor receptor type 17 (BCMA) affinity Cynomolgus monkey receptor Surface plasmon resonance assay Kd
Tumor necrosis factor receptor type 17 (BCMA) affinity Recombinant human receptor Surface plasmon resonance assay Kd
Tumor necrosis factor receptor type 17 (BCMA) affinity Recombinant monkey receptor Surface plasmon resonance assay Kd

Toll Like Receptor 4

Toll Like Receptor 4 (TLR4) plays a key role in mediating immune responses implicated in food allergy pathogenesis. TLR4 testing is essential for evaluating the immunomodulatory effects of drug candidates. Our service utilizes a sensitive gene reporter assay to quantify TLR4 activation. Main parameters include measurement of the minimum inhibitory concentration (MIC), providing critical data for optimizing food allergy drug development.

Pharmacological Activity Material Method Parameter
Gene transcription (NF-kappaB-dependent) (endotoxin-induced), inhibition HEK293 human embryonic kidney cells transfected with mouse TLR4 (+MD2/CD14) receptor Gene reporter assay MIC
HOW WE WORK

Make Order

Make Order

Experimental Scheme

Experimental Scheme

Implementation

Implementation

Conclusion

Conclusion
Make an Inquiry