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.
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 (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 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 (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 (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 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 (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 (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 |
Make Order
Experimental Scheme
Implementation
Conclusion