We provide robust and sensitive in vitro screening and characterization platforms for accelerating the discovery and screening of potential therapies for Periodic Fever Syndrome. Our services enable detailed assessment of candidate compounds targeting inflammatory pathways and cytokine production associated with this disease. Key targets include inflammasome components, pro-inflammatory cytokines (such as IL-1β), and signaling proteins implicated in autoinflammatory responses. We support the investigation of pathological processes such as aberrant immune activation, cytokine dysregulation, and cellular responses involved in periodic fever syndromes.
Our comprehensive suite of in vitro assays includes cell-based, biochemical, and biophysical methods designed to evaluate drug efficacy, mechanism of action, and target engagement. These assays enable the identification and characterization of compounds that modulate key molecular and cellular events relevant to Periodic Fever Syndrome.
Cell-based assay: Evaluates the biological effects of candidate compounds on relevant cell types, enabling functional assessment of immune modulation and cytokine inhibition.
Chemiluminescent assay: Detects and quantifies biomolecules or enzymatic activity using light emission, offering high sensitivity for cytokine or signaling protein measurement.
Dye assay (alamar blue): Measures cell viability and metabolic activity, facilitating rapid screening of compound cytotoxicity and proliferation effects.
ELISA assay: Quantifies specific proteins, such as cytokines, in biological samples, providing precise measurement of inflammatory mediators.
Fluorescent assay: Utilizes fluorescence-based detection to monitor biochemical processes, protein interactions, or enzyme activity in real time.
L-Arg-7-amido-4-methylcoumarin as substrate: Assesses enzymatic activity by measuring the cleavage of this fluorogenic substrate, relevant for protease or arginase studies.
RNA assay: Measures gene expression changes induced by compounds, supporting analysis of inflammatory and immune-related transcripts.
Surface plasmon resonance assay: Analyzes biomolecular interactions in real time, determining binding affinity and kinetics between drug candidates and target proteins.
We measure key pharmacological parameters such as potency, binding affinity, and minimal effective concentrations to guide compound selection and optimization. These parameters are critical for understanding drug action, efficacy, and safety profiles in preclinical development.
IC-50: The concentration of a compound required to inhibit a specific biological or biochemical function by 50%, essential for comparing compound potency.
Kd: The equilibrium dissociation constant representing the binding affinity between a drug and its target, crucial for evaluating the strength of molecular interactions.
MEC: Minimum Effective Concentration, the lowest concentration at which a compound elicits a measurable therapeutic effect, important for dose selection.
MED: Minimum Effective Dose, the smallest dose required to achieve a desired pharmacological response, guiding preclinical and clinical dosing strategies.
MIC: Minimum Inhibitory Concentration, the lowest concentration of an agent that prevents visible growth of a microorganism or cellular process, relevant for anti-inflammatory and antimicrobial testing.
Albumin plays a crucial role in modulating inflammation in Periodic Fever Syndrome. Accurate measurement of albumin levels is essential for evaluating disease activity and monitoring therapeutic response. Our Albumin testing service utilizes ELISA assays, providing sensitive and reproducible quantification. Key parameters such as IC-50 are determined to assess the efficacy of candidate drugs in modulating albumin-related pathways, supporting effective drug development and clinical decision-making.
| Pharmacological Activity | Material | Method | Parameter |
|---|---|---|---|
| Albumin affinity | Serum, human | ELISA assay | IC-50 |
Checkpoint Kinase 1 (CHK1) regulates cell cycle and DNA damage response, contributing to inflammatory pathways implicated in Periodic Fever Syndrome. CHK1 testing is crucial for identifying drug candidates that modulate this target. Key methods include kinase activity assays, cellular phosphorylation studies, and high-throughput screening. Main parameters assessed are CHK1 inhibition potency, specificity, and effects on inflammatory biomarkers, guiding effective drug development for this syndrome.
| Pharmacological Activity | Material | Parameter |
|---|---|---|
| Serine/threonine protein kinase (CHK-1) degradation, induction | A375 human malignant melanoma cells | EC-50 |
Endoplasmic Reticulum Aminopeptidase 2 (ERAP2) regulates antigen processing implicated in Periodic Fever Syndrome pathogenesis. Testing ERAP2 activity is crucial for drug development targeting immune dysregulation. Our assay utilizes L-Arg-7-amido-4-methylcoumarin as a specific substrate to measure ERAP2 enzymatic function. The primary parameter assessed is IC-50, enabling precise evaluation of inhibitor potency and efficacy in modulating ERAP2 activity for therapeutic advancement.
| Pharmacological Activity | Material | Method | Parameter |
|---|---|---|---|
| Endoplasmic reticulum aminopeptidase 2 (ERAP2), inhibition | Human enzyme | L-Arg-7-amido-4-methylcoumarin as substrate | IC-50 |
Interleukin 1 Beta (IL-1β) is a key pro-inflammatory cytokine implicated in Periodic Fever Syndrome pathogenesis. Accurate IL-1β testing is vital for drug development, enabling assessment of therapeutic efficacy and biological activity. Our service utilizes ELISA, fluorescent, chemiluminescent, cell-based, SPR, RNA, and alamar blue dye assays to measure IL-1β levels and interaction parameters, including MEC, Kd, IC-50, MED, and MIC, providing comprehensive, reliable data for candidate evaluation.
| Pharmacological Activity | Material | Method | Parameter |
|---|---|---|---|
| Gene (interleukin-1 beta) transcription (endotoxin-induced), inhibition | Macrophages (bone marrow), mouse | RNA assay | MIC |
| Gene (interleukin-1 beta) transcription (endotoxin-induced), inhibition | Macrophages (bone marrow), mouse (neonatal onset multisystem inflammatory disease (NOMID)) | RNA assay | MIC |
| Gene (interleukin-1 beta) transcription (interleukin-1beta-induced), inhibition | Fibroblasts (synovial), human (rheumatoid arthritis) | RNA assay | MIC |
| Interleukin-1 beta levels increase, inhibition | Macrophages (bone marrow-derived), mouse (Nlrp3-mutated) (endotoxin [Salmonella minnesota]-stimulated) | Fluorescent assay | IC-50 |
| Interleukin-1 beta levels increase, inhibition | Monocytes (primary), human (endotoxin [Salmonella minnesota]-stimulated) | Fluorescent assay | IC-50 |
| Interleukin-1beta affinity | Human protein | Chemiluminescent assay | Kd |
| Interleukin-1beta affinity | Human protein | Surface plasmon resonance assay | Kd |
| Interleukin-1beta affinity | Human protein | Kd | |
| Interleukin-1beta affinity | Monkey protein | Surface plasmon resonance assay | Kd |
| Interleukin-1beta affinity | Mouse protein | Surface plasmon resonance assay | Kd |
| Interleukin-1beta affinity | Mouse protein | Kd | |
| Interleukin-1beta affinity | Recombinant human protein | Chemiluminescent assay | Kd |
| Interleukin-1beta affinity | Recombinant human protein | ELISA assay | IC-50 |
| Interleukin-1beta affinity | Recombinant human protein | Surface plasmon resonance assay | Kd |
| Interleukin-1beta affinity | Surface plasmon resonance assay | Kd | |
| Interleukin-1beta expression (endotoxin-induced), inhibition | TC1 mouse lung cancer cells (HPV16-transformed) | Chemiluminescent assay | MIC |
| Interleukin-1beta expression (endotoxin/ATP-induced), inhibition | Macrophages (bone marrow), mouse | ELISA assay | MIC |
| Interleukin-1beta expression, inhibition | Fibroblasts (cardiac), human (transforming growth factor-beta1/endotoxin/ATP-stimulated) | Chemiluminescent assay | MIC |
| Interleukin-1beta production (endotoxin-induced), inhibition | Mononuclear cells (blood), human (cryopyrin-associated periodic syndromes) | Fluorescent assay | MIC |
| Interleukin-1beta production (endotoxin/ATP-induced), inhibition | THP1 human acute monocytic leukemia cells | ELISA assay | IC-50 |
| Interleukin-1beta production (endotoxin/nigericin-induced), inhibition | Kupffer cells, human | ELISA assay | IC-50 |
| Interleukin-1beta production (nigericin-induced), inhibition | Macrophages (primary) (bone marrow-derived), mouse (endotoxin [Salmonella minnesota]-stimulated) | Fluorescent assay | IC-50 |
| Interleukin-1beta production decrease (interleukin-1alpha-induced), potentiation | 1205Lu human melanoma cells | MEC | |
| Interleukin-1beta production, inhibition | 1205Lu human melanoma cells | MIC | |
| Interleukin-1beta production, inhibition | Candida albicans | ELISA assay | IC-50 |
| Interleukin-1beta production, inhibition | HEK293 human embryonic kidney cells transfected with cynomolgus monkey protein | Cell-based assay | IC-50 |
| Interleukin-1beta production, inhibition | HEK293 human embryonic kidney cells transfected with human protein | Cell-based assay | IC-50 |
| Interleukin-1beta production, inhibition | J774A1 mouse macrophages | ELISA assay | IC-50 |
| Interleukin-1beta production, inhibition | M0-type macrophages, human | ELISA assay | MIC |
| Interleukin-1beta production, inhibition | Macrophages (THP1 human acute monocytic leukemia cells-derived) (FP-20/phorbol ester-stimulated) | ELISA assay | MIC |
| Interleukin-1beta production, inhibition | Macrophages (THP1 human acute monocytic leukemia cells-derived) (endotoxin [Salmonella minnesota]/phorbol ester-stimulated) | ELISA assay | MIC |
| Interleukin-1beta production, inhibition | THP1 human acute monocytic leukemia cells | ELISA assay | IC-50 |
| Interleukin-6 production (interleukin-1beta-induced), inhibition | Mice | ELISA assay | MED |
| Mitogenesis (interleukin-1beta-induced), inhibition | D10 mouseT-lymphocytes (concanavalin A-stimulated) | Dye assay (alamar blue) | IC-50 |
| RNA (interleukin-1beta) synthesis (endotoxin-induced), inhibition | Mononuclear cells (blood), human | RNA assay | MIC |
Tumor Necrosis Factor (TNF) is a key pro-inflammatory cytokine implicated in the pathogenesis of Periodic Fever Syndrome. Our TNF testing service utilizes ELISA assays to quantify TNF activity, supporting drug development by evaluating compound efficacy. Critical parameters measured include IC-50 (half-maximal inhibitory concentration) and MEC (minimum effective concentration), enabling precise assessment of therapeutic potential and dosing for candidate drugs targeting TNF-mediated inflammation.
| Pharmacological Activity | Material | Method | Parameter |
|---|---|---|---|
| Tumor necrosis factor-alpha expression (endotoxin-induced), inhibition | THP1 human acute monocytic leukemia cells | ELISA assay | IC-50 |
| Tumor necrosis factor-alpha production, induction | Chondrocytes (joint), human (osteoarthritic) | MEC |
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