In Vitro Efficacy Testing Services for Periodic Fever Syndrome
Drug R&D Solutions

In Vitro Efficacy Testing Services for Periodic Fever Syndrome

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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.

Recommended In Vitro Efficacy Tests

Albumin

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

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

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

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

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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