In Vitro Efficacy Testing Services for Pancreatic Cancer

We provide robust and sensitive in vitro screening and characterization platforms for accelerating the discovery and screening of potential therapies for Pancreatic Cancer. Our services offer comprehensive evaluation of candidate compounds, biologics, and immunotherapies targeting key pathways and molecular mechanisms implicated in pancreatic tumorigenesis. We focus on targets such as PARP, PD-1/PD-L1, and metabolic enzymes, as well as signaling cascades and immune checkpoint interactions relevant to pancreatic cancer progression and resistance. Our assays enable investigation of cell viability, apoptosis, DNA repair, immune modulation, and other critical pathological processes associated with this aggressive malignancy.

Our portfolio encompasses a broad range of in vitro testing methods, including biochemical, cell-based, and biophysical assays. These methods enable the evaluation of drug efficacy, mechanism of action, target engagement, and immunological response, supporting comprehensive preclinical screening for pancreatic cancer therapeutics. Each assay is selected to provide detailed insights into drug performance and molecular interactions.

ATP assay: Measures cellular ATP levels as an indicator of cell viability and cytotoxicity, essential for assessing anti-cancer effects of test compounds.

Bioluminescence resonance energy transfer (BRET) assay: Detects protein-protein interactions or compound binding in real time, facilitating the study of signaling pathways and target engagement.

CHO-K1 Chinese hamster ovary cells transfected with human CD274/aAPC: Utilized for evaluating immune checkpoint modulation and antibody activities in a controlled cellular context.

Chemiluminescent assay: Provides sensitive detection of biomolecular interactions or enzymatic activity via chemiluminescence, useful for quantifying target engagement or pathway activation.

DNA-PARP trapping: Assesses the ability of compounds to trap PARP on DNA, a key mechanism in targeting DNA repair pathways in cancer cells.

ELISA assay: Quantifies specific proteins, cytokines, or biomarkers in cell culture supernatants, supporting immune response and pathway analysis.

Flow cytometry assay: Enables multiparametric analysis of cell populations, including apoptosis, cell cycle, and surface marker expression relevant to tumor progression.

Fluorescent assay: Utilizes fluorescence-based detection for assessing enzyme activity, cell viability, or target binding in vitro.

Fluorescent polarization assay: Measures molecular interactions and binding affinities in solution, supporting drug-target binding studies.

Fluorescent-activated cell sorting (FACS) assay: Allows isolation and analysis of distinct cell subsets, enabling functional and phenotypic characterization.

Homogeneous Time Resolved Fluorescence (HTRF) assay: Combines fluorescence resonance energy transfer with time-resolved detection for high-sensitivity quantification of biomolecular interactions.

Jurkat human T-cell leukemia cells transfected with PD1/NFAT/luciferase: Used to study T cell activation and immune checkpoint modulation in response to candidate immunotherapies.

Jurkat human T-cell leukemia cells transfected with human PD1/NFAT/luciferase: Assesses immune signaling and checkpoint inhibition using humanized T cell models.

NAD(+) as substrate: Supports enzymatic assays, particularly for enzymes involved in cellular metabolism and DNA repair, relevant to cancer cell survival.

Surface plasmon resonance assay: Provides real-time, label-free analysis of molecular interactions and binding kinetics between drugs and targets.

Surface plasmon resonance assay (At 25 degree Celsius): Conducts binding studies at controlled room temperature to evaluate interaction kinetics under standard conditions.

Surface plasmon resonance assay (At 37 degree Celsius): Performs binding analysis at physiological temperature, offering insights into drug-target interactions in biologically relevant settings.

We quantify key pharmacological parameters such as potency, affinity, and efficacy to comprehensively profile each compound's activity. These parameters are critical for guiding lead optimization, dose selection, and risk assessment during drug development. Accurate measurement of these values ensures reliable comparison and selection of promising therapeutic candidates.

EC-50: The concentration of a drug that produces 50% of its maximal effect, indicating compound potency in biological assays.

IC-50: The concentration of inhibitor required to reduce a specific biological or biochemical function by 50%, essential for evaluating inhibitory activity.

Kd: The equilibrium dissociation constant that quantifies the binding affinity between a ligand and its target, a fundamental parameter for drug-target interactions.

MEC: Minimum effective concentration, representing the lowest concentration at which a compound elicits a detectable biological response.

MIC: Minimum inhibitory concentration, the lowest concentration required to inhibit visible growth of target cells or organisms, important for cytotoxic or antimicrobial assessment.

pEC-50: The negative logarithm of the EC-50, providing a standardized and more precise measure of compound potency in pharmacological studies.

Recommended In Vitro Efficacy Tests

Dna Topoisomerase I

DNA Topoisomerase I is crucial for DNA replication and is often overexpressed in pancreatic cancer, making it a vital drug target. Testing its inhibition helps identify promising therapeutics. Our service utilizes a chemiluminescent assay to accurately evaluate compound efficacy, providing key parameters such as the Minimum Inhibitory Concentration (MIC) to guide drug development decisions efficiently.

Epidermal Growth Factor Receptor

Epidermal Growth Factor Receptor (EGFR) plays a crucial role in pancreatic cancer progression and therapy resistance. EGFR testing informs targeted drug development by identifying effective inhibitors. Our service employs advanced methods—FACS, chemiluminescence, fluorescent polarization, HTRF, flow cytometry, fluorescent, ATP, and surface plasmon resonance assays—to evaluate key parameters including MEC, IC₅₀, and Kd, ensuring precise assessment of drug efficacy and binding affinity for optimal therapeutic outcomes.

Poly(Adp-Ribose) Polymerase 1

Poly(ADP-Ribose) Polymerase 1 (PARP1) is crucial in DNA repair and is often overactive in pancreatic cancer, making it a key therapeutic target. Our PARP1 testing service uses methods such as BRET, chemiluminescent and fluorescent assays (with NAD+ as substrate), and DNA-PARP trapping to evaluate drug efficacy. Main parameters measured include binding affinity (Kd) and inhibitor potency (IC-50), supporting effective pancreatic cancer drug development.

Poly(Adp-Ribose) Polymerase 2

Poly(ADP-Ribose) Polymerase 2 (PARP2) plays a crucial role in DNA repair pathways implicated in pancreatic cancer progression and therapy resistance. Testing PARP2 activity is essential for evaluating drug efficacy and developing targeted therapeutics. Our service utilizes NAD(+) as a substrate and assesses DNA-PARP trapping using sensitive fluorescent and chemiluminescent assays. The primary parameter measured is IC-50, enabling precise quantification of inhibitor potency in pancreatic cancer drug development.

Poly(Adp-Ribose) Polymerase Family Member 3

Poly(ADP-Ribose) Polymerase Family Member 3 (PARP3) is implicated in DNA repair and genomic stability, influencing pancreatic cancer progression and response to therapy. PARP3 testing is vital for identifying therapeutic targets and predicting drug sensitivity. Key methods include qPCR, immunohistochemistry, and sequencing. Main parameters assessed are PARP3 expression levels, mutation status, and activity, supporting drug development and personalized treatment strategies in pancreatic cancer.

Programmed Cell Death 1

Programmed Cell Death 1 (PD-1) is a key immune checkpoint involved in pancreatic cancer immune evasion. Testing PD-1 interactions is crucial for developing effective immunotherapies. We offer comprehensive assays—including FACS, flow cytometry, ELISA, fluorescent assays, and surface plasmon resonance (at 25°C and 37°C)—using specialized cell lines (CHO-K1, Jurkat T-cells) to evaluate drug efficacy. Key parameters measured include EC-50, Kd, IC-50, and MIC for quantitative assessment.

Receptor Interacting Serine/Threonine Kinase 2

Receptor Interacting Serine/Threonine Kinase 2 (RIPK2) is implicated in pancreatic cancer progression and inflammatory signaling. Testing RIPK2 activity is crucial for evaluating potential drug candidates targeting this kinase. Our service employs chemiluminescent and ATP assays to accurately measure RIPK2 inhibition, with IC-50 determination as the primary parameter, enabling precise assessment of compound potency in pancreatic cancer drug development.

Somatostatin Receptor 2

Somatostatin Receptor 2 (SSTR2) is frequently overexpressed in pancreatic cancer, influencing tumor growth and response to therapy. SSTR2 testing is crucial for identifying targeted treatment strategies and evaluating drug efficacy. Our service utilizes a chemiluminescent assay to assess ligand-receptor interactions, providing precise measurement of receptor activity. The main parameter reported is pEC-50, enabling accurate comparison of drug potency and aiding in the development of effective pancreatic cancer therapeutics.

Somatostatin Receptor 3

The Somatostatin Receptor 3 (SSTR3) testing service assesses SSTR3 function, a key modulator of tumor growth in pancreatic cancer. This testing is vital for evaluating drug candidates targeting SSTR3-mediated pathways. Using a sensitive chemiluminescent assay, the service quantifies receptor activity and determines pEC-50 values, providing essential data on compound potency and efficacy for pancreatic cancer drug development.