In Vitro Efficacy Testing Services for Neuroendocrine Cancer
Drug R&D Solutions

In Vitro Efficacy Testing Services for Neuroendocrine Cancer

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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 Neuroendocrine Cancer. Our services are tailored to evaluate drug candidates by targeting critical proteins and pathways such as somatostatin receptors, PD1/PDL1 immune checkpoints, and key peptide hormones involved in neuroendocrine tumor biology. We offer comprehensive testing of therapeutic efficacy, receptor binding, signal transduction, and immune modulation relevant to neuroendocrine malignancies. These platforms enable the assessment of tumor cell viability, receptor-ligand interactions, and mechanisms underlying tumor progression and immune evasion.

Our in vitro testing methods encompass a diverse array of biochemical, molecular, and cellular assays designed to assess compound efficacy, receptor interactions, and cellular responses in Neuroendocrine Cancer models. These platforms enable precise evaluation of drug potency, selectivity, and mechanism of action, supporting informed decision-making in therapeutic development.

ATP assay: Measures cellular ATP levels to evaluate cell viability and cytotoxicity following drug treatment, providing a quantitative assessment of anti-tumor activity.

CHO-K1 Chinese hamster ovary cells transfected with PDL1/OKT3: A cellular system used to investigate immune checkpoint interactions and the efficacy of immunomodulatory compounds.

Chemiluminescent assay: Utilizes light emission to detect specific biomolecular interactions or enzymatic activities, enabling sensitive quantification of assay targets.

Competitive binding assay: Assesses the ability of test compounds to compete with labeled ligands for receptor binding, indicating affinity and potential mechanism of action.

Competitive binding assay (qPCR): Combines binding competition with quantitative PCR to detect and quantify specific DNA or RNA sequences, enhancing sensitivity and specificity.

Displacement of [125I]-[Tyr11]-somatostatin-14: Evaluates the binding of candidate drugs to somatostatin receptors by measuring their ability to displace radiolabeled somatostatin analogues.

Displacement of [18F]-AlF-NOTA-JR11: Measures receptor binding by tracking displacement of radiolabeled peptide ligands, aiding in the characterization of drug-receptor interactions.

ELISA assay: Enzyme-linked immunosorbent assay used for quantifying proteins, peptides, or antibodies, supporting biomarker and pharmacodynamic studies.

Flow cytometry assay: Analyzes cell populations for phenotype and functional markers, enabling multiparametric assessment of immune and tumor cells.

Fluorescent assay: Employs fluorescent probes to detect cellular or molecular events such as receptor binding or enzyme activity, allowing for high-throughput analysis.

Fluorescent-activated cell sorting (FACS) assay: Sorts and analyzes cells based on fluorescence markers, facilitating the study of heterogeneous cell populations and drug effects.

Homogeneous Time Resolved Fluorescence (HTRF) assay: Detects molecular interactions in a homogeneous format with high sensitivity, useful for screening ligand-receptor binding or signal transduction.

Jurkat human T-cell leukemia cells transfected with PD1/NFAT/luciferase: A reporter cell assay system for evaluating T-cell activation and the impact of immuno-oncology agents.

Luciferine/luciferase assay: Measures luminescence as an indicator of ATP levels or gene expression, providing a sensitive readout for cell viability and reporter assays.

Poly(glutamine/tyrosine) peptide as substrate: Used to assess enzymatic activity against synthetic peptide substrates relevant to neuroendocrine signaling.

RNA assay: Quantifies mRNA expression levels to assess gene regulation by candidate drugs, informing on molecular mechanism of action.

Radioactivity assay: Detects radiolabeled compounds or metabolites, offering quantitative insights into drug binding and metabolic fate.

Surface plasmon resonance assay: Measures real-time biomolecular interactions and binding kinetics without labeling, supporting high-resolution characterization of drug-target affinity.

We measure a range of pharmacological parameters including potency, binding affinity, efficacy thresholds, and inhibitory concentrations. These metrics are essential for determining the therapeutic window, selectivity, and mechanistic profile of drug candidates. Accurate parameter assessment guides optimization and advancement of compounds in the drug development pipeline.

IC-50: The concentration of a compound required to inhibit a specific biological or biochemical function by 50%, indicating drug potency.

Kd: The equilibrium dissociation constant reflecting the affinity between a ligand and its target, with lower values signifying stronger binding.

MEC: Minimum Effective Concentration, the lowest concentration of a drug that produces a detectable therapeutic response, important for dose selection.

MIC: Minimum Inhibitory Concentration, the lowest concentration needed to inhibit cell growth or activity, often used in cytotoxicity evaluations.

pEC-50: The negative logarithm of the EC50 (effective concentration for 50% maximal response), providing a standardized measure of agonist potency.

pIC-50: The negative logarithm of the IC50, offering a normalized scale for comparing inhibitory potency across compounds.

Recommended In Vitro Efficacy Tests

Axl Receptor Tyrosine Kinase

Axl Receptor Tyrosine Kinase is implicated in neuroendocrine cancer progression and therapy resistance. Testing Axl activity is crucial for identifying and optimizing targeted drug candidates. Our service utilizes ATP assays to evaluate compound efficacy, quantifying inhibition through IC-50 determination. This enables precise assessment of drug potency against Axl, supporting effective neuroendocrine cancer drug development.

Pharmacological Activity Material Method Parameter
Protein-tyrosine kinase (Axl), inhibition Recombinant human enzyme ATP assay IC-50
Protein-tyrosine kinase (Axl), inhibition IC-50

Colony Stimulating Factor 1 Receptor

The Colony Stimulating Factor 1 Receptor (CSF1R) plays a critical role in neuroendocrine cancer by mediating tumor-associated macrophage recruitment and supporting tumor growth. CSF1R testing is essential for evaluating drug efficacy targeting this pathway. Our service utilizes chemiluminescent and ATP assays to measure drug inhibition, providing precise IC-50 values to assess compound potency and guide neuroendocrine cancer drug development.

Pharmacological Activity Material Method Parameter
Protein-tyrosine kinase (CSF-1 receptor) phosphorylation, inhibition DEL human anaplastic large-cell lymphoma cells Chemiluminescent assay IC-50
Protein-tyrosine kinase (CSF-1 receptor), inhibition Recombinant human enzyme ATP assay IC-50

Fibroblast Growth Factor Receptor 1

Fibroblast Growth Factor Receptor 1 (FGFR1) plays a crucial role in neuroendocrine cancer by promoting tumor growth and angiogenesis. FGFR1 testing is essential for identifying patients who may benefit from targeted therapies. Key methods include immunohistochemistry, FISH, and PCR-based assays. Main parameters assessed are FGFR1 gene amplification, protein expression, and mutation status, enabling precise patient stratification and supporting effective drug development.

Pharmacological Activity Method Parameter
Protein-tyrosine kinase (FGF receptor-1), inhibition ELISA assay IC-50
Protein-tyrosine kinase (FGF receptor-1), inhibition Radioactivity assay IC-50
Protein-tyrosine kinase (FGF receptor-1), inhibition IC-50

Fms Related Receptor Tyrosine Kinase 1

Fms Related Receptor Tyrosine Kinase 1 (FLT1/VEGFR1) is implicated in angiogenesis and tumor growth in neuroendocrine cancer. Testing FLT1 activity is crucial for evaluating drug efficacy and mechanism of action. Our service utilizes HTRF, ELISA, and ATP assays to accurately measure FLT1 inhibition, with IC-50 as the primary readout. This enables rapid, quantitative assessment of candidate compounds for neuroendocrine cancer drug development.

Pharmacological Activity Material Method Parameter
Protein-tyrosine kinase (flt-1 [VEGF receptor-1])/Vascular endothelial growth factor A (VEGF165) interaction, inhibition Recombinant human enzyme ELISA assay IC-50
Protein-tyrosine kinase (flt-1[VEGF receptor-1]), inhibition ATP assay IC-50
Protein-tyrosine kinase (flt-1[VEGF receptor-1]), inhibition ELISA assay IC-50
Protein-tyrosine kinase (flt-1[VEGF receptor-1]), inhibition Homogeneous Time Resolved Fluorescence (HTRF) assay IC-50
Protein-tyrosine kinase (flt-1[VEGF receptor-1]), inhibition IC-50

Fms Related Receptor Tyrosine Kinase 3

Fms Related Receptor Tyrosine Kinase 3 (FLT3) is implicated in the proliferation and survival of neuroendocrine cancer cells. FLT3 testing is crucial for identifying therapeutic targets and predicting drug response. Key methods include qPCR, immunohistochemistry, and next-generation sequencing. Main parameters assessed are FLT3 gene expression, mutation status, and protein phosphorylation levels, enabling precise evaluation during neuroendocrine cancer drug development.

Pharmacological Activity Method Parameter
Protein-tyrosine kinase (FLT3) (D835Y-mutated), inhibition IC-50
Protein-tyrosine kinase (FLT3), inhibition Chemiluminescent assay IC-50
Protein-tyrosine kinase (FLT3), inhibition ELISA assay IC-50
Protein-tyrosine kinase (FLT3), inhibition Radioactivity assay IC-50
Protein-tyrosine kinase (FLT3), inhibition IC-50
Protein-tyrosine kinase (FLT3-ITD), inhibition IC-50

Fms Related Receptor Tyrosine Kinase 4

Fms Related Receptor Tyrosine Kinase 4 (FLT4/VEGFR-3) regulates lymphangiogenesis and tumor metastasis in neuroendocrine cancer. FLT4 testing is crucial for identifying therapeutic targets and evaluating drug efficacy. Key methods include IHC, qPCR, and ELISA. Main parameters assessed are FLT4 expression levels, activation status (phosphorylation), and correlation with tumor progression, supporting informed drug development and patient stratification.

Pharmacological Activity Method Parameter
Protein-tyrosine kinase (FLT4 [VEGF receptor-3]), inhibition ATP assay IC-50
Protein-tyrosine kinase (FLT4 [VEGF receptor-3]), inhibition Homogeneous Time Resolved Fluorescence (HTRF) assay IC-50
Protein-tyrosine kinase (FLT4 [VEGF receptor-3]), inhibition Radioactivity assay IC-50
Protein-tyrosine kinase (FLT4 [VEGF receptor-3]), inhibition IC-50

Kinase Insert Domain Receptor

Our Kinase Insert Domain Receptor (KDR) testing service supports Neuroendocrine Cancer drug development by evaluating KDR’s role in tumor angiogenesis. This testing is crucial for identifying inhibitors that may slow cancer progression. Using advanced methods—HTRF, ATP, competitive binding (qPCR), luciferin/luciferase, RNA, and ELISA assays—we assess drug effects on KDR activity. Key parameters measured include pIC-50, MIC, and IC-50, ensuring precise evaluation of compound efficacy.

Pharmacological Activity Material Method Parameter
Gene (KDR [VEGF receptor-2]) transcription, inhibition Chorioallantoic membrane, chicken (embryo) RNA assay MIC
Gene transcription (NFAT-dependent) (vascular endothelial growth factor-A-induced), inhibition HEK293 human embryonic kidney cells transfected with KDR (VEGF receptor-2)/NFAT response element Luciferine/luciferase assay pIC-50
Protein-tyrosine kinase (KDR [VEGF receptor-2]) affinity Recombinant human receptor Competitive binding assay (qPCR) IC-50
Protein-tyrosine kinase (KDR [VEGF receptor-2]) affinity IC-50
Protein-tyrosine kinase (KDR [VEGF receptor-2]), inhibition Recombinant human enzyme ATP assay IC-50
Protein-tyrosine kinase (KDR [VEGF receptor-2]), inhibition ATP assay IC-50
Protein-tyrosine kinase (KDR [VEGF receptor-2]), inhibition ELISA assay IC-50
Protein-tyrosine kinase (KDR [VEGF receptor-2]), inhibition Homogeneous Time Resolved Fluorescence (HTRF) assay IC-50
Protein-tyrosine kinase (KDR [VEGF receptor-2]), inhibition IC-50

Kit Proto-Oncogene, Receptor Tyrosine Kinase

The Kit Proto-Oncogene, Receptor Tyrosine Kinase (KIT) plays a pivotal role in neuroendocrine cancer by driving cell proliferation and survival. Testing KIT status is crucial for patient stratification and targeted therapy development. Our service utilizes methods such as immunohistochemistry (IHC), PCR, and sequencing, assessing parameters including KIT expression, activating mutations, and gene amplification, providing actionable insights for drug development and personalized treatment approaches.

Pharmacological Activity Method Parameter
Protein-tyrosine kinase (c-Kit), inhibition ELISA assay IC-50
Protein-tyrosine kinase (c-Kit), inhibition IC-50

Mechanistic Target Of Rapamycin Kinase

The Mechanistic Target Of Rapamycin (mTOR) kinase regulates cell growth and survival in neuroendocrine cancers, making it a critical therapeutic target. mTOR kinase testing assesses pathway activation, supporting drug development and patient stratification. Key methods include immunohistochemistry, Western blot, and phospho-protein assays. Main parameters measured are mTOR phosphorylation status, downstream effector activation (e.g., pS6, 4EBP1), and pathway inhibition in response to candidate drugs.

Pharmacological Activity Method Parameter
Mammalian target of rapamycin mTOR, inhibition ELISA assay IC-50
Mammalian target of rapamycin mTOR, inhibition IC-50

Met Proto-Oncogene, Receptor Tyrosine Kinase

The Met Proto-Oncogene, Receptor Tyrosine Kinase is implicated in neuroendocrine cancer progression and metastasis. Testing its activity is essential for targeted drug development and therapy optimization. Our service utilizes RNA, ELISA, and chemiluminescent assays to measure expression and functional activity. Key parameters include MEC, IC-50, and MIC, enabling precise evaluation of drug efficacy and potency against Met-driven neuroendocrine tumors.

Pharmacological Activity Material Method Parameter
Gene (hepatocyte growth factor) transcription, induction U87MG human glioblastoma cells RNA assay MEC
Gene (hepatocyte growth factor) transcription, induction U87MG human glioblastoma cells (temozolomide-resistant) RNA assay MEC
Protein-tyrosine kinase (c-Met) (D1228H-mutated), inhibition IC-50
Protein-tyrosine kinase (c-Met) (D1228N-mutated), inhibition IC-50
Protein-tyrosine kinase (c-Met) (F1200I-mutated), inhibition IC-50
Protein-tyrosine kinase (c-Met) (M1250T-mutated), inhibition IC-50
Protein-tyrosine kinase (c-Met) (Y1230A-mutated), inhibition IC-50
Protein-tyrosine kinase (c-Met) (Y1230C-mutated), inhibition IC-50
Protein-tyrosine kinase (c-Met) (Y1230D-mutated), inhibition IC-50
Protein-tyrosine kinase (c-Met) (Y1230H-mutated), inhibition IC-50
Protein-tyrosine kinase (c-Met) expression, inhibition DBTRG05MG human glioblastoma cells Chemiluminescent assay MIC
Protein-tyrosine kinase (c-Met) expression, inhibition U87MG human glioblastoma cells Chemiluminescent assay MIC
Protein-tyrosine kinase (c-Met) expression, inhibition U87MG human glioblastoma cells (temozolomide-resistant) Chemiluminescent assay MIC
Protein-tyrosine kinase (c-Met) phosphorylation, inhibition U87MG human glioblastoma cells Chemiluminescent assay MIC
Protein-tyrosine kinase (c-Met) phosphorylation, inhibition U87MG human glioblastoma cells (temozolomide-resistant) Chemiluminescent assay MIC
Protein-tyrosine kinase (c-Met), inhibition ELISA assay IC-50
Protein-tyrosine kinase (c-Met), inhibition IC-50

Programmed Cell Death 1

Our Programmed Cell Death 1 (PD1) testing service supports Neuroendocrine Cancer drug development by evaluating PD1/PDL1 pathway interactions—key in tumor immune evasion. Using advanced methods including FACS, flow cytometry, surface plasmon resonance, ELISA, and engineered CHO-K1 and Jurkat cell assays, we measure drug binding affinity (Kd) and inhibitory potency (IC-50). This testing is essential for identifying and optimizing immunotherapeutic candidates targeting PD1-mediated immune checkpoints.

Pharmacological Activity Material Method Parameter
Gene transcription (NFAT-dependent), inhibition Jurkat human T-cell leukemia cells transfected with human PD1/NFAT responsible element CHO-K1 Chinese hamster ovary cells transfected with PDL1/OKT3 IC-50
Programmed cell death 1 (PD-1) affinity CHO-K1 Chinese hamster ovary cells transfected with human protein Fluorescent-activated cell sorting (FACS) assay IC-50
Programmed cell death 1 (PD-1) affinity Cynomolgus monkey protein ELISA assay IC-50
Programmed cell death 1 (PD-1) affinity Cynomolgus monkey protein Surface plasmon resonance assay Kd
Programmed cell death 1 (PD-1) affinity Human protein ELISA assay IC-50
Programmed cell death 1 (PD-1) affinity Human protein Surface plasmon resonance assay Kd
Programmed cell death 1 (PD-1) affinity Jurkat human T-cell leukemia cells transfected with human protein Fluorescent-activated cell sorting (FACS) assay IC-50
Programmed cell death 1 (PD-1) affinity Recombinant cynomolgus monkey protein Surface plasmon resonance assay Kd
Programmed cell death 1 (PD-1) affinity Recombinant human protein ELISA assay IC-50
Programmed cell death 1 (PD-1) affinity Recombinant human protein Surface plasmon resonance assay Kd
Programmed cell death 1 (PD-1) affinity Surface plasmon resonance assay Kd
Programmed cell death 1 (PD-1) affinity Kd
Programmed cell death 1 (PD-1)/B7-H1 (CD274 antigen, PDL1) complex interaction, inhibition CHO-K1 Chinese hamster ovary cells (CD274-overexpressing) Jurkat human T-cell leukemia cells transfected with PD1/NFAT/luciferase IC-50
Programmed cell death 1 (PD-1)/B7-H1 (CD274 antigen, PDL1) complex interaction, inhibition CHO-K1 Chinese hamster ovary cells transfected with human CD274/aAPC Jurkat human T-cell leukemia cells transfected with PD1/NFAT/luciferase IC-50
Programmed cell death 1 (PD-1)/B7-H1 (CD274 antigen, PDL1) complex interaction, inhibition CHO-K1 Chinese hamster ovary cells transfected with human protein Flow cytometry assay IC-50
Programmed cell death 1 (PD-1)/B7-H1 (CD274 antigen, PDL1) complex interaction, inhibition Recombinant human protein ELISA assay IC-50
Programmed cell death 1 (PD-1)/B7-H1 (CD274 antigen, PDL1) complex interaction, inhibition IC-50

Ret Proto-Oncogene

Ret Proto-Oncogene (RET) mutations drive tumorigenesis in neuroendocrine cancers, making RET a crucial therapeutic target. RET testing identifies mutations or fusions crucial for patient stratification and drug efficacy assessment. Key methods include PCR, NGS, and FISH, analyzing parameters such as mutation type, allele frequency, and gene rearrangements. Accurate RET profiling guides targeted therapy development and optimizes clinical trial enrollment for neuroendocrine cancer treatments.

Pharmacological Activity Method Parameter
Protein-tyrosine kinase (RET) (G810R-mutated), inhibition IC-50
Protein-tyrosine kinase (RET) (M918T-mutated), inhibition IC-50
Protein-tyrosine kinase (RET) (V804L-mutated), inhibition IC-50
Protein-tyrosine kinase (RET), inhibition ELISA assay IC-50
Protein-tyrosine kinase (RET), inhibition IC-50

Somatostatin Receptor 2

Somatostatin Receptor 2 (SSTR2) is a key therapeutic target in neuroendocrine cancer, mediating tumor growth inhibition. SSTR2 testing is crucial for drug development to assess compound binding and efficacy. Our service employs chemiluminescent, HTRF, competitive binding, radioactivity, and surface plasmon resonance assays, including displacement of [125I]-[Tyr11]-somatostatin-14 and [18F]-AlF-NOTA-JR11. We determine critical parameters such as Kd, IC-50, and pEC-50 to support candidate selection.

Pharmacological Activity Material Method Parameter
Somatostatin sst2 receptor affinity AR42J rat pancreas acinar cancer cells Displacement of [18F]-AlF-NOTA-JR11 IC-50
Somatostatin sst2 receptor affinity CHO-K1 Chinese hamster ovary cells transfected with human receptor Radioactivity assay IC-50
Somatostatin sst2 receptor affinity HEK293 human embryonic kidney cells transfected with receptor Displacement of [125I]-[Tyr11]-somatostatin-14 IC-50
Somatostatin sst2 receptor affinity HEK293 human embryonic kidney cells transfected with receptor Surface plasmon resonance assay Kd
Somatostatin sst2 receptor affinity U2OS human osteosarcoma cells transfected with receptor Competitive binding assay IC-50
cAMP production (NKH-477-induced), inhibition CHO-K1 Chinese hamster ovary cells transfected with human sst2 receptor Homogeneous Time Resolved Fluorescence (HTRF) assay IC-50
cAMP production, induction HEK293 human embryonic kidney cells transfected with SST2 (Mut4-mutated) receptor Chemiluminescent assay pEC-50
cAMP production, induction HEK293 human embryonic kidney cells transfected with SST2 receptor Chemiluminescent assay pEC-50

Tek Receptor Tyrosine Kinase

Tek Receptor Tyrosine Kinase plays a crucial role in neuroendocrine cancer progression by regulating angiogenesis and tumor growth. Our testing service enables drug developers to assess inhibitor efficacy using poly(glutamine/tyrosine) peptide substrates with advanced detection methods, including fluorescent, ATP, radioactivity, and ELISA assays. The primary parameter measured is IC-50, providing critical data on compound potency and supporting targeted therapy development for neuroendocrine cancers.

Pharmacological Activity Material Method Parameter
Protein-tyrosine kinase (TIE2) phosphorylation (vanadate-induced), inhibition CHO Chinese hamster ovary cells transfected with human enzyme ELISA assay IC-50
Protein-tyrosine kinase (TIE2) phosphorylation, inhibition CHO Chinese hamster ovary cells transfected with enzyme ELISA assay IC-50
Protein-tyrosine kinase (TIE2) phosphorylation, inhibition CHO Chinese hamster ovary cells transfected with human enzyme ELISA assay IC-50
Protein-tyrosine kinase (TIE2), inhibition Recombinant enzyme Fluorescent assay IC-50
Protein-tyrosine kinase (TIE2), inhibition Recombinant enzyme Poly(glutamine/tyrosine) peptide as substrate IC-50
Protein-tyrosine kinase (TIE2), inhibition Recombinant enzyme Radioactivity assay IC-50
Protein-tyrosine kinase (TIE2), inhibition Recombinant human enzyme Poly(glutamine/tyrosine) peptide as substrate IC-50
Protein-tyrosine kinase (TIE2), inhibition ATP assay IC-50
Protein-tyrosine kinase (TIE2), inhibition ELISA assay IC-50
Protein-tyrosine kinase (TIE2), inhibition IC-50
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