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.
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 |
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 (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 (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 (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 (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 |
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 |
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 |
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 |
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 |
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) 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 (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 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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