We provide robust and sensitive in vitro screening and characterization platforms for accelerating the discovery and screening of potential therapies for Liver Cancer. Our services offer comprehensive assessment of compound efficacy, cytotoxicity, and mechanism of action specifically tailored to hepatocellular carcinoma and related liver malignancies. Key targets evaluated include oncogenic signaling pathways such as PI3K/AKT, Wnt/β-catenin, and proteins like AFP and VEGF, which are central to liver tumorigenesis. We are equipped to analyze processes including cell proliferation, apoptosis, angiogenesis, and drug resistance relevant to liver cancer pathology.
Our testing portfolio includes a range of biochemical and molecular assays, enabling precise evaluation of compound effects on liver cancer cells. We employ ATP, chemiluminescent, ELISA, fluorescent, and RNA-based assays to assess viability, protein expression, signaling activity, and gene modulation. These methodologies collectively provide a robust framework for evaluating therapeutic efficacy in vitro.
ATP assay: Measures cellular viability and metabolic activity by quantifying intracellular ATP levels, providing a sensitive indicator of cytotoxic and antiproliferative effects on liver cancer cells.
Chemiluminescent assay: Detects specific biomolecules or cellular responses using chemiluminescent substrates, enabling high-sensitivity quantification of proteins, enzymes, or reporter gene activity relevant to liver cancer.
ELISA assay: Utilized for quantifying the presence and concentration of specific proteins (e.g., AFP, VEGF) in cell lysates or supernatants, aiding in the assessment of target engagement and pathway modulation.
Fluorescent assay: Employs fluorescent probes to monitor cell proliferation, apoptosis, or specific molecular events, allowing multi-parametric analysis of compound effects in liver cancer models.
RNA assay: Involves the quantification and analysis of mRNA levels for genes of interest, facilitating the understanding of transcriptional changes and pathway regulation in response to therapeutic intervention.
We measure key pharmacological parameters such as IC-50, MEC, and MIC to quantify the potency and efficacy of candidate compounds. These metrics are critical for comparing compound activities and determining therapeutic windows during drug development. Accurate parameter determination guides lead optimization and preclinical decision-making.
IC-50: The half-maximal inhibitory concentration; a key indicator of compound potency, representing the concentration required to inhibit a specific biological function or cell viability by 50%.
MEC: Minimum effective concentration; the lowest concentration at which a compound demonstrates a desired biological effect, important for establishing dosing strategies.
MIC: Minimum inhibitory concentration; the lowest concentration required to inhibit visible growth or activity of cancer cells, crucial for assessing compound efficacy and selectivity.
Our B-Raf Proto-Oncogene, Serine/Threonine Kinase testing service supports liver cancer drug development by assessing inhibitors targeting B-Raf, a key driver of tumor cell proliferation. Accurate testing is crucial for identifying effective therapeutics. We utilize ELISA, chemiluminescent, and ATP assays to measure B-Raf activity. Main parameters reported include Minimum Effective Concentration (MEC), Minimum Inhibitory Concentration (MIC), and half-maximal inhibitory concentration (IC-50) for comprehensive compound profiling.
| Pharmacological Activity | Material | Method | Parameter |
|---|---|---|---|
| Serine/threonine protein kinase (B-Raf) (V600E-mutated), inhibition | Recombinant human enzyme | ATP assay | IC-50 |
| Serine/threonine protein kinase (B-Raf) (V600E-mutated), inhibition | Chemiluminescent assay | IC-50 | |
| Serine/threonine protein kinase (B-Raf) expression, inhibition | HCCLM3 human hepatocellular carcinoma cells | Chemiluminescent assay | MIC |
| Serine/threonine protein kinase (B-Raf) expression, inhibition | HuH7 human liver cancer cells | Chemiluminescent assay | MIC |
| Serine/threonine protein kinase (B-Raf) phosphorylation, induction | MCF7 human breast adenocarcinoma cells (hormone-dependent) | Chemiluminescent assay | MEC |
| Serine/threonine protein kinase (B-Raf), inhibition | Chemiluminescent assay | IC-50 | |
| Serine/threonine protein kinase (B-Raf), inhibition | ELISA assay | IC-50 | |
| Serine/threonine protein kinase (B-Raf), inhibition | IC-50 |
Our Bcl2 Apoptosis Regulator testing service for Liver Cancer drug development evaluates the anti-apoptotic role of Bcl2, a key driver of tumor survival and chemoresistance. Accurate assessment is vital for identifying effective therapeutics. We utilize RNA, fluorescent, and chemiluminescent assays to measure Bcl2 expression and activity, providing quantitative analysis of drug efficacy through MIC and IC-50 parameters, enabling precise optimization of anti-cancer candidates.
| Pharmacological Activity | Material | Method | Parameter |
|---|---|---|---|
| Gene (Bcl2) transcription, inhibition | HuH7 human liver cancer cells | RNA assay | MIC |
| Protein (Bcl2) affinity | IC-50 | ||
| Protein (Bcl2) expression decrease, inhibition | HepG2 human hepatoblastoma cells | Chemiluminescent assay | MIC |
| Protein (Bcl2) expression, inhibition | A375 human malignant melanoma cells | Chemiluminescent assay | MIC |
| Protein (Bcl2) expression, inhibition | HepG2 human hepatoblastoma cells | Chemiluminescent assay | MIC |
| Protein (Bcl2) expression, inhibition | HuH7 human liver cancer cells | Chemiluminescent assay | MIC |
| Protein (Bcl2) expression, inhibition | MCF7 human breast adenocarcinoma cells (hormone-dependent) (doxorubicin-resistant) (PK-11195-treated) | Chemiluminescent assay | MIC |
| Protein (Bcl2) expression, inhibition | MHCC-97H human hepatocellular carcinoma cells | Chemiluminescent assay | MIC |
| Protein (Bcl2) expression, inhibition | SKMEL2 human melanoma cells | Chemiluminescent assay | MIC |
| Protein (Bcl2) expression, inhibition | SKMEL2 human melanoma cells | Fluorescent assay | MIC |
| Protein (Bcl2) expression, inhibition | SKMEL28 human melanoma cells | Chemiluminescent assay | MIC |
| Protein (Bcl2) expression, inhibition | SKMEL28 human melanoma cells | Fluorescent assay | MIC |
| Protein (Bcl2) expression, inhibition | SMMC7721 human hepatocellular carcinoma cells | Chemiluminescent assay | MIC |
| Protein (Bcl2), inhibition | SET2 human megakaryoblastic leukemia cells | IC-50 | |
| Protein (Bcl2), inhibition | SET2 human megakaryoblastic leukemia cells (ruxolitinib-persister) | IC-50 |
Ret Proto-Oncogene (RET) alterations can drive liver cancer progression via aberrant signaling pathways. RET testing is crucial for identifying patients who may benefit from targeted therapies in drug development. Key methods include PCR, next-generation sequencing (NGS), and immunohistochemistry. Main parameters assessed are RET mutations, fusions, and expression levels, enabling precise patient stratification and optimizing therapeutic strategies in liver cancer clinical trials.
| Pharmacological Activity | 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 | IC-50 |
The Src Proto-Oncogene, Non-Receptor Tyrosine Kinase plays a crucial role in liver cancer progression by promoting cell proliferation, invasion, and metastasis. Testing its activity is vital for drug development, enabling identification of effective Src inhibitors. Key methods include kinase activity assays, Western blotting, and immunohistochemistry. Main parameters assessed are phosphorylation levels, Src expression, and downstream signaling pathway activation, providing critical insights for targeted therapy development.
| Pharmacological Activity | Method | Parameter |
|---|---|---|
| Protein-tyrosine kinase (Src), inhibition | Bioluminescence resonance energy transfer (BRET) assay | IC-50 |
| Protein-tyrosine kinase (Src), inhibition | Chemiluminescent assay | IC-50 |
| Protein-tyrosine kinase (Src), inhibition | Homogeneous Time Resolved Fluorescence (HTRF) assay | IC-50 |
Tumor Necrosis Factor (TNF) is a key cytokine involved in liver cancer progression and inflammation. Accurate TNF testing is crucial for drug development, enabling assessment of therapeutic efficacy and safety. Our service uses ELISA assays to quantify TNF levels, providing main parameters such as Minimum Effective Concentration (MEC) and Minimum Inhibitory Concentration (MIC), supporting optimal dose selection and candidate evaluation in liver cancer research.
| Pharmacological Activity | Material | Method | Parameter |
|---|---|---|---|
| Tumor necrosis factor-alpha production (endotoxin-induced), inhibition | Macrophages (bone marrow-derived), mouse | ELISA assay | MIC |
| Tumor necrosis factor-alpha production, induction | Endothelial cells (Induced pluripotent stem cells-derived), human | ELISA assay | MEC |
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