In Vitro Efficacy Testing Services for Glioma
Drug R&D Solutions

In Vitro Efficacy Testing Services for Glioma

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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 Glioma. Our services offer comprehensive efficacy assessment using a variety of cell-based and biochemical assays specifically tailored to evaluate anti-glioma compounds. Key targets and pathways include EGFR, PI3K/Akt/mTOR, IDH mutations, and angiogenesis-related factors, all of which are central to glioma progression and resistance mechanisms. We are equipped to analyze critical pathological processes such as cell proliferation, apoptosis, migration, invasion, and drug resistance.

Our in vitro testing portfolio for Glioma encompasses a diverse range of biochemical and cell-based assays designed to evaluate compound efficacy, mechanism of action, and target engagement. These assays enable high-throughput screening, detailed molecular profiling, and quantitative analysis of drug responses in glioma models.

ATP assay: Measures cellular ATP levels as an indicator of cell viability and cytotoxicity, providing a direct readout of compound-induced cell death in glioma cells.

Chemiluminescent assay: Utilizes light emission to quantify specific analytes or enzymatic activities, offering sensitive detection of biomolecular interactions or cellular responses.

Fluorescence resonance energy transfer (FRET) assay: Detects molecular interactions and conformational changes by measuring energy transfer between fluorophores, useful for studying protein–protein interactions in glioma signaling.

Fluorescent assay: Employs fluorescent tags to monitor cellular events such as apoptosis, proliferation, and marker expression, enabling multiplexed and real-time analysis.

Fluorescent-activated cell sorting (FACS) assay: Analyzes and sorts cell populations based on fluorescent labeling, allowing detailed characterization of subpopulations and assessment of drug-induced phenotypic changes.

Homogeneous Time Resolved Fluorescence (HTRF) assay: Combines FRET with time-resolved measurement to reduce background and enhance sensitivity, ideal for quantifying protein–protein or protein–ligand interactions relevant to glioma pathways.

RNA assay: Quantifies gene expression changes in response to treatment, providing insights into drug effects on glioma-associated genes and pathways.

Surface plasmon resonance assay: Measures real-time binding kinetics and affinities between biomolecules, critical for evaluating compound–target interactions in glioma research.

We assess a comprehensive set of pharmacological parameters to quantify drug potency, efficacy, and binding characteristics. These parameters provide crucial insights for lead compound optimization and prediction of in vivo activity, guiding rational drug development for glioma.

IC-50: The concentration of compound required to inhibit a biological process by 50%, serving as a key indicator of drug potency in vitro.

Kd: The dissociation constant reflecting the affinity between a drug and its target, essential for understanding drug–target interactions.

MEC: The minimum effective concentration at which a compound elicits a desired biological response, aiding in effective dose selection.

MIC: The minimum inhibitory concentration necessary to suppress cell proliferation or survival, important for evaluating cytotoxic efficacy against glioma cells.

Recommended In Vitro Efficacy Tests

B-Raf Proto-Oncogene, Serine/Threonine Kinase

The B-Raf Proto-Oncogene, Serine/Threonine Kinase is a critical driver in glioma pathogenesis, making it a prime target for therapeutic intervention. Our testing service evaluates glioma drug efficacy by measuring B-Raf kinase activity using chemiluminescent and ATP assays. Key parameters include IC-50, indicating drug potency, and MEC (minimum effective concentration), supporting precise candidate selection and accelerated drug development.

Pharmacological Activity Material Method Parameter
Serine/threonine protein kinase (B-Raf) (V600E-mutated), inhibition Chemiluminescent assay IC-50
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 Recombinant enzyme ATP assay IC-50
Serine/threonine protein kinase (B-Raf), inhibition Recombinant human enzyme ATP assay IC-50
Serine/threonine protein kinase (B-Raf), inhibition ATP assay IC-50
Serine/threonine protein kinase (B-Raf), inhibition Chemiluminescent assay IC-50
Serine/threonine protein kinase (B-Raf), inhibition IC-50

Epidermal Growth Factor Receptor

Epidermal Growth Factor Receptor (EGFR) plays a pivotal role in glioma progression by promoting cell proliferation and survival. EGFR testing enables precise evaluation of drug efficacy and mechanism of action, which is crucial for glioma drug development. Key assays—ATP, fluorescent, chemiluminescent, HTRF, surface plasmon resonance, RNA, and FACS—quantify parameters such as IC-50, MEC, Kd, and MIC, ensuring rigorous assessment of candidate therapeutics targeting EGFR pathways.

Pharmacological Activity Material Method Parameter
Epidermal growth factor EGF receptor (EGFR) degradation, induction CCK81 human colon adenocarcinoma cells Fluorescent assay MEC
Epidermal growth factor EGF receptor (EGFR) degradation, induction HCT8 human ileocecal adenocarcinoma cells Fluorescent assay MEC
Gene (ErbB1/HER1) transcription, inhibition K562 human myeloid leukemia cells RNA assay MIC
Protein-tyrosine kinase (EGF receptor) (A263P-mutated], inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (A289D-mutated], inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (A289V-mutated], inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (G598V-mutated], inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (L718Q-mutated), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (L858R-mutated), inhibition Recombinant human enzyme ATP assay IC-50
Protein-tyrosine kinase (EGF receptor) (L858R-mutated), inhibition Sf9 insect cells transfected with enzyme ATP assay IC-50
Protein-tyrosine kinase (EGF receptor) (L858R-mutated), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (L858R/C797S-mutated), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (L858R/T790M-mutated), inhibition Sf9 insect cells transfected with enzyme ATP assay IC-50
Protein-tyrosine kinase (EGF receptor) (L858R/T790M-mutated), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (L858R/T790M/C797S-mutated), inhibition Sf9 insect cells transfected with enzyme ATP assay IC-50
Protein-tyrosine kinase (EGF receptor) (L858R/T790M/C797S-mutated), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (T790M-mutated), inhibition Recombinant human enzyme ATP assay IC-50
Protein-tyrosine kinase (EGF receptor) (T790M-mutated), inhibition Homogeneous Time Resolved Fluorescence (HTRF) assay IC-50
Protein-tyrosine kinase (EGF receptor) (exon 19-deleted), inhibition Recombinant human enzyme ATP assay IC-50
Protein-tyrosine kinase (EGF receptor) (exon 19-deleted), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (exon 19-deleted/C797S-mutated), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (exon 19-deleted/T790M-mutated), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (exon 19-deleted/T790M/C797S-mutated), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (variant III-mutated), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) affinity CT26 murine colon adenocarcinoma cells Fluorescent-activated cell sorting (FACS) assay IC-50
Protein-tyrosine kinase (EGF receptor) affinity Surface plasmon resonance assay Kd
Protein-tyrosine kinase (EGF receptor) phosphorylation, inhibition Glioblastoma cells IC-50
Protein-tyrosine kinase (EGF receptor) phosphorylation, inhibition HaCaT human keratinocytes IC-50
Protein-tyrosine kinase (EGF receptor) phosphorylation, inhibition IC-50
Protein-tyrosine kinase (EGF receptor), inhibition Recombinant human enzyme ATP assay IC-50
Protein-tyrosine kinase (EGF receptor), inhibition Sf9 insect cells transfected with enzyme ATP assay IC-50
Protein-tyrosine kinase (EGF receptor), inhibition ATP assay IC-50
Protein-tyrosine kinase (EGF receptor), inhibition Chemiluminescent assay IC-50
Protein-tyrosine kinase (EGF receptor), inhibition IC-50

Janus Kinase 3

Janus Kinase 3 (JAK3) plays a pivotal role in signaling pathways driving glioma progression. Our testing service enables the evaluation of candidate drugs targeting JAK3, crucial for identifying effective glioma therapies. Using ATP and FRET assays, we precisely measure JAK3 inhibition, with IC-50 as the key parameter to determine drug potency. This service accelerates discovery of novel inhibitors for glioma treatment.

Pharmacological Activity Material Method Parameter
Protein-tyrosine kinase (JAK3), inhibition Human enzyme ATP assay IC-50
Protein-tyrosine kinase (JAK3), inhibition ATP assay IC-50
Protein-tyrosine kinase (JAK3), inhibition Fluorescence resonance energy transfer (FRET) assay IC-50

Receptor Interacting Serine/Threonine Kinase 3

Receptor Interacting Serine/Threonine Kinase 3 (RIPK3) is pivotal in regulating necroptosis, influencing glioma cell death and tumor progression. RIPK3 testing is crucial for identifying and optimizing therapeutic candidates in glioma drug development. Our service employs a sensitive chemiluminescent assay to quantify RIPK3 activity, with Minimum Effective Concentration (MEC) as a primary parameter, enabling precise assessment of compound efficacy in modulating RIPK3-mediated pathways.

Pharmacological Activity Material Method Parameter
Serine/threonine protein kinase (RIPK3) phosphorylation, induction GBM9 human glioblastoma multiforme cells Chemiluminescent assay MEC
Serine/threonine protein kinase (RIPK3) phosphorylation, induction GSC28 human glioblastoma stem cells Chemiluminescent assay MEC
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