We provide robust and sensitive in vitro screening and characterization platforms for accelerating the discovery and screening of potential therapies for kidney diseases. Our service offers tailored assays to evaluate compound efficacy, cellular responses, and molecular interactions specific to renal injury, nephrotoxicity, and kidney cell function. Key targets include renal transporters, ion channels, ATPases, and signaling pathways involved in kidney health and disease. We assess pathological processes such as cell viability, apoptosis, fibrosis, and drug-induced nephrotoxicity relevant to kidney disorders.
Our comprehensive suite of testing methods includes biochemical, cellular, and molecular assays designed to evaluate drug effects on kidney cells and related pathways. These methods enable detailed analysis of compound activity, target engagement, and mechanistic insights to support preclinical drug development.
ATP assay: Measures cellular ATP levels as an indicator of cell viability and metabolic activity, important for assessing nephrotoxicity and cytoprotection.
ATP assay (at 0.01 mM): Quantifies ATP content under low substrate conditions to evaluate compound effects on energy metabolism in sensitive settings.
ATP assay (at 1 mM): Assesses ATP levels at higher substrate concentrations, useful for determining maximal metabolic response.
ATPase assay: Evaluates ATPase enzyme activity, critical for understanding compound interactions with renal transporters and pumps.
Chemiluminescent assay: Detects specific biomolecules or cellular responses using luminescent signals, providing sensitive quantitation of targets.
Dissociation enhanced lanthanide fluorescent immunoassay (DELFIA): Offers highly sensitive detection of proteins or biomarkers via time-resolved fluorescence.
ELISA assay: Quantifies proteins, cytokines, or biomarkers relevant to kidney pathology using antibody-based detection.
Flow cytometry assay: Analyzes cell populations, apoptosis, and surface marker expression in kidney cells, enabling multiparametric profiling.
Fluorescence resonance energy transfer (FRET) assay: Detects molecular interactions or conformational changes in real-time within renal pathways.
Fluorescent assay: Measures cellular or biochemical changes using fluorescence, applicable for viability, signaling, or metabolite detection.
Fluorescent-activated cell sorting (FACS) assay: Sorts and analyzes kidney cell subpopulations based on fluorescent markers, aiding in functional studies.
Homogeneous Time Resolved Fluorescence (HTRF) assay: Quantifies protein-protein interactions or signaling events with minimal sample processing.
Paclitaxel accumulation assay: Assesses drug accumulation and efflux in kidney cells to evaluate transporter activity and drug disposition.
Poly(L-alanine/L-glutamic acid/L-lysine/L-tyrosine) as substrate: Used to evaluate protease or enzyme activity relevant to extracellular matrix remodeling in renal disease.
Poly(glutamine/tyrosine) peptide as substrate: Serves as a substrate for enzymatic assays targeting renal proteolytic pathways.
RNA assay: Measures gene expression changes in kidney cells, providing insights into transcriptional responses to treatments.
Radioactivity assay: Quantifies uptake, binding, or enzyme activity using radiolabeled substrates for high sensitivity.
Rhodamine 123 accumulation assay: Evaluates mitochondrial function and efflux transporter activity in kidney cells.
Surface plasmon resonance assay: Measures real-time binding kinetics of drugs to kidney-relevant targets without labeling.
We measure a comprehensive range of pharmacological parameters to quantify compound potency, efficacy, and binding characteristics in kidney models. These parameters are critical for comparing drug candidates, optimizing dosing, and predicting in vivo performance.
EC-50 (half-maximal effective concentration): Indicates the concentration of a compound required to achieve 50% of its maximal effect, reflecting potency.
IC-50 (half-maximal inhibitory concentration): Represents the concentration needed to inhibit a biological or biochemical function by 50%, essential for evaluating inhibitor efficacy.
Kd (dissociation constant): Measures the binding affinity between a drug and its target, with lower values indicating stronger binding.
MEC (minimum effective concentration): The lowest concentration of a drug that produces a detectable effect, used for dosing considerations.
MIC (minimum inhibitory concentration): The lowest concentration of a compound that inhibits visible growth of a microorganism or cell, important in anti-infective and cytostatic studies.
pIC-50 (negative logarithm of IC-50): Provides a logarithmic scale of inhibitory potency, allowing easier comparison between compounds.
The Atp Binding Cassette Subfamily B Member 1 (ABCB1) actively exports drugs from kidney cells, impacting renal drug disposition and resistance. Testing ABCB1 activity is crucial for optimizing kidney drug development and minimizing adverse interactions. Key assays include Rhodamine 123 and Paclitaxel accumulation assays, and ATPase assay, which assess transporter function. Main parameters measured are MIC (minimum inhibitory concentration) and IC-50 (half-maximal inhibitory concentration).
Pharmacological Activity | Material | Method | Parameter |
---|---|---|---|
P-Glycoprotein [MDR1] activation, inhibition | ECA109 human esophagus cancer cells (vincristine-resistant) | Rhodamine 123 accumulation assay | MIC |
P-Glycoprotein [MDR1], inhibition | CaCo2 human colon adenocarcinoma cells | Paclitaxel accumulation assay | IC-50 |
P-Glycoprotein [MDR1], inhibition | MES-SA/Dx5 human uterine sarcoma cells | Paclitaxel accumulation assay | IC-50 |
P-Glycoprotein [MDR1], inhibition | NCI-H460 human large-cell lung carcinoma cells (multidrug-resistant) | Rhodamine 123 accumulation assay | MIC |
P-Glycoprotein [MDR1], inhibition | ATPase assay | IC-50 |
B-Raf Proto-Oncogene, Serine/Threonine Kinase regulates cell growth and survival pathways in the kidney, impacting drug response and disease progression. Testing B-Raf activity is crucial for identifying therapeutic targets and optimizing kidney drug development. Our service utilizes ELISA, chemiluminescent, and ATP assays to assess B-Raf function, providing key parameters such as MIC and IC-50 for evaluating compound potency and efficacy.
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), 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 |
The Bcl2 Apoptosis Regulator plays a crucial role in controlling kidney cell survival and apoptosis, impacting drug-induced nephrotoxicity. Our testing service evaluates Bcl2 activity using sensitive fluorescent and chemiluminescent assays, enabling precise measurement of drug effects. Key parameters such as EC-50 and MIC are determined, providing essential data for optimizing kidney drug efficacy and safety during preclinical development.
Pharmacological Activity | Material | Method | Parameter |
---|---|---|---|
Protein (Bcl2) degradation, induction | 4T1 mouse mammary cancer cells (paclitaxel-resistant) | Chemiluminescent assay | EC-50 |
Protein (Bcl2) expression, inhibition | MDAMB453 human breast carcinoma cells (HER2 [ERBB2]-overexpressing) | Chemiluminescent assay | MIC |
Protein (Bcl2) expression, inhibition | OCI-Ly10 human diffuse large B-cell lymphoma cells | Chemiluminescent assay | MIC |
Protein (Bcl2) expression, inhibition | SKBr3 human breast adenocarcinoma cells (HER2 [ERBB2]-overexpressing) | 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 |
DNA Topoisomerase I regulates DNA supercoiling during replication and transcription in kidney cells, impacting cellular health and drug response. Testing its activity is crucial for developing effective kidney therapeutics. Our service uses a sensitive chemiluminescent assay to quantify Topoisomerase I function, determining the Minimum Inhibitory Concentration (MIC) of candidate drugs. This enables precise evaluation of drug efficacy and safety in kidney drug development.
Pharmacological Activity | Material | Method | Parameter |
---|---|---|---|
DNA topoisomerase I expression, inhibition | LoVo human colon adenocarcinoma cells | Chemiluminescent assay | MIC |
DNA topoisomerase I expression, inhibition | LoVo human colon adenocarcinoma cells (irinotecan-resistant) | Chemiluminescent assay | MIC |
The Enhancer Of Zeste 2 Polycomb Repressive Complex 2 Subunit (EZH2/PRC2) regulates gene silencing and epigenetic remodeling in kidney development and disease. Testing EZH2/PRC2 is vital for kidney drug development to assess target engagement, efficacy, and off-target effects. Key methods include qPCR, Western blot, and ChIP-seq. Main parameters analyzed are EZH2 expression, H3K27me3 levels, and downstream gene repression, ensuring precise evaluation of therapeutic interventions.
Pharmacological Activity | Method | Parameter |
---|---|---|
Histone-lysine N-methyltransferase EZH2 (A682G-mutated), inhibition | IC-50 | |
Histone-lysine N-methyltransferase EZH2 (A692V-mutated), inhibition | IC-50 | |
Histone-lysine N-methyltransferase EZH2 (Y641F-mutated), inhibition | Fluorescent assay | IC-50 |
Histone-lysine N-methyltransferase EZH2 (Y641F-mutated), inhibition | IC-50 | |
Histone-lysine N-methyltransferase EZH2 (Y641N-mutated), inhibition | Fluorescent assay | IC-50 |
Histone-lysine N-methyltransferase EZH2 (Y646C-mutated), inhibition | IC-50 | |
Histone-lysine N-methyltransferase EZH2 (Y646F-mutated), inhibition | IC-50 | |
Histone-lysine N-methyltransferase EZH2 (Y646H-mutated), inhibition | IC-50 | |
Histone-lysine N-methyltransferase EZH2 (Y646N-mutated), inhibition | IC-50 | |
Histone-lysine N-methyltransferase EZH2 (Y646S-mutated), inhibition | IC-50 | |
Histone-lysine N-methyltransferase EZH2, inhibition | Fluorescent assay | IC-50 |
Histone-lysine N-methyltransferase EZH2, inhibition | S-adenosyl methionine as substrate | IC-50 |
Histone-lysine N-methyltransferase EZH2, inhibition | IC-50 |
Epidermal Growth Factor Receptor (EGFR) plays a crucial role in kidney cell proliferation, survival, and repair. EGFR testing is vital in kidney drug development to evaluate therapeutic efficacy and safety. Our service employs advanced methods, including FACS, DELFIA, chemiluminescent, HTRF, flow cytometry, FRET, SPR, ELISA, and ATP/fluorescent assays. Key parameters measured include IC-50, MIC, Kd, pIC-50, and MEC, enabling precise assessment of drug-target interactions.
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 |
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) (L858R-mutated), inhibition | Recombinant enzyme | Fluorescence resonance energy transfer (FRET) assay | IC-50 |
Protein-tyrosine kinase (EGF receptor) (L858R-mutated), inhibition | IC-50 | ||
Protein-tyrosine kinase (EGF receptor) (L858R/C797S-mutated), inhibition | Recombinant enzyme | Fluorescence resonance energy transfer (FRET) assay | IC-50 |
Protein-tyrosine kinase (EGF receptor) (L858R/C797S-mutated), inhibition | IC-50 | ||
Protein-tyrosine kinase (EGF receptor) (L858R/T790M-mutated), inhibition | Recombinant enzyme | Fluorescence resonance energy transfer (FRET) assay | IC-50 |
Protein-tyrosine kinase (EGF receptor) (L858R/T790M-mutated), inhibition | IC-50 | ||
Protein-tyrosine kinase (EGF receptor) (L858R/T790M/C797S-mutated), inhibition | Recombinant enzyme | Fluorescence resonance energy transfer (FRET) 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 | 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 | A431 human vulvar epidermoid carcinoma cells (EGF receptor-overexpressing) | Flow cytometry assay | IC-50 |
Protein-tyrosine kinase (EGF receptor) affinity | A431 human vulvar epidermoid carcinoma cells (EGF receptor-overexpressing) | Fluorescent-activated cell sorting (FACS) assay | 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 | DiFi human colorectal carcinoma cells | Flow cytometry assay | IC-50 |
Protein-tyrosine kinase (EGF receptor) affinity | FaDu human squamous-cell nasopharyngeal cancer cells | Flow cytometry assay | IC-50 |
Protein-tyrosine kinase (EGF receptor) affinity | HCT116 human colon carcinoma cells | Fluorescent-activated cell sorting (FACS) assay | IC-50 |
Protein-tyrosine kinase (EGF receptor) affinity | LIM1215 human colorectal carcinoma cells | Flow cytometry assay | IC-50 |
Protein-tyrosine kinase (EGF receptor) affinity | PANC1 human pancreas adenocarcinoma cells | Fluorescent-activated cell sorting (FACS) assay | IC-50 |
Protein-tyrosine kinase (EGF receptor) affinity | Recombinant cynomolgus monkey enzyme | Surface plasmon resonance assay | Kd |
Protein-tyrosine kinase (EGF receptor) affinity | Recombinant cynomolgus monkey receptor | Surface plasmon resonance assay | Kd |
Protein-tyrosine kinase (EGF receptor) affinity | Recombinant human enzyme | Surface plasmon resonance assay | Kd |
Protein-tyrosine kinase (EGF receptor) affinity | Surface plasmon resonance assay | Kd | |
Protein-tyrosine kinase (EGF receptor) phosphorylation, inhibition | FaDu human squamous-cell nasopharyngeal cancer cells | Chemiluminescent assay | MIC |
Protein-tyrosine kinase (EGF receptor) phosphorylation, inhibition | MDAMB453 human breast carcinoma cells (HER2 [ERBB2]-overexpressing) | Chemiluminescent assay | MIC |
Protein-tyrosine kinase (EGF receptor) phosphorylation, inhibition | SKBr3 human breast adenocarcinoma cells (HER2 [ERBB2]-overexpressing) | Chemiluminescent assay | MIC |
Protein-tyrosine kinase (EGF receptor) phosphorylation, inhibition | IC-50 | ||
Protein-tyrosine kinase (EGF receptor), inhibition | BAF3 mouse lymphoblasts (epidermal growth factor-treated) | IC-50 | |
Protein-tyrosine kinase (EGF receptor), inhibition | Human enzyme | ATP assay | IC-50 |
Protein-tyrosine kinase (EGF receptor), inhibition | PC3 human prostate adenocarcinoma cells | ATP assay | IC-50 |
Protein-tyrosine kinase (EGF receptor), inhibition | Recombinant enzyme | ATP assay (at 0.01 mM) | pIC-50 |
Protein-tyrosine kinase (EGF receptor), inhibition | Recombinant enzyme | ATP assay (at 1 mM) | pIC-50 |
Protein-tyrosine kinase (EGF receptor), inhibition | Recombinant enzyme | Chemiluminescent assay | IC-50 |
Protein-tyrosine kinase (EGF receptor), inhibition | Recombinant enzyme | Dissociation enhanced lanthanide fluorescent immunoassay (DELFIA) | IC-50 |
Protein-tyrosine kinase (EGF receptor), inhibition | Recombinant enzyme | Fluorescence resonance energy transfer (FRET) assay | IC-50 |
Protein-tyrosine kinase (EGF receptor), inhibition | Recombinant enzyme | Poly(glutamine/tyrosine) peptide as substrate | pIC-50 |
Protein-tyrosine kinase (EGF receptor), inhibition | Recombinant human enzyme | ATP assay | IC-50 |
Protein-tyrosine kinase (EGF receptor), inhibition | Recombinant human enzyme | ELISA 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 | Chemiluminescent assay | IC-50 | |
Protein-tyrosine kinase (EGF receptor), inhibition | ELISA assay | IC-50 | |
Protein-tyrosine kinase (EGF receptor), inhibition | Fluorescence resonance energy transfer (FRET) assay | IC-50 | |
Protein-tyrosine kinase (EGF receptor), inhibition | IC-50 |
Erb-B2 Receptor Tyrosine Kinase 2 (HER2/ERBB2) plays a crucial role in kidney cell signaling and pathology. Testing its activity is vital for kidney drug development to assess efficacy and safety. Our service offers sensitive detection using FRET and chemiluminescent assays, providing key parameters such as Minimum Effective Concentration (MEC), IC-50, and Minimum Inhibitory Concentration (MIC) for comprehensive compound profiling.
Pharmacological Activity | Material | Method | Parameter |
---|---|---|---|
Protein-tyrosine kinase (HER2 [ErbB2]) expression, induction | Calu3 human lung carcinoma cells (HER2 [ERBB2]-overexpressing) | MEC | |
Protein-tyrosine kinase (HER2 [ErbB2]) expression, induction | NCI-H2170 human non-small-cell lung cancer cells (HER2 [ERBB2] amplification-expressing) | MEC | |
Protein-tyrosine kinase (HER2 [ErbB2]) phosphorylation, inhibition | MDAMB453 human breast carcinoma cells (HER2 [ERBB2]-overexpressing) | Chemiluminescent assay | MIC |
Protein-tyrosine kinase (HER2 [ErbB2]) phosphorylation, inhibition | SKBr3 human breast adenocarcinoma cells (HER2 [ERBB2]-overexpressing) | Chemiluminescent assay | MIC |
Protein-tyrosine kinase (HER2 [ErbB2]), inhibition | Purified enzyme | IC-50 | |
Protein-tyrosine kinase (HER2 [ErbB2]), inhibition | Recombinant enzyme | Fluorescence resonance energy transfer (FRET) assay | IC-50 |
Protein-tyrosine kinase (HER2 [ErbB2]), inhibition | IC-50 |
Fms Related Receptor Tyrosine Kinase 1 (FLT1/VEGFR1) regulates angiogenesis and vascular permeability in the kidney, impacting disease pathogenesis and drug response. Testing FLT1 activity is crucial for identifying and optimizing kidney drug candidates. Our service employs HTRF, ELISA, and ATP assays to accurately quantify FLT1 inhibition, with IC-50 determination as the primary efficacy parameter, enabling precise evaluation of compound potency for renal therapeutics 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 |
Fms Related Receptor Tyrosine Kinase 3 (FLT3) plays a key role in kidney cell signaling, proliferation, and survival. Testing FLT3 activity is crucial for developing targeted kidney therapeutics and assessing drug efficacy. We offer FLT3 testing using chemiluminescent, fluorescent, ATP, radioactivity, and ELISA assays, with Poly(L-alanine/L-glutamic acid/L-lysine/L-tyrosine) as substrate. The primary parameter measured is IC-50, enabling precise evaluation of compound potency in kidney drug development.
Pharmacological Activity | Material | Method | Parameter |
---|---|---|---|
Protein-tyrosine kinase (FLT3) (D835Y-mutated), inhibition | IC-50 | ||
Protein-tyrosine kinase (FLT3), inhibition | ATP assay | 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 | Fluorescent 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 | Recombinant human enzyme | Poly(L-alanine/L-glutamic acid/L-lysine/L-tyrosine) as substrate | IC-50 |
Protein-tyrosine kinase (FLT3-ITD), inhibition | IC-50 |
Fms Related Receptor Tyrosine Kinase 4 (FLT4/VEGFR-3) regulates lymphangiogenesis in the kidney, influencing fluid balance and fibrosis. FLT4 testing is crucial for assessing drug effects on kidney lymphatic function and disease progression. Key methods include ELISA, immunohistochemistry, and qPCR. Main parameters measured are FLT4 protein expression, gene transcription levels, and downstream signaling activity, providing vital insights for kidney drug development.
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 |
The Raf-1 Proto-Oncogene, Serine/Threonine Kinase plays a pivotal role in kidney cell signaling and survival, impacting responses to drug candidates. Our testing service quantifies Raf-1 activity using RNA and chemiluminescent assays, enabling assessment of drug efficacy and toxicity. Minimum Inhibitory Concentration (MIC) is determined to guide dose optimization, supporting effective and safe kidney drug development.
Pharmacological Activity | Material | Method | Parameter |
---|---|---|---|
Gene (c-Raf) transcription, inhibition | PC9 human non-small-cell lung adenocarcinoma cells | RNA assay | MIC |
Gene (c-Raf) transcription, inhibition | PC9 human non-small-cell lung adenocarcinoma cells (anlotinib-resistant) | RNA assay | MIC |
Protein (C-raf) expression, inhibition | HCCLM3 human hepatocellular carcinoma cells | Chemiluminescent assay | MIC |
Protein (C-raf) expression, inhibition | HuH7 human liver cancer cells | Chemiluminescent assay | MIC |
Protein (C-raf) expression, inhibition | PC9 human non-small-cell lung adenocarcinoma cells | Chemiluminescent assay | MIC |
Protein (C-raf) expression, inhibition | PC9 human non-small-cell lung adenocarcinoma cells (anlotinib-resistant) | Chemiluminescent assay | MIC |
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