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           Search results for: DiscoveryPak™ EGFR Tyrosine Kinase Inhibitor Set   

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#28921872   2017/09/18 Save this To Up

First-line therapy with dacomitinib, an orally available pan-HER tyrosine kinase inhibitor, for locally-advanced or metastatic penile squamous cell carcinoma: results of an open label, single-arm, single-center, phase 2 study.

To harness the frontline therapy in advanced penile squamous cell carcinoma (PSCC), for which chemotherapy exerts moderate activity but poor efficacy. Dacomitinib is an irreversible, pan-epidermal growth factor receptor (HER) inhibitor.

1124 related Products with: First-line therapy with dacomitinib, an orally available pan-HER tyrosine kinase inhibitor, for locally-advanced or metastatic penile squamous cell carcinoma: results of an open label, single-arm, single-center, phase 2 study.

Esophageal squamous cell Breast cancer and matched Human tumor cell array, 1 Human Squamous Cell Carci Human squamous cell carci Esophagus squamous cell c Esophageal squamous cell Kidney clear cell carcino Non small cell lung carci Lung small cell carcinoma Mouse Anti-Human CD19 (pa Oral cavity squamous cell

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#28852500   2017/08/30 Save this To Up

Metabolic profiling of triple-negative breast cancer cells reveals metabolic vulnerabilities.

Among breast cancers, the triple-negative breast cancer (TNBC) subtype has the worst prognosis with no approved targeted therapies and only standard chemotherapy as the backbone of systemic therapy. Unique metabolic changes in cancer progression provide innovative therapeutic opportunities. The receptor tyrosine kinases (RTKs) epidermal growth factor receptor (EGFR), and MET receptor are highly expressed in TNBC, making both promising therapeutic targets. RTK signaling profoundly alters cellular metabolism by increasing glucose consumption and subsequently diverting glucose carbon sources into metabolic pathways necessary to support the tumorigenesis. Therefore, detailed metabolic profiles of TNBC subtypes and their response to tyrosine kinase inhibitors may identify therapeutic sensitivities.

2349 related Products with: Metabolic profiling of triple-negative breast cancer cells reveals metabolic vulnerabilities.

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#28801995   2017/08/12 Save this To Up

INST OX-05-024: first line gemcitabine, oxaliplatin, and erlotinib for primary hepatocellular carcinoma and bile duct cancers: a multicenter Phase II trial.

Hepatocellular Carcinoma (HCC) incidence is increasing in the USA. Gemcitabine (G) and oxaliplatin (O) are active in HCC and biliary duct cancer (BDC). Erlotinib (E) is an EGFR tyrosine kinase inhibitor (TKI) with known activity against both. We sought to evaluate the efficacy of the combination G+O+E. Patients with either of the two diagnosis were treated in a phase II trial. Simons 2 stage design was used. A disease-control rate (DCR), complete response (CR) + partial response (PR)+ stable disease (SD) at 24 weeks of ≤20% and >40% (P0 and P1 of 0.2 and 0.4, respectively) were set as undesirable (null) and desirable results. 26 HCC and 7 BDC patients were accrued. In HCC, 1 PR, 10 SD, and 9 PDs were seen. DCR in HCC was 42%. Among seven (7) patients with BDC, one patient was not evaluable; one achieved a long lasting PR, and five patients had SD and DCR was 86%. Median overall survival (OS) times and progression-free survivals (PFS) were 196 and 149 days in HCC and 238 days and not reached in BDC. PFS at 26 weeks in HCC was 41% and at 21 weeks in BDC was 60%. Grade 3 toxicities in >5% of patients were fatigue (12.9%), neutropenia (9.6%), thrombocytopenia (9.6%), and diarrhea (6.4%). G+O+E exceeded both preset P0a and P1 of the primary objective with a PFS of 41% at 26 weeks for HCC and preliminary BDC data may warrant further investigations.

1563 related Products with: INST OX-05-024: first line gemcitabine, oxaliplatin, and erlotinib for primary hepatocellular carcinoma and bile duct cancers: a multicenter Phase II trial.

Breast invasive ductal ca 4 Androstene 3,17 dione C Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 Primary antibody Caspase Primary antibody FLIP An Primary antibody DNase I AZD-3514 Mechanisms: Andr 17β-Acetoxy-2α-bromo-5

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#28746211   2017/07/26 Save this To Up

Epidermal growth factor promotes proliferation and maintains multipotency of continuous cultured adipose stem cells via activating STAT signal pathway in vitro.

This study aimed to investigate the effects of epidermal growth factor (EGF) on the proliferation and differentiation of adipose stem cells (ASC) during the repeated passaging and probe the underlying signal pathway. Results showed that the Ki67 positive rate remained at a high level, the number of ASCs in G0/G1 phase reduced significantly, but ASCs in G2/M phase and S phase increased markedly in ASCs treated with EGF when compared with ASCs without EGF treatment, indicating that EGF made more ASCs in proliferation phase. The adipogenic capability of ASCs without EGF was compromised when compared with that of ASCs after EGF treatment, although significant difference was not observed. The osteogenic and chondrogenic potencies increased significantly in ASC with EGF treatment indicating EGF could maintain differentiative capacity of ASCs. Gene Set Enrichment Analysis showed EGF upregulated the expression of molecules in the epithelial mesenchymal transition and G2/M checkpoint signal pathways. GeneMANIA database analysis indicated the network interaction between EGF and STAT. EGF receptor (EGFR) inhibitor and STAT3 inhibitor were independently used to validate the role of both pathways in these effects. After inhibition of EGFR or STAT3, the proliferation of ASCs was significantly inhibited, and Western blotting showed EGF was able to markedly increase the expression of EGFR and STAT3. These findings suggest EGF not only promotes the proliferation of ASCs and delays their senescence, but also maintains the differentiation potency of ASCs, which are related to the EGF-induced activation of STAT signal pathway.

2411 related Products with: Epidermal growth factor promotes proliferation and maintains multipotency of continuous cultured adipose stem cells via activating STAT signal pathway in vitro.

Epidermal Growth Factor ( Epidermal Growth Factor ( IGF-1R Signaling Phospho- Macrophage Colony Stimula Macrophage Colony Stimula PathwayReady™ JAK STAT Epidermal Growth Factor ( Epidermal Growth Factor ( Human Insulin-like Growth Human Epidermal Growth Fa Human Insulin-like Growth Mouse Insulin-like Growth

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#28705152   2017/07/14 Save this To Up

Elevated serum CEA levels are associated with the explosive progression of lung adenocarcinoma harboring EGFR mutations.

Serum carcinoembryonic antigen (CEA) levels are a predictor of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) efficacy and are associated with epidermal growth factor receptor (EGFR) gene mutations. However, the clinical significance of plasma CEA level changes during different cycles of target therapy is unknown for lung adenocarcinoma patients with sensitizing EGFR mutations.

2114 related Products with: Elevated serum CEA levels are associated with the explosive progression of lung adenocarcinoma harboring EGFR mutations.

Lung adenocarcinoma and n Lung adenocarcinoma tissu Lung adenocarcinoma (grad Cancer samples: Colorect Cancer samples: Lung Car Cancer samples: Rectum A Lung adenocarcinoma tissu Lung adenocarcinoma (grad Lung carcinoma progressio Lung adenocarcinoma tissu Lung disease spectrum (pu Lung disease spectrum (pu

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#28561591   2017/05/31 Save this To Up

Development of Selective Clk1 and -4 Inhibitors for Cellular Depletion of Cancer-Relevant Proteins.

In cancer cells, kinases of the Clk family control the supply of full-length, functional mRNAs coding for a variety of proteins essential to cell growth and survival. Thus, inhibition of Clks might become a novel anticancer strategy, leading to a selective depletion of cancer-relevant proteins after turnover. On the basis of a Weinreb amide hit compound, we designed and synthesized a diverse set of methoxybenzothiophene-2-carboxamides, of which the N-benzylated derivative showed enhanced Clk1 inhibitory activity. Introduction of a m-fluorine in the benzyl moiety eventually led to the discovery of compound 21b, a potent inhibitor of Clk1 and -4 (IC50 = 7 and 2.3 nM, respectively), exhibiting an unprecedented selectivity over Dyrk1A. 21b triggered the depletion of EGFR, HDAC1, and p70S6 kinase from the cancer cells, with potencies in line with the measured GI50 values. In contrast, the cellular effects of congener 21a, which inhibited Clk1 only weakly, were substantially lower.

2566 related Products with: Development of Selective Clk1 and -4 Inhibitors for Cellular Depletion of Cancer-Relevant Proteins.

Recombinant C. trachomati Recombinant C. trachomati Recombinant C. trachomati Recombinant Tick-Borne En Recombinant Tick-Borne En Recombinant Tick-Borne En Recombinant HEV ORF2 (aa Recombinant HEV ORF2 (aa Recombinant HEV ORF2 (aa Recombinant HEV ORF2 (aa Recombinant HEV ORF2 (aa Recombinant HEV ORF2 (aa

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#28482151   2017/05/08 Save this To Up

Trisubstituted Imidazoles with a Rigidized Hinge Binding Motif Act As Single Digit nM Inhibitors of Clinically Relevant EGFR L858R/T790M and L858R/T790M/C797S Mutants: An Example of Target Hopping.

The high genomic instability of non-small cell lung cancer tumors leads to the rapid development of resistance against promising EGFR tyrosine kinase inhibitors (TKIs). A recently detected triple mutation compromises the activity of the gold standard third-generation EGFR inhibitors. We have prepared a set of trisubstituted imidazoles with a rigidized 7-azaindole hinge binding motif as a new structural class of EGFR inhibitors by a target hopping approach from p38α MAPK inhibitor templates. On the basis of an iterative approach of docking, compound preparation, biological testing, and SAR interpretation, robust and flexible synthetic routes were established. As a result, we report two reversible inhibitors 11d and 11e of the clinically challenging triple mutant L858R/T790M/C797S with IC50 values in the low nanomolar range. Furthermore, we developed a kinome selective irreversible inhibitor 45a with an IC50 value of 1 nM against the EGFR L858R/T790M double mutant. Target binding kinetics and metabolic stability data are included. These potent mutant EGFR inhibitors may serve as a basis for the development of structurally novel EGFR probes, tools, or candidates.

2426 related Products with: Trisubstituted Imidazoles with a Rigidized Hinge Binding Motif Act As Single Digit nM Inhibitors of Clinically Relevant EGFR L858R/T790M and L858R/T790M/C797S Mutants: An Example of Target Hopping.

Cell Meter™ Annexin V B Cell Meter™ Annexin V B Cell Meter™ Annexin V B Cell Meter™ Annexin V B Cell Meter™ Annexin V B Cell Meter™ Annexin V B Cell Meter™ Annexin V B RNA binding motif protein Alkaline Phospatase (ALP) Bovine Androstenedione,AS Rabbit Anti-Rat Androgen CAR,CAR,Constitutive acti

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#28319808   2017/03/20 Save this To Up

Identifying Regulatory Posttranslational Modifications of PD-L1: A Focus on Monoubiquitinaton.

A set of high-affinity, high-specificity posttranslational modification (PTM) enrichment tools was developed to generate an unbiased snapshot of four key PTM profiles (tyrosine phosphorylation, acetylation, ubiquitination, and SUMOylation 2/3) for the clinically important protein programmed cell death ligand 1 (PD-L1). The results showed that epidermal growth factor (EGF) treatment induced tyrosine phosphorylation, acetylation, and ubiquitination of PD-L1. Further characterization of EGF-induced PD-L1 ubiquitination revealed a significant increase in mono- and multiubiquitination of PD-L1 that occurred on glycosylated PD-L1. EGF induced mono- and multiubiquitination of PD-L1 preceded EGF-induced increases in PD-L1 protein levels. Chemical inhibitors of the EGFR pathway, gefitnib and SCH772984, suppressed PD-L1 mono- and multiubiquitination, and inhibition of the ubiquitin E1 activating enzyme, with the chemical inhibitor PYR41, was sufficient to block EGF-stimulated increases in PD-L1 protein levels. This study highlights the significance of identifying novel PTMs for PD-L1 and reveals potentially critical regulatory mechanisms that may be valuable therapeutic targets. In a broader context, this report validates an approach whereby one can gain insight into novel mechanisms of action by a simple and unbiased analysis of a PTM profile of potentially any endogenous protein of interest.

1534 related Products with: Identifying Regulatory Posttranslational Modifications of PD-L1: A Focus on Monoubiquitinaton.

Goat Anti-Human CD274 PD- Rat anti mouse B7-H1 (PD- AGTR L1 Active Cathepsin L1 mg Rabbit Anti-Human Myosin Mouse Anti-Bovine PKA Reg Mouse Anti-Human UCH-L1 Canertinib (CI-1033, PD-1 Canertinib (CI-1033, PD-1 PD-0325901; Appearance Of PD-0325901; Appearance Of PD-0325901; Appearance Of

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#28057155   2017/01/06 Save this To Up

[Level of soluble programmed death-1 ligand 1 in peripheral blood of patients with advanced epidermal growth factor receptor mutated lung adenocarcinoma and its clinical implications].

Objective: To analyze the expression of soluble programmed death ligand 1 (sPD-L1) in the serum of patients with advanced epidermal growth factor receptor (EGFR) mutated lung adenocarcinoma and to explore its clinical implications. Methods: Seventy-two patients with EGFR mutated advanced lung adenocarcinoma (EGFR mutation group) were included from the Department of Respiratory Diseases in The Second Affiliated Hospital of Soochow University from May 2015 to July 2016. Thirty-one patients with advanced EGFR wild type (WT) lung adenocarcinoma [EGFR WT group, diagnosed via mini specimens from bronchoscopy or transthoracic needle aspiration biopsy (TNAB), matching in sex, age and tumor stage with EGFR mutation group] were also enrolled as controls. The sPD-L1 protein expression in serum was determined by enzyme-linked immunosorbent assay (ELISA) kit. According to the clinical response of two-month EGFR-tyrosine kinase inhibitor (TKI) treatment, all patients were divided into two groups: 36 cases in disease progression groups (PD group) and 36 cases in disease control group (DC group). The sPD-L1 level in peripheral blood between the two groups was analyzed. In EGFR mutation group, the relationship of serum sPD-L1 with TNM staging was analyzed. At the same time, the value of serum sPD-L1 and cancer embryo antigen (CEA) in clinical evaluation of advanced EGFR mutated lung adenocarcinoma was evaluated by analyzing the receiver operating characteristic (ROC) curve. Results: A lower level of sPD-L1 level in EGFR mutation group [0.75(0.15-2.78) μg/L] was found compared with the control group [1.56(0.85-3.29) μg/L] (P<0.001). The expression of sPD-L1 in PD group was significantly higher than that in DC group [1.175(0.62-2.78) μg/L vs 0.625(0.15-2.27) μg/L, P<0.001]. High expression of sPD-L1 in the serum of patients with advanced EGFR mutated lung adenocarcinoma was closely correlated to lymph node metastasis and distant metastasis (χ(2)=10.985, 4.662; both P<0.05). The area under ROC curve of serum sPD-L1 and CEA was 0.893 (95%CI: 0.830-0.956) and 0.745(95%CI: 0.652-0.839) respectively. Youden index was the maximum when the cutoff value of sPD-L1 was set to 0.815 μg/L, and the sensitivity and specificity were 77.8% and 91.4%, respectively. Conclusions: After EGFR-TKI treatment, the level of sPD-L1 in the serum of patients with advanced EGFR mutated lung adenocarcinoma is lower, which suggests that sPD-L1 expression may depend on the regulation of EGFR signaling pathway. The level of sPD-L1 can reflect the clinical response of EGFR mutated lung adenocarcinoma to EGFR-TKI.

2002 related Products with: [Level of soluble programmed death-1 ligand 1 in peripheral blood of patients with advanced epidermal growth factor receptor mutated lung adenocarcinoma and its clinical implications].

RANK Ligand Soluble, Huma IGF-1R Signaling Phospho- Human Insulin-like Growth Human Epidermal Growth Fa Mouse Insulin-like Growth Mouse Epidermal Growth Fa Rat Insulin-like Growth F Anti RAGE (Receptor for A Stomach adenocarcinoma wi Lung disease spectrum tis Lung carcinoma and normal Lung carcinoma and normal

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#27934896   2016/12/09 Save this To Up

Transient appearance of circulating tumor DNA associated with de novo treatment.

The limitation of circulating tumor DNA (ctDNA) is its inability to detect cancer cell subpopulations with few or no dying cells. Lung cancer patients subjected to the EGFR tyrosine kinase inhibitor (EGFR-TKI) treatment were prospectively collected, and ctDNA levels represented by the activating and T790M mutations were measured. The first data set (21 patients) consisting of samples collected in the period from before initiation of EGFR-TKI to at least 2 weeks after initiation: the ctDNA dynamics generally exhibited a rapid decrease and/or a transient increase. In 4 patients, we detected a transient increase of ctDNA bearing activating mutations not identified in biopsy samples. ctDNA with the same genotypical pattern was identified in 7 out of the 39 patients of the second data set intended to include samples until the onset of disease progression. In 6 of the 7 patients, this unique ctDNA appeared in the early period after treatment initiation, and did not reappear even after disease progression or chemotherapy. In another patient, similar ctDNA appeared upon radiation therapy. The identification of ctDNA with a unique genotype indicates the presence of cancer cell subpopulations that normally contain few or no dying cells, but generate dead cells because of the treatment.

2970 related Products with: Transient appearance of circulating tumor DNA associated with de novo treatment.

DNA (cytosine 5) methyltr Caspase-3 Substrate DEVD- Caspase-3 Substrate DEVD- Caspase-3 Substrate DEVD- Caspase-3 Substrate DEVD- Caspase-3 Inhibitor Z-DEV Caspase-3 Inhibitor Z-DEV Dexamethasone (10 mM); Ap Dexamethasone ; Appearanc Dexamethasone ; Appearanc Biotin-DEVD-FMK; Appearan Z-DEVD-FMK; Appearance Ly

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