Nvp tae684

Manufactured by Selleck Chemicals

Sourced in United States

NVP-TAE684 is a laboratory reagent used for research purposes. It is a tyrosine kinase inhibitor that targets the TAE684 protein. The core function of NVP-TAE684 is to inhibit the activity of the TAE684 protein in in vitro experiments.

Automatically generated - may contain errors

Lab products found in correlation

Ag 1024, by Selleck Chemicals (1 mentions) Bkm120, by Selleck Chemicals (1 mentions) Recombinant murine igf 1, by Thermo Fisher Scientific (1 mentions) Ly294002, by Bio-Techne (1 mentions) Kanamycin, by Thermo Fisher Scientific (1 mentions) Sureprint g3 human ge 8x60k microarray, by Agilent Technologies (1 mentions) Experion, by Bio-Rad (1 mentions) Dimethyl sulfoxide (dmso), by Avantor (1 mentions) Penicillin streptomycin, by Thermo Fisher Scientific (1 mentions) L glutamine, by Thermo Fisher Scientific (1 mentions) Hepes, by Thermo Fisher Scientific (1 mentions) Rpmi 1640 medium, by Thermo Fisher Scientific (1 mentions) Total alk, by Cell Signaling Technology (1 mentions) Pt202 y204 erk, by Cell Signaling Technology (1 mentions) Total erk, by Cell Signaling Technology (1 mentions) Mg132, by Selleck Chemicals (1 mentions) Nih3t3 cells, by American Type Culture Collection (1 mentions) Crizotinib, by Pfizer (1 mentions) Crizotinib, by Selleck Chemicals (1 mentions) Nvp tae684, by MedChemExpress (1 mentions)

7 protocols using nvp tae684

Cortical Neuron Signaling Pathway Analysis

Cited 1 time

Check if the same lab product or an alternative is used in the 5 most similar protocols

Cortical neurons were treated with inhibitors or ligands 4 h after plating and were fixed 33–38 h after treatment for analysis. For IGF‐1R, inhibitors or activators were added in starvation medium (serum‐free Neurobasal medium, supplemented with 2% B27 minus insulin, 1% L‐glutamine, 50 IU/ml penicillin, and 50 μg/ml streptomycin). The following inhibitors and ligands were used: TAE684 (NVP‐TAE684, Selleckchem, #1108), crizotinib (PR‐02341066, Selleckchem #1068), LY 294002 (Tocris), BKM120 (Buparlisib) (Selleckchem, #S2247), AG1024 (Selleckchem #S1234), PPP (CAS 477‐47‐4, Santa Cruz, scbt #24008), and recombinant murine IGF‐1 (Peprotech).
ALKAL2‐containing conditioned medium (ACM) was generated as described previously (Guan et al, 2015 (link)) with slight modifications. Briefly, HEK293T cells, in 10 cm plates, were transfected with 8.0 μg pcDNA3‐FAM150B‐HA using the calcium phosphate method. After 16 h, media was replaced with starvation medium (DMEM, supplemented with 0.2% FBS, 50 IU/ml penicillin, and 50 μg/ml streptomycin) and ALKAL2‐conditioned medium was collected after 36 h. Cortical neurons were treated with CCM and ACM, supplemented with 2% B27 and 1% N2. Activation of wild‐type endogenous ALK was confirmed in IMR‐32 human neuroblastoma cells.

Christova T., Ho S.K., Liu Y., Gill M, & Attisano L. (2023). LTK and ALK promote neuronal polarity and cortical migration by inhibiting IGF1R activity. EMBO Reports, 24(7), e56937.

+ Open protocol

+ Expand

Gene Expression Profiling of ALK-Mutant Neuroblastoma

Check if the same lab product or an alternative is used in the 5 most similar protocols

The CLB-GA time series dataset has been described before [31 (link)]. The neuroblastoma CLB-GA cell line (ALK^R1275Q) was cultured in RPMI-1640 medium (Invitrogen), supplemented with fetal bovine serum (10%), kanamycin (100 μg/ml) penicillin/streptomycin (100 IU/ml), L-glutamine (2 mM) and HEPES (25 mM) (Life Technologies), and maintained at 37°C in a 5% C02-humidified environment. At different time points (10, 30 minutes, 1, 2, 4 and 6 hours) after treatment with 0.32 μM of the small molecule ALK inhibitor NVP-TAE684 (hereafter TAE684) (SelleckChem, S1108) or DMSO (VWR) as solvent control, cells were harvested and RNA quality was analysed using Experion (Bio-Rad) prior to gene-expression profiling. Samples were labelled and hybridized to the Sureprint G3 human GE 8x60K microarrays (Agilent Technologies), according to the manufacturer’s guidelines and starting from 200 ng RNA. The data was normalized with the vsn method in R version 3.3.3 (packages vsn and limma). The R package BioMart was used to annotate gene names to their corresponding probes. Probes detecting at least a two-fold higher expression than the negative control probes of the array in at least 60% of the DMSO or TAE samples, were selected as background correction. Data can be accessed through ArrayExpress (accession number E-MTAB-3206) [31 (link)].

Claeys S., Denecker G., Cannoodt R., Kumps C., Durinck K., Speleman F, & De Preter K. (2017). Early and late effects of pharmacological ALK inhibition on the neuroblastoma transcriptome. Oncotarget, 8(63), 106820-106832.

+ Open protocol

+ Expand

Detailed Cell Line Characterization and Treatments

Check if the same lab product or an alternative is used in the 5 most similar protocols

H2228, H3122, and HCC78 were a kind gift from Dr. John D. Minna (The University of Texas, Southwestern Medical Center, Dallas, TX) and STE-1 were a kind gift from Dr. Christine M. Lovly (Vanderbilt University School of Medicine, Nashville, TN). ROS1 fusion cell lines CUTO2 (SDC4-ROS1), CUTO23 and CUTO27 (CD74-ROS1), and CUTO28 (TPM3-ROS1) were generated at the University of Colorado from patient tumor samples following informed consent under an IRB-approved protocol. ALK and ROS1 fusion cell lines were grown in RPMI supplemented with 10% FBS. H1299, A549, H460, H1650, HCC827 were obtained from the University of Colorado Cancer Center Tissue Culture Core and cultured in RPMI supplemented with 5% FBS. NIH3T3 cells were obtained from American Type Culture collection and grown in Dulbecco’s Modified Eagle’s Media with 5% FBS. Crizotinib (PF-02341066) was obtained from Pfizer, Inc. NVP-TAE684 and MG132 were purchased from Selleck Chemicals. Antibodies used were ALK pY1278/1282/1283 (#3983), total ALK (#3791), ERK pT202/Y204 (#9191), total ERK (#9107), c-MYC (#5605), c-MYC pS62 (#13748) were purchased from Cell Signaling Technology. MYCBP (ab172444) c-MYC pT58 (28842) was purchased from Abcam, and alpha-tubulin (sc-8035), was purchased from Santa Cruz biotechnology.

Pilling A.B., Kim J., Estrada-Bernal A., Zhou Q., Le A.T., Singleton K.R., Heasley L.E., Tan A.C., DeGregori J, & Doebele R.C. (2018). ALK is a critical regulator of the MYC-signaling axis in ALK positive lung cancer. Oncotarget, 9(10), 8823-8835.

+ Open protocol

+ Expand

Inhibitors and Chemotherapeutics for ALK+ Cell Lines

Check if the same lab product or an alternative is used in the 5 most similar protocols

Crizotinib, NVP-TAE684 and LDK-378 for use in tissue culture studies were purchased from Selleck Chemicals (Houston, TX), dissolved in DMSO and stored at −20C. For in vivo use, Crizotinib was obtained from Aok Bio (Shanghai, China), and NVP-TAE684 and LDK-378 were sourced from MedChemExpress (Monmouth Junction, NJ). The purity of all drugs were greater than 95%, as assessed by LC-MS analysis. ALK inhibitors were suspended in capryol 90 (Gattefosse Corp., Paramus, NJ) for oral gavage of animals. Vincristine (V), actinomycin D (A) and cyclophosphamide (C) were all obtained from the St. Jude pharmacy and were dissolved in sterile saline. They were administered by i.p. injection using a schedule deemed efficacious in pediatric patients (V given weekly at 0.38mg/kg; A given once at 0.5mg/kg; C given once at 125mg/kg).
Antibodies for ALK (31F12 mouse monoclonal, cat# 3791) and G3PDH (D16H11 rabbit HRP-conjugated monoclonal, cat# 8884) were purchased from Cell Signaling (Danvers, MA). siRNA targeting ALK and GFP-tagged RNA used as a control for transfection efficiency were obtained from OriGene (Rockville, MD). The former consists of 3 unique 27mer siRNA duplexes targeting different regions of the ALK mRNA and scrambled siRNA were used as negative controls.

Wierdl M., Tsurkan L., Chi L., Hatfield M.J., Tollemar V., Bradley C., Chen X., Qu C, & Potter P.M. (2018). Targeting ALK in pediatric RMS does not induce antitumor activity in vivo. Cancer chemotherapy and pharmacology, 82(2), 251-263.

+ Open protocol

+ Expand

ALK Inhibitors and Antibodies Protocol

Check if the same lab product or an alternative is used in the 5 most similar protocols

ALK small-molecule inhibitors PF-02341066 (Crizotinib) and NVP-TAE684 were purchased from Selleckchem (Selleck Chemicals, Houston, TX, USA), whereas anti-ALK monoclonal antibodies (mAb46 and 30) were a generous gift of Dr. Marc Vigny [39 (link)]. The primary antibodies for Western blot analysis were from Cell Signalling (ALK^Y1604; AKT^S473; ERK^T202/Y204; c-Met^Y1234/1235; EGFR^Y1068; IGF1-Rβ^Y1135/1136; IGF1-Rβ) (Cell Signaling Technology, Inc., Danvers, MA, USA); SIGMA (γ-tubulin) (SIGMA Aldrivh Co., USA); Invitrogen (ALK) (Invitrogen, Life Technologies Co); or Santa Cruz (AKT; ERK) (Santa Cruz Biotechnology, Inc., Santa Cruz, CA, USA). Horseradish peroxidase (HRP)-conjugated sheep anti-mouse or donkey anti-rabbit antibodies, were purchased from GE Healthcare (GE Healthcare Life Sciences, Uppsala, Sweden), whereas recombinant human HGF, EGF, and IGF-1 growth factors were purchased from Peprotech (Peprotech, NJ, USA). Pervanadate stock solution (100mM) was prepared as indicated by Huyer et al. [40 (link)]; while MTT salt (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) was available from SIGMA (SIGMA Aldrich Co., USA).

Peron M., Lovisa F., Poli E., Basso G, & Bonvini P. (2015). Understanding the Interplay between Expression, Mutation and Activity of ALK Receptor in Rhabdomyosarcoma Cells for Clinical Application of Small-Molecule Inhibitors. PLoS ONE, 10(7), e0132330.

+ Open protocol

+ Expand

Cytostatic Drug Combination Protocol

Check if the same lab product or an alternative is used in the 5 most similar protocols

Novartis Pharma generously provided Smac mimetic LCL161. Cytostatic drugs daunorubicin, doxorubicin, etoposide, idarubicin, topotecan, SN-38 (active metabolite of irinotecan), vinblastine, vincristine and vindesine were obtained from Sigma-Aldrich (Munich, Germany). NVP-TAE684 was purchased from Selleckchem (Munich, Germany). Working solutions were prepared by dilution of drugs with medium or ddH₂O to designated concentrations.

Najem S., Langemann D., Appl B., Trochimiuk M., Hundsdoerfer P., Reinshagen K, & Eschenburg G. (2016). Smac mimetic LCL161 supports neuroblastoma chemotherapy in a drug class-dependent manner and synergistically interacts with ALK inhibitor TAE684 in cells with ALK mutation F1174L. Oncotarget, 7(45), 72634-72653.

+ Open protocol

+ Expand

Cytotoxic Drug Screening Assay

Check if the same lab product or an alternative is used in the 5 most similar protocols

The drugs, TG-101209, NVP-TAE684, MK-0752, actinomycin-d, and panobinostat were purchased from Selleckchem (S2692, S1108, S2660, S8964, S1030, Selleckchem, Houston, TX, USA), and withaferin-a was purchased from Sigma (W4394, Sigma-Aldrich, Saint Louis, MO, USA). These drugs were dissolved in DMSO. The cells were seeded in a 96-well plate at 20×10³ cells per well. Day after seeding, drugs were added to the wells at a proper concentration, TG-101209 (6nM), NVP-TAE684 (3nM), MK-0752 (5nM), withaferin-a (4uM), actinomycin-d (0.3nM), and panobinostat (5nM) and treated for one day. The cells in the negative control group were only treated by DMSO for one day.

Li X., Shong K., Kim W., Yuan M., Yang H., Sato Y., Kume H., Ogawa S., Turkez H., Shoaie S., Boren J., Nielsen J., Uhlen M., Zhang C, & Mardinoglu A. (2022). Prediction of drug candidates for clear cell renal cell carcinoma using a systems biology-based drug repositioning approach. EBioMedicine, 78, 103963.

+ Open protocol

+ Expand

About PubCompare

Our mission is to provide scientists with the largest repository of trustworthy protocols and intelligent analytical tools, thereby offering them extensive information to design robust protocols aimed at minimizing the risk of failures.

We believe that the most crucial aspect is to grant scientists access to a wide range of reliable sources and new useful tools that surpass human capabilities.

However, we trust in allowing scientists to determine how to construct their own protocols based on this information, as they are the experts in their field.

Ready to get started?

Revolutionizing how scientists
search and build protocols!