Ars 1620

Manufactured by MedChemExpress

Sourced in United States

ARS-1620 is a laboratory instrument designed for the reliable quantification of cellular oxygen consumption rates (OCR) and extracellular acidification rates (ECAR). The device utilizes a highly sensitive optical sensor technology to accurately measure these metabolic parameters in a variety of cell types and experimental conditions.

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Lab products found in correlation

Sphingosine 1 phosphate (s1p), by Cayman Chemical (1 mentions) Tgf β neutralizing antibody, by BioXCell (1 mentions) Galunisertib, by Selleck Chemicals (1 mentions) Trametinib, by Selleck Chemicals (1 mentions) Rmil 6, by Thermo Fisher Scientific (1 mentions) Pgf2α, by Cayman Chemical (1 mentions) Alpelisib, by Selleck Chemicals (1 mentions) Lmk 235, by MedChemExpress (1 mentions) Rs 504393, by Cayman Chemical (1 mentions) Ccr2 inhibitor, by Santa Cruz Biotechnology (1 mentions) Rmtgf β1, by R&D Systems (1 mentions) Glutamax, by Thermo Fisher Scientific (1 mentions) Chir99021, by Selleck Chemicals (1 mentions) Torin1, by Selleck Chemicals (1 mentions) Trametinib, by MedChemExpress (1 mentions) Fetal bovine serum (fbs), by Wisent (1 mentions) Bafilomycin a1, by LC Laboratories (1 mentions) Gemcitabine, by LC Laboratories (1 mentions) Doxorubicin, by LC Laboratories (1 mentions) Hepes, by Wisent (1 mentions)

5 protocols using ars 1620

Pharmacological Modulation of Signaling Pathways

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For in vitro studies: PGF2α (Cayman), rmFGF1 (Peprotech), rmPDGFBB (Peprotech), rmPDGFAA (Peprotech), rh/mWnt-5a (R&D), LPA (Santa Cruz biotech), rmIL6 (Peprotech), S1P (Cayman), Adapalene (Selleckchem), SAG (Tocris), rmTGFβ1(R&D), rmTGFβ2(R&D), rmTGFβ3 (R&D), CCL2 (BioLegend), CCR2 inhibitor (Santa Cruz Biotechnology), MEKi (PD0324901, 2 μM, Selleckchem), PI3Ki (LY294002, 2 μM, Selleckchem) , mTORi (Rapamycin, 100 nM, Selleckchem), Trametinib (Selleckchem, 50 nM), Alpelisib (Selleckchem, 5 μM) and ARS-1620 (MedChemExpress).
For in vivo studies: TGFβ neutralizing antibody (BioXCell, Clone 1D11, 200 μg, every other day, i.p), Clodronate liposome (Liposoma, 0.1 ml per 10 mg weight, every 5 days, i.p), Trametinib (Selleckchem, 0.3 or 1 or 3 mg/kg as indicated, q.d., oral), Alpelisib (Selleckchem, 50 mg/kg, once per day, oral), ARS-1620 (MedChemExpress, 200 mg/kg, q.d., oral), LMK-235 (MedChemExpress, 5 mg/kg, q.d., i.p.), Galunisertib (Selleckchem, 50 mg/kg, b.i.d., oral), mouse CCL2 neutralizing antibody (BioXCell, 5 mg/kg, every 2 days, i.p.), and RS 504393 (Cayman, 2 mg/kg, q.d., i.p.).

Hou P., Kapoor A., Zhang Q., Li J., Wu C.J., Li J., Lan Z., Tang M., Ma X., Ackroyd J.J., Kalluri R., Zhang J., Jiang S., Spring D.J., Wang Y.A, & DePinho R.A. (2020). Tumor microenvironment remodeling enables bypass of oncogenic KRAS dependency in pancreatic cancer. Cancer discovery, 10(7), 1058-1077.

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Pancreatic Cancer Cell Culture and Treatment

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HeLa and MIA PaCa-2 cells were obtained from ATCC and cultured in DMEM supplemented with 10% fetal bovine serum (Wisent Bioproducts, St-Bruno, QC, Canada), 10 mM HEPES (Wisent Bioproducts), and 2 mM GlutaMAX^TM (Thermo Fisher Scientific Inc., Mississauga, ON, Canada) at 37 °C under a humidified 5% CO₂ atmosphere. The generation of MIA PaCa-2 cells stably expressing a non-targeting shRNA (shNT) or shRNA targeting TFEB (shTFEB) was identical to the method we described for PANC1 [33 (link)]. Non-tumoral human pancreatic duct epithelial (HPDE) cells were kindly provided by Ming-Sound Tsao (University of Toronto, ON, Canada) and cultured in keratinocyte Serum-Free Growth Medium (SFM) (Thermo Fisher Scientific Inc.) as described [33 (link), 57 (link), 58 (link)]. Cells were incubated with gemcitabine (LC Laboratories, Woburn, MA, USA), doxorubicin (LC Laboratories), or 5-fluorouracil (5-FU; Sigma-Aldrich Canada Corp., Oakville, ON, Canada) for the indicated periods. The following inhibitors were purchased from the listed suppliers: the mTOR inhibitor Torin1 and GSK3 inhibitor CHIR99021 (Selleck Chemicals LLC., Houston, TX, USA), MEK inhibitor trametinib, and the KRAS^G12C inhibitor ARS-1620 (MedChemExpress, Monmouth Junction, NJ, USA), and Bafilomycin A1 (LC Laboratories).

Marchand B., Poulin M.A., Lawson C., Tai L.H., Jean S, & Boucher M.J. (2023). Gemcitabine promotes autophagy and lysosomal function through ERK- and TFEB-dependent mechanisms. Cell Death Discovery, 9, 45.

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Combination Drug Synergy Analysis

Cited 1 time

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ARS-1620 and BI-3406 was purchased from MedChemExpress. AMG-510, Erlotinib, Afatinib, AZD-4547, Linsitinib, Imatinib, Cabozantinib, Ceritinib, GDC-0941 and RXDX-106 were purchased from Selleckchem. Drugs were reconstituted in DMSO to 10 mM stock concentrations and stored at −80^oC. The combination index (CI) was calculated using CompuSyn software (20 (link)). The coefficient of drug interaction (CDI) was calculated using the following formula; CDI = AB/(A × B) (21 (link)).

Solanki H.S., Welsh E.A., Fang B., Izumi V., Darville L., Stone B., Franzese R., Chavan S., Kinose F., Imbody D., Koomen J.M., Rix U, & Haura E.B. (2021). Cell-type Specific Adaptive Signaling Responses to KRASG12C inhibition. Clinical cancer research : an official journal of the American Association for Cancer Research, 27(9), 2533-2548.

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Cell Line Maintenance and Compound Acquisition

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The pancreatic cancer cell line MIA PaCa-2 was purchased from the Bioresource Collection and Research Center (Hsinchu, Taiwan). The lung cancer cell lines LU65 and NCI-H23 were obtained from the RIKEN Cell Bank (Ibaraki, Japan) and American Type Culture Collection (Manassas, VA, USA), respectively. MIA PaCa-2 cells were maintained in Dulbecco’s modified Eagle medium supplemented with 10% fetal bovine serum (FBS), 0.1 mM nonessential amino acids, and 1 mM sodium pyruvate. NCI-H23 and LU65 cells were maintained in Roswell Park Memorial Institute 1640 medium supplemented with 10% FBS. In all culture media, 100 U/mL penicillin and 100 μg/mL streptomycin were added to prevent bacterial contamination. All cell culture reagents were purchased from Gibco, Thermo Fisher Scientific (Waltham, MA, USA). The cell lines were incubated in a humidified incubator at 37 °C under 5% CO₂ and 95% air atmosphere. All cells were verified through short-tandem repeat (STR) profiling and tested negative for mycoplasma contamination.
Sotorasib, ARS-1620, Q-VD-OPh (QVD), cobimetinib, N-acetyl-l-cysteine (NAC), and encorafenib were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Chiou L.W., Chan C.H., Jhuang Y.L., Yang C.Y, & Jeng Y.M. (2023). DNA replication stress and mitotic catastrophe mediate sotorasib addiction in KRASG12C-mutant cancer. Journal of Biomedical Science, 30, 50.

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KRAS siRNA and shRNA Knockdown Assay

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siRNA oligonucleotides targeting KRAS were: KRAS 1, CUAUGGUCCUAGUAGGAAAtt (Thermo Fisher, 4390824, s7939), and KRAS 2, GCCUUGACGAUACAGCUAAtt (Thermo Fisher, 4390824, s7940). The target sequence for the validated shRNA construct used to target KRAS was CAGTTGAGACCTTCTAATTGG. To determine the levels of activated proteins, immunoblot analyses were done using phosphospecific antibodies to AMPKα (T172; 40H9), Beclin-1 (S93; D9A5G), DRP1 (S616) and RSK (T395/S363). Antibodies recognized total LC3B, KRAS (234–4.2), AMPKα (Δ63Γ4) Beclin-1 (2A4), PINK1 (D8G3), VDAC (D73D12), DRP1 (D8H5), RSK (32D7), ATG5, ATG7 (EP1759Y), β-actin (AC-15), vinculin (hVIN-1) or GAPDH (GAPDH-71.1) to control for total protein expression. All antibodies were obtained from Cell Signaling Technologies except ATG7 (Abcam), KRAS (Calbiochem), β-actin (Sigma) and vinculin (Sigma). Immunochemical labeling of mitochondria was performed using TOMM20 (Santa Cruz). Chemical reagents used were bafilomycin A1, oligomycin A, rotenone, antimycin, FCCP, CCCP, doxycycline, MTT and chloroquine diphosphate (Sigma); calcein AM and AlamarBlue (Invitrogen); hydroxychloroquine (SelleckChem); binimetinib (SelleckChem); ARS-1620 (Medchem Express); Spautin-1, SBI-0206965 and MRT68921 (Xcessbio); SCH772984 (provided by Merck) and BVD-523 (provided by Biomed Valley Discoveries).

Bryant K.L., Stalnecker C.A., Zeitouni D., Klomp J.E., Peng S., Tikunov A.P., Gunda V., Pierobon M., Waters A.M., George S.D., Tomar G., Papke B., Hobbs G.A., Yan L., Hayes T.K., Diehl J.N., Goode G.D., Chaika N.V., Wang Y., Zhang G.F., Witkiewicz A.K., Knudsen E.S., Petricoin EF I.I.I., Singh P.K., Macdonald J.M., Tran N.L., Lyssiotis C.A., Ying H., Kimmelman A.C., Cox A.D, & Der C.J. (2019). Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer. Nature medicine, 25(4), 628-640.

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