Sch772984

Manufactured by Selleck Chemicals

Sourced in United States, China, Germany, United Kingdom, Switzerland

SCH772984 is a chemical compound used in laboratory research. It functions as a small molecule inhibitor. The core purpose of this product is for use in scientific experimentation and analysis.

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Lab products found in correlation

Spelling variants of this product

ERK inhibitor (SCH772984) (3 citations) ERKi SCH772984 (2 citations) Erk1/2 inhibitor (SCH772984) (2 citations)

223 protocols using sch772984

Embryonic Angiogenesis Modulation

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Eggs with embryos were incubated at 37 °C in an incubator with 70% humidity. After 6 to 7 days of incubation, an air chamber was made, the shell membrane and chorioallantoic membrane were separated, and a window was opened on the shell membrane for injection. The CM from GC-shESM1 cells with or without recombinant ESM1, MAPK/ERK inhibitor SCH772984 (Selleck, Houston, TX, USA) or c-Met-inhibitor AMG-337 (Shanghai Ulva test), and the CM from GC cells with or without the ESM1-neutralizing antibody and MAPK/ERK stimulator Ceramide C6 (Santa Cruz, CA, USA) or MAPK/ERK inhibitor SCH772984 (Selleck, USA) were added to the loop by window injection. After 3 days, the CAM area was isolated, unfolded on a glass slide, and imaged under a stereomicroscope. Vascularization was assessed using image J/FIJI.

Yang J., Shu G., Chen T., Dong A., Dong C., Li W., Sun X., Zhou Y., Li D, & Zhou J. (2023). ESM1 Interacts with c-Met to Promote Gastric Cancer Peritoneal Metastasis by Inducing Angiogenesis. Cancers, 16(1), 194.

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Establishment and Characterization of Melanoma Cell Lines

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1205Lu cells (donated by Dr. Meenhard Herlyn, Wistar Institute, Philadelphia, PA in 2005) were cultured in MCDB153 medium containing 2% FBS, 20% Leibovitz L-15 medium, with 5 μg/mL insulin. A375 cells (purchased from ATCC in 2005) were cultured in DMEM with 10% FBS. Cell lines were authenticated by sequencing at the NRAS and BRAF loci, and by STR analysis (completed July 2016). CRT cells were cultured in the same medium as parental cells with the addition of PLX4720 (1 μM) and PD0325901 (35 nM) (15 (link),16 (link)). These levels maintain the same RAF inhibitor to MEK inhibitor ratio as used for in vivo experiments. PLX4720 was provided by Dr. Gideon Bollag (Plexxikon Inc., Berkeley, CA). PD0325901, SCH772984, GSK461364, and BI 6727 were purchased from Selleck Chemicals (Houston, TX).

Sanchez I.M., Purwin T.J., Chervoneva I., Erkes D.A., Nguyen M.Q., Davies M.A., Nathanson K.L., Kemper K., Peeper D.S, & Aplin A.E. (2019). In vivo ERK½ reporter predictively models response and resistance to combined BRAF and MEK inhibitors in melanoma. Molecular cancer therapeutics, 18(9), 1637-1648.

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Investigating Stress Response Signaling Pathways

Cited 2 times

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The following inhibitors were purchased from Selleck Chemicals, catalogue numbers as follows: GSK2656157 (hearefter referred to as PERKi), S7033; pictilisib (GDC-0941), S1065; AZD8055, S1555; apitolisib (GDC-0980), S2696; selumetinib (AZD6244), S1008; GDC-0879, S1104; RO5126766, S7170; SCH772984, S7101. AKT inhibitor VIII (AKTi VIII) was purchased from Merck Millipore, catalogue number 124018. Concentrations were selected from a dilution series performed to ensure activity. Concentrations used for all experiments are shown in Table 1. Cells were treated with inhibitor 1 h prior to induction of ER-stress.Table 1

Inhibitors, major targets and concentrations used in this study.

Table 1

Inhibitor	Major target(s)	Concentration	Reference
GSK2656157	PERK	50 and 500 nM	[42 (link)]
pictilisib (GDC-0941)	PI3K	500 nM	[43 (link)]
AKT inhibitor VIII	AKT PH domain	5 μM	[44 (link)]
AZD8055	MTOR	500 nM	[45 (link)]
apitolisib (GDC-0980)	PI3K and MTOR	500 nM	[46 (link)]
selumetinib (AZD6244)	MEK1	50 nM	[47 (link)]
GDC-0879	BRAF/CRAF	50 nM	[48 (link)]
RO5126766	BRAF/CRAF/MEK	50 nM	[49 (link)]
SCH772984	ERK1/2	50 nM	[50 (link)]

Bright M.D., Clarke P.A., Workman P, & Davies F.E. (2018). Oncogenic RAC1 and NRAS drive resistance to endoplasmic reticulum stress through MEK/ERK signalling. Cellular Signalling, 44, 127-137.

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Synthesis and Characterization of DDP Prodrug

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DDP (P3494) and doxorubicin (D1515) were purchased from Sigma. Docetaxel (T1034) was purchased from TargetMol. Carboplatin (C805203) was purchased from Macklin, ERK inhibitor SCH772984 and Rac1 inhibitor NCS23766 was from Selleck.
The DDP prodrug was synthesized according previous report^{51 (link)}, by using the reaction between cis, trans, cis-[PtCl₂(OH)₂(NH₃)₂], and sebacic anhydride. The structure of this DDP prodrug was analyzed by proton nuclear magnetic resonance (HNMR) to confirm successful synthesis (Supplementary Fig. 8). Details of the drugs including their targets and concentrations noted in the figure legends.

Li Q., Qin T., Bi Z., Hong H., Ding L., Chen J., Wu W., Lin X., Fu W., Zheng F., Yao Y., Luo M.L., Saw P.E., Wulf G.M., Xu X., Song E., Yao H, & Hu H. (2020). Rac1 activates non-oxidative pentose phosphate pathway to induce chemoresistance of breast cancer. Nature Communications, 11, 1456.

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High-Throughput Screening of Tyrosine Kinase Inhibitors

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HGF: 20 ng/ml, EGF: 30 ng/ml, bFGF: 100 ng/ml (all from Preprotech). Drugs: (all from Selleckchem, Pittsburg, PA, USA): SCH772984: 1 µM, Staurosporin: 1 µM, H₂O₂: 800 mM. Axitinib: 1 µM, 5 µM, 10 µM, NPV-BEZ35: 250 nM, 500 nM, 1 µM, 5 µM, 10 µM, dasatinib (BMS-354825): 250 nM, 1 µM, 5 µM, 10 µM, Erlotinib HCI: 250 nM, 500 nM, 1 µM, 5 µM, 10 µM, Imatinib mesylate: 1 µM, 5 µM, 10 µM, Nilotinib (AMN-107): 1 µM, 5 µM, 10 µM, Rapamycin (sirolimus): 250 nM, 500 nM, 1 µM, 5 µM, 10 µM, Sunitinib malate (sutent): 1 µM, 5 µM, 10 µM, Temsirolimus (torisel): 1 µM, 5 µM, 10 µM, Masitinib (AB1010): 500 nM, 1 µM, 5 µM, 10 µM, Crizotinib (PF-02341066): 250 nM, 500 nM, 1 µM, 5 µM, 10 µM, Foretinib: 500 nM, 1 µM, 5 µM, 10 µM (Selleckchem), XL-184: 1 µM, 5 µM, 10 µM, Vermurafenib (PLX4032): 1 µM, 5 µM, 10 µM, Zoledronic acid (zoledronate): 1 µM, 5 µM, 10 µM, Ruxolitinib (INCB018424): 500 nM, 1 µM, 5 µM, 10 µM, Nystatin (mycostatin): 1 µM, 5 µM, 10 µM, lapatinib: 1 µM, 5 µM, 10 µM, Pazopanib: 1 µM, 5 µM, 10 µM, dequalinium chloride: 1 µM, 5 µM, 10 µM, Tofacitinib citrate (CP-690550 citrate): 500 nM, 1 µM, 5 µM, 10 µM. H-1152 (from Alexis Biochemicals): 1 µM.

Schönholzer M.T., Migliavacca J., Alvarez E., Santhana Kumar K., Neve A., Gries A., Ma M., Grotzer M.A, & Baumgartner M. (2020). Real-time sensing of MAPK signaling in medulloblastoma cells reveals cellular evasion mechanism counteracting dasatinib blockade of ERK activation during invasion. Neoplasia (New York, N.Y.), 22(10), 470-483.

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Modulation of Fibroblast-Macrophage Crosstalk

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Term human FM explants were collected as described above, rested in DMEM/F12 media supplemented with 10% FBS overnight and then treated with neutrophil CM for 24 hrs. In some experiments, FMs were pre-treated with the ERK inhibitor, SCH772984 (10nM, Selleckchem, Houston, TX); or the TLR9 antagonist, ODN2088 (TTAGGG, 1μM, Invivogen, A151, San Diego, CA) for 1 hr at 37°C prior to the addition of neutrophil CM. In other cases, DNase I derived from bovine pancreas (1U/ml, Roche, #10104159001, Roche, Switizerland) was added to neutrophil CM for 30 min at room temperature then the CM incubated at 70°C for 20 min and cooled prior to adding to the FMs. Neutrophil CM was incubated at 70°C for 20 min without DNase I as the baseline control. Incubation of activated neutrophil CM at 70°C for 20 min without DNase I did not affect its ability to alter FM function. After 24 hr of co-culture, the neutrophil CM and any associated factors was removed and FMs were transferred to a serum-free OptiMEM culture system for an additional 24 hrs to collect freshly secreted FM-derived factors for downstream analysis. FM supernatants and tissues are collected and stored at −80°C until analysis.

Tong M., Smith A.H, & Abrahams V.M. (2021). Activated Neutrophils Propagate Fetal Membrane Inflammation and Weakening through ERK and Neutrophil Extracellular Trap-induced TLR-9 Signaling. Journal of immunology (Baltimore, Md. : 1950), 206(5), 1039-1045.

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Selective Inhibition of Cancer Pathways

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ABT-199 was generously provided by Abbvie (Chicago, IL, USA). AZD6244, MEK162, SCH772984, SAHA, LBH589, MS275 and FK228 were purchased from Selleckchem (Houston, TX, USA). Tubacin was purchased from Sigma-Aldrich (St. Louis, MO, USA). Stock solutions were made in dimethylsulfoxide, aliquoted and stored at −20°C.

Ramakrishnan V.G., Miller K.C., Macon E.P., Kimlinger T.K., Haug J., Kumar S., Gonsalves W.I., Rajkumar S.V, & Kumar S.K. (2019). Histone deacetylase inhibition in combination with MEK or BCL-2 inhibition in multiple myeloma. Haematologica, 104(10), 2061-2074.

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Signaling Pathway Analysis in Cells

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p-p38 (9215), p38 (9212), p-ERK (4370), ERK (9102), p-AKT(S473) (4060), and AKT (4691) antibodies were purchased from Cell Signaling Technology (Danvers, MA, USA). α-SMA (ab7817), collagen 1 (ab34710), HIF-1α (ab179483 for western blot, ab1 for immunofluorescence), alpha tubulin (ab18251), vimentin (ab 8978), goat anti-mouse IgG H&L (HRP, ab6789), and goat anti-rabbit IgG H&L (HRP, ab6721) antibodies were purchased from Abcam (Cambridge, UK). AFAP (NBP1-90216) antibody was purchased from Novus (Littleton, CO, USA). Alexa Fluor 488 goat anti-mouse IgG and Alexa Fluor 555 goat anti-rabbit IgG antibodies were purchased from Invitrogen (Carlsbad, CA, USA). Beta-actin (sc-47778) was purchased from Santa Cruz Biotechnology (Dallas, TX, USA). SCH772984 was purchased from Selleckchem (Houston, TX, USA) and stored in 5 mM dimethyl sulfoxide (DMSO) at −20 °C.

Kim J., Kim B., Kim S.M., Yang C.E., Song S.Y., Lee W.J, & Lee J.H. (2019). Hypoxia-Induced Epithelial-To-Mesenchymal Transition Mediates Fibroblast Abnormalities via EKR Activation in Cutaneous Wound Healing. International Journal of Molecular Sciences, 20(10), 2546.

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Selective Kinase Inhibitor Protocol

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VS-5584, GSK1120212, SCH772984, and BVD-523 were purchased from Selleck Chemicals (Houston, TX, USA).

Ning C., Liang M., Liu S., Wang G., Edwards H., Xia Y., Polin L., Dyson G., Taub J.W., Mohammad R.M., Azmi A.S., Zhao L, & Ge Y. (2017). Targeting ERK enhances the cytotoxic effect of the novel PI3K and mTOR dual inhibitor VS-5584 in preclinical models of pancreatic cancer. Oncotarget, 8(27), 44295-44311.

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Inhibition of Oncogenic Pathways

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BRAF inhibitors dabrafenib and PLX4720, MEK inhibitor trametinib, ERK
inhibitor SCH772984 and EGFR tyrosine kinase inhibitor CL-387,785 were purchased
from Selleck Chemicals (Houston, TX, USA). Dacarbazine was obtained from the
pharmacy of the Slotervaart hospital (Amsterdam, The Netherlands).

Kong X., Kuilman T., Shahrabi A., Boshuizen J., Kemper K., Song J.Y., Niessen H.W., Rozeman E.A., Geukes Foppen M.H., Blank C.U, & Peeper D.S. (2017). Cancer Drug Addiction is Relayed by an ERK2-Dependent Phenotype Switch. Nature, 550(7675), 270-274.

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