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Rmc 4550

Manufactured by Selleck Chemicals
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The RMC-4550 is a laboratory centrifuge designed for general-purpose applications. It features a maximum speed of 4,550 rpm and a maximum relative centrifugal force of 3,000 x g. The RMC-4550 is capable of accommodating a variety of sample containers and rotor configurations.

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Lab products found in correlation

Trametinib, by Selleck Chemicals (4 mentions) Alectinib, by Selleck Chemicals (3 mentions) Osimertinib, by Selleck Chemicals (3 mentions) Crizotinib, by Selleck Chemicals (3 mentions) Shp099, by Selleck Chemicals (3 mentions) Gefitinib, by Selleck Chemicals (2 mentions) Azd5363, by Selleck Chemicals (2 mentions) Lorlatinib, by Selleck Chemicals (2 mentions) Sotorasib, by Selleck Chemicals (2 mentions) Adagrasib, by Selleck Chemicals (2 mentions) Afatinib, by Selleck Chemicals (2 mentions) Erlotinib, by Selleck Chemicals (2 mentions) Amg 511, by Selleck Chemicals (2 mentions) Rpmi 1640, by Merck Group (2 mentions) Mrtx849, by MedChemExpress (2 mentions) Bgj398, by Selleck Chemicals (2 mentions) Amg510, by MedChemExpress (2 mentions) Ars 1620, by Selleck Chemicals (2 mentions) Gilteritinib, by Selleck Chemicals (2 mentions) Cobimetinib, by Selleck Chemicals (2 mentions)

11 protocols using rmc 4550

1

Decidualization and PR Translocation in hESCs

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To induce decidualization, hESCs were incubated with 1 μM MPA (Targetmol) and 0.5 mM db-cAMP (Targetmol). Subsequently, the SHP2 inhibitor RMC-4550 (Selleck) was added in the process of decidualization induction or hESCs knocked down SHP2 were used for decidualization induction. Decidualization was verified by the changes in cell morphology from a fibroblastic to a round shape, as observed with light microscopy, and five randomly selected microscopic fields in each group were used to calculate the relative ratio of round cells. To observe the translocation of PR, hESCs cells were treated with 2 μM P4 (Targetmol) and SHP2 inhibitor RMC-4550 (Selleck) or hESCs knocked down SHP2 were treated with 2 μM P4 (Targetmol). Concurrently, the MEK inhibitor trametinib (MCE) or ERK inhibitor U0126 (M Millipore) was added in the process of the translocation of PR. The PR translocation ratio was calculated as percentage of nuclear PR cells in five randomly selected microscopic fields.
Chen L., Zhao W., Li M., Yang Y., Tian C., Zhang D., Chang Z., Zhang Y., Zhao Z.J., Chen Y, & Ma L. (2023). SHP2 participates in decidualization by activating ERK to maintain normal nuclear localization of progesterone receptor. Reproduction (Cambridge, England), 166(1), 37-53.
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2

Targeted Therapies in Cancer Research

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The following targeted therapies were used in this study: erlotinib, gefitinib, osimertinib, crizotinib, alectinib, lorlatinib, sotorasib, and adagrasib (Selleckchem). MAPK pathway inhibitors included afatinib, erlotinib, RMC-4550, sotorasib, trametinib, AMG 511, and AZD5363 (Selleckchem).
Vaccaro K., Allen J., Whitfield T.W., Maoz A., Reeves S., Velarde J., Yang D., Meglan A., Ribeiro J., Blandin J., Phan N., Bell G.W., Hata A.N, & Weiskopf K. (2024). Targeted therapies prime oncogene-driven lung cancers for macrophage-mediated destruction. The Journal of Clinical Investigation, 134(9), e169315.
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3

Authentication and Culture of Cell Lines for Research

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Cell lines were obtained from ATCC, Millipore Sigma or the Center for Molecular Therapeutics at the MGH Cancer Center (Boston, MA) (Crystal et al., 2014 (link)), which routinely performs cell line authentication testing by SNP and short tandem repeat analysis, and maintained in DMEM/F12 or RPMI 1640 supplemented with 10% fetal calf serum, and were not cultured longer than 6 months after receipt from cell banks. AMG 510 and MRTX849 used for in vitro and in vivo studies were purchased from MedChemExpress and ARS-1620, RMC-4550, BGJ398, and trametinib used for in vitro studies were purchased from Selleckchem. RM-018 used for in vitro studies and RMC-4550 used in in vivo studies were kindly provided by Revolution Medicines. Panitumumab was obtained from McKesson Pharmaceuticals.
Ryan M.B., Coker O., Sorokin A., Fella K., Barnes H., Wong E., Kanikarla P., Gao F., Zhang Y., Zhou L., Kopetz S, & Corcoran R.B. (2022). KRASG12C-independent feedback activation of wild-type RAS constrains KRASG12C inhibitor efficacy. Cell reports, 39(12), 110993.
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4

Acquired Resistance Generation Protocol

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SHP099, RMC-4550, cobimetinib, gilteritinib, and KW-2449 were purchased from Selleckchem. II-B08 was purchased from Sigma-Aldrich. Recombinant human, animal free EGF was purchased from Peprotech.
For acquired resistance generation, cells were initially treated with SHP099 at their respective IC50, followed by dose increase at each passage for over 3 weeks, stopping the increase at doses corresponding approximately 5× IC50 (2.5 μmol/L for MV-4-11 and 10 μmol/L for MOLM-13), and continuing cultivation at those doses of SHP099 for a maximum of 6 weeks.
Pfeiffer A., Franciosa G., Locard-Paulet M., Piga I., Reckzeh K., Vemulapalli V., Blacklow S.C., Theilgaard-Mönch K., Jensen L.J, & Olsen J.V. (2022). Phosphorylation of SHP2 at Tyr62 Enables Acquired Resistance to SHP2 Allosteric Inhibitors in FLT3-ITD–Driven AML. Cancer Research, 82(11), 2141-2155.
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5

Comprehensive Western Blotting Antibody Panel

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Primary antibodies used for Western blotting were as follows: p-Tyr (sc-508), GAPDH (sc-32233), SHP2 (sc-7384), MCL-1 (sc-819) from Santa Cruz Biotechnology; p-EGFR (1068) (3777), p-ErbB2 (1248) (2247), ErbB3 (4754), p-ErbB3 (1289) (4791), p-ErbB3 (1328) (14525), p-ErbB4 (1284) (4757), p-Akt (308) (4056), p-Akt (473) (4060), p-Erk (202/204) (4370), p-P70S6K (389) (9205), p-4EBP1 (37/46) (2855), BIM (2933), BCL-xL (2764), p-P90RSK (380) (9341), p-S6 (235/6) (4858), p-S6 (240/4) (5364), c-Myc (5605), p-SHP2 (542) (3751), GAB1 (3232), p-GAB1 (627) (3233), p-GAB1 (659) (12745), β-ACTIN (4970), from Cell Signaling Technology. Secondary antibodies used were mouse IgG (GE Healthcare Life Sciences; NXA931) and rabbit IgG (GE Healthcare Life Sciences; NA934). Alpelisib and trametinib were purchased from AbMole Biosciences. RMC-4550 was purchased from Selleckchem. The SHP2 inhibitor (SHP099) for cell culture and in vivo experiments was purchased from MedchemExpress and AbMole Biosciences and was dissolved in DMSO at a stock concentration of 10 mmol/L for in vitro experiments. Human recombinant growth factors epiregulin (EREG) was purchased from Sigma-Aldrich (SRP3033) and neuregulin-1 (5898-NR) was purchased from R&D Systems.
Kurupi R., Floros K.V., Jacob S., Chawla A.T., Cai J., Hu B., Puchalapalli M., Coon C.M., Khatri R., Crowther G.S., Egan R.K., Murchie E., Greninger P., Dalton K.M., Ghotra M.S., Boikos S.A., Koblinski J.E., Harada H., Sun Y., Morgan I.M., Basu D., Dozmorov M.G., Benes C.H, & Faber A.C. (2022). Pharmacologic Inhibition of SHP2 Blocks Both PI3K and MEK Signaling in Low-epiregulin HNSCC via GAB1. Cancer Research Communications, 2(9), 1061-1074.
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6

Authenticating and Culturing Cell Lines

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Human cancer cell lines originated from the CCLE [18 (link)] were authenticated by single-nucleotide polymorphism analysis and tested for mycoplasma infection using a PCR-based detection technology (RADIL, University of Missouri, Columbia, MO; now IDEXX Laboratories). All cell lines used were directly thawed from the CCLE collection stock and cultured as previously described [18 (link)] except SW1736 (Creative Bioarray). Cell lines were used within 15 passages of thawing and continuously cultured for less than 6 months. All small molecule inhibitors used were synthesized and structurally verified by NMR and LC/MS according to cited references at Novartis except RMC-4550 (Selleck Chemicals), NSC-87877 (Selleck Chemicals), and IIB-08 (Millipore Sigma). EGF and FGF19 were purchased from R&D Systems.
Lu H., Liu C., Huynh H., Le T.B., LaMarche M.J., Mohseni M., Engelman J.A., Hammerman P.S., Caponigro G, & Hao H.X. (2020). Resistance to allosteric SHP2 inhibition in FGFR-driven cancers through rapid feedback activation of FGFR. Oncotarget, 11(3), 265-281.
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7

In Vitro and In Vivo Compound Synthesis

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AZD4625, SHP099, and afatinib were synthesized in-house as per published methods (22, 23 (link)). RMC-4550 was purchased from Selleckchem. Anti-mPD-L1 (mouse IgG1, clone D265A), anti-mPD-1 (mouse IgG2a, clone RMP1-14), and isotype controls were synthesized in-house. For in vitro studies, compounds were solubilized in DMSO. For animal studies, AZD4625, afatinib, and RMC-4550 were formulated in 0.5% HPMC/0.1% Tween 80 (HPMC/Tween), SHP099 in 1% Pluronic and antibodies in PBS (phosphate-buffered saline).
Cells were routinely grown in RPMI or DMEM supplemented with 10% FCS and 2 mmol/L glutamine at 37°C in 5% CO2. Cells were used in studies between passage 2 and 10. All cell lines were authenticated by short tandem repeat analysis upon banking and/or stock replenishment and periodically screened by PCR for Mycoplasma and rodent pathogens for in vivo studies. Details of cells including cancer type and source are in Supplementary Table S1.
Chakraborty A., Hanson L., Robinson D., Lewis H., Bickerton S., Davies M., Polanski R., Whiteley R., Koers A., Atkinson J., Baker T., del Barco Barrantes I., Ciotta G., Kettle J.G., Magiera L., Martins C.P., Peter A., Wigmore E., Underwood Z., Cosulich S., Niedbala M, & Ross S. (2022). AZD4625 is a Potent and Selective Inhibitor of KRASG12C. Molecular Cancer Therapeutics, 21(10), 1535-1546.
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8

Targeted Therapies and MAPK Inhibitors

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The following targeted therapies were used in this study: erlotinib, gefitinib, osimertinib, crizotinib, alectinib, lorlatinib, sotorasib, adagrasib (Selleckchem). MAPK pathway inhibitors included: afatinib, erlotinib, RMC-4550, sotorasib, trametinib, AMG 511, AZD5363 (Selleckchem).
Vaccaro K., Allen J., Whitfield T.W., Maoz A., Reeves S., Velarde J., Yang D., Phan N., Bell G.W., Hata A.N, & Weiskopf K. (2023). Targeted therapies prime oncogene-driven lung cancers for macrophage-mediated destruction. bioRxiv.
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9

Authentication and Culture of Cell Lines for Research

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Cell lines were obtained from ATCC, Millipore Sigma or the Center for Molecular Therapeutics at the MGH Cancer Center (Boston, MA) (Crystal et al., 2014 (link)), which routinely performs cell line authentication testing by SNP and short tandem repeat analysis, and maintained in DMEM/F12 or RPMI 1640 supplemented with 10% fetal calf serum, and were not cultured longer than 6 months after receipt from cell banks. AMG 510 and MRTX849 used for in vitro and in vivo studies were purchased from MedChemExpress and ARS-1620, RMC-4550, BGJ398, and trametinib used for in vitro studies were purchased from Selleckchem. RM-018 used for in vitro studies and RMC-4550 used in in vivo studies were kindly provided by Revolution Medicines. Panitumumab was obtained from McKesson Pharmaceuticals.
Ryan M.B., Coker O., Sorokin A., Fella K., Barnes H., Wong E., Kanikarla P., Gao F., Zhang Y., Zhou L., Kopetz S, & Corcoran R.B. (2022). KRASG12C-independent feedback activation of wild-type RAS constrains KRASG12C inhibitor efficacy. Cell reports, 39(12), 110993.
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10

Acquired Resistance Generation Protocol

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SHP099, RMC-4550, cobimetinib, gilteritinib and KW-2449 were purchased from Selleckchem. II-B08 was purchased from Sigma Aldrich. Recombinant human, animal free EGF was purchased from Peprotech.
For acquired resistance generation, cells were initially treated with SHP099 at their respective IC50, followed by dose increase at each passage for over three weeks, stopping the increase at doses corresponding approximately 5x IC50 (2.5 μM for MV-4–11 and 10 μM for MOLM-13), and continuing cultivation at those doses of SHP099 for a maximum of 6 weeks.
Pfeiffer A., Franciosa G., Locard-Paulet M., Piga I., Reckzeh K., Vemulapalli V., Blacklow S.C., Theilgaard-Mönch K., Jensen L.J, & Olsen J.V. (2022). Phosphorylation of SHP2 at Tyr62 Enables Acquired Resistance to SHP2 Allosteric Inhibitors in FLT3-ITD–Driven AML. Cancer Research, 82(11), 2141-2155.
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