Pd0325901

Manufactured by Chemietek

Sourced in Germany, United States

PD0325901 is a small-molecule inhibitor that targets the mitogen-activated protein kinase (MAPK) pathway. It acts as a potent and selective inhibitor of the MEK1/2 kinases, which are critical components of the MAPK signaling cascade. This compound is commonly used in cell-based assays and research applications to study the role of the MAPK pathway in various biological processes.

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Lab products found in correlation

7 protocols using pd0325901

Inhibitors of MAPK Pathway

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Trametinib, afatinib, erlotinib were purchased from Selleckchem (Selleckchem, Munich, Germany), PD0325901, refametinib (RDEA119), triciribine (MK2206) and selumetinib (AZD6244) were purchased from ChemieTek (Indianapolis, IN, USA).

Brauswetter D., Gurbi B., Varga A., Várkondi E., Schwab R., Bánhegyi G., Fábián O., Kéri G., Vályi-Nagy I, & Peták I. (2017). Molecular subtype specific efficacy of MEK inhibitors in pancreatic cancers. PLoS ONE, 12(9), e0185687.

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NCI-60 Cell Line Anticancer Drug Screen

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The complete NCI-60 panel was obtained from National Cancer Institute (NCI) Anticancer Drug Screen (Bethesda, MD, USA). Pancreatic cell lines were obtained from ATCC (Manassas, VA, USA). All cells were cultivated in RPMI including 2 mM glutamine and 11.11 mM glucose supplemented by 10% FBS and penicillin/streptomycin (GIBCO, Grand Island, NY, USA).
Romidepsin (depsipeptide, NSC 630176) was provided by the Cancer Therapy Evaluation Program, NCI. Tariquidar was provided by the NCI Anticancer Drug Screen. PD-0325901 (MEK inhibitor), MK-2206 (AKT inhibitor) were purchased from ChemieTek (Indianapolis, IN, USA). Glutaminase inhibitor 968 compound was obtained from Millipore (Burlington, MA, USA); oligomycinA, NAC, glutathione, dimethyl-α-ketoglutarate, dimethyl-glutamate, sodium citrate, and sodium acetate were obtained from Sigma-Aldrich (St. Louis, MO, USA); DPI, ML171, and etomoxir was obtained from Selleckchem (Houston, TX). MitoQ was provided by Dan L. Sackett (NIH, NICHD).
Unless otherwise specified, t-tests were performed to evaluate significance of results, and asterisks were added to graphs when the p-value was lower than 0.05.

Basseville A., Violet P.C., Safari M., Sourbier C., Linehan W.M., Robey R.W., Levine M., Sackett D.L, & Bates S.E. (2022). A Histone Deacetylase Inhibitor Induces Acetyl-CoA Depletion Leading to Lethal Metabolic Stress in RAS-Pathway Activated Cells. Cancers, 14(11), 2643.

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Evaluation of MEK Inhibitors and 5-Aza in Mice

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For binimetinib study, mice were treated twice a day (BID) using oral gavage with either vehicle (1% carboxymethyl cellulose (CMC) in water) or binimetinib at 20 mg/kg. Binimetinib was suspended in 1 % CMC. For selumetinib and PD-0325901 study, mice were treated once a day (QD) using oral gavage with either vehicle (50 mM 2-hydroxypropyl β cyclodextrin in water for selumetinib study or 5 % hydroxypropyl methylcellulose/2 % Tween80 in water for PD-0325901), selumetinib at 25mg/kg or PD-0325901 at 5 mg/kg. Selumetinib was suspended in 50 mM 2-hydroxypropyl β cyclodextrin and PD-0325901 was suspended in 5 % hydroxypropyl methylcellulose/2 % Tween80. Binimetinib (CT-A162), selumetinib (CT-A6244) and PD-0325901 (CT-PD03) were all purchased from ChemieTek. For 5-Aza study, mice were treated once a day using intraperitoneal injection (IP) with either vehicle (PBS) or 5-Aza at 5 mg/kg. 5-Aza was suspended in PBS and was purchased from SIGMA-ALDRICH (A2385). See Supplemental Information for details of treatment schedule.

Kunimoto H., Meydan C., Nazir A., Whitfield J., Shank K., Rapaport F., Maher R., Pronier E., Meyer S.C., Garrett-Bakelman F.E., Tallman M., Melnick A., Levine R.L, & Shih A.H. (2017). Cooperative Epigenetic Remodeling by TET2 Loss and NRAS Mutation Drives Myeloid Transformation and MEK Inhibitor Sensitivity. Cancer cell, 33(1), 44-59.e8.

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Evaluating Efficacy of Targeted Therapies

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NVP-BEZ235 (BEZ235), NVP-BKM120 (Buparlisib, BKM120), GSK1120212 (Trametinib, JTP-74057), PD0325901, and AZD6244 were purchased from Chemie Tek (Indianapolis, IN). Temozolomide, doxorubicin and paclitaxel were purchased from Sigma. For in vivo studies, BEZ235 and BKM120 were resuspended in NMP (N-methyl-2-pyrrolidone):PEG300 1:9 v:v, and GSK1120212 and PD0325901 were resuspended in 0.5% hydroxypropyl-methylcellulose (Sigma):0.2% Tween 80 (Sigma) (Gilmartin et al., 2011 (link); Kinross et al., 2011 (link)). BKM120, GSK1120212 and PD0325901 were given once daily by oral gavage at 10 ml/kg. Mice were treated with BEZ235 on a 5 days on, 2 days off schedule (Liu et al., 2009 (link)). Vehicle- and drug-treated mice were closely monitored on a daily basis for clinical signs as described above.

El Meskini R., Iacovelli A.J., Kulaga A., Gumprecht M., Martin P.L., Baran M., Householder D.B., Van Dyke T, & Weaver Ohler Z. (2014). A preclinical orthotopic model for glioblastoma recapitulates key features of human tumors and demonstrates sensitivity to a combination of MEK and PI3K pathway inhibitors. Disease Models & Mechanisms, 8(1), 45-56.

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Inhibitors of Cell Signaling Pathways

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Romidepsin was obtained from the Developmental Therapeutics Program of the National Cancer Institute (Bethesda MD). The MEK inhibitor PD-0325901, the AKT inhibitor MK-2206, the ERK inhibitor Vx-11e and the PI3K inhibitor GDC-0941 were purchased from ChemieTek (Indianapolis, IN). Q-VD-OPh was from R&D Systems (Minneapolis, MN). The dual pathway inhibitor, D-87503, was synthesized in-house by the Chemical Biology Laboratory, Center for Cancer Research (Frederick, MD).

Bahr J.C., Robey R.W., Luchenko V., Basseville A., Chakraborty A.R., Kozlowski H., Pauly G.T., Patel P., Schneider J.P., Gottesman M.M, & Bates S.E. (2016). Blocking downstream signaling pathways in the context of HDAC inhibition promotes apoptosis preferentially in cells harboring mutant Ras. Oncotarget, 7(43), 69804-69815.

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Ex vivo and in vivo drug administration

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For the drug administration under ex vivo culture conditions, (-)-Blebbistatin (FUJIFILM Wako Pure Chemical Corporation, #021-17041) and PD0325901 (FUJIFILM Wako Pure Chemical Corporation, #162-25291) were mixed in the culture medium. Equivalent amounts of DMSO were used as a vehicle control for each drug. For administration by oral gavage, PD0325901 (ChemieTek, #CT-PD03) in 30% PEG400, 0.5% Tween 80 in PBS was administered to pregnant mice at a dose of 25 mg/kg body weight twice a day (at 8:00 a.m and 6:00 p.m) for 2 days from E13.5, i.e., 4 times in total.

Yoshida T., Matsuda M, & Hirashima T. (2020). Incoherent Feedforward Regulation via Sox9 and ERK Underpins Mouse Tracheal Cartilage Development. Frontiers in Cell and Developmental Biology, 8, 585640.

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Ex vivo and in vivo PD0325901 administration

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For the drug administration under ex vivo culture conditions, (-)-Blebbistatin (FUJIFILM Wako Pure Chemical Corporation, #021-17041) and PD0325901 (FUJIFILM Wako Pure Chemical Corporation, #162-25291) were mixed in the culture medium. Equivalent amounts of DMSO were used as a vehicle control for each drug. For administration by oral gavage, PD0325901 (ChemieTek, #CT-PD03) in 30% PEG400, 0.5% Tween 80 in PBS was administered to pregnant mice at a dose of 25 mg/kg body weight twice a day (at 8:00am and 6:00pm) for two days from E13.5, i.e., 4 times in total.

Yoshida T., Matsuda M., & Hirashima T. (2020). Incoherent feedforward regulation via Sox9 and Erk underpins mouse tracheal cartilage development.

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