S2101

Manufactured by Merck Group

Sourced in United States

The S2101 is a general-purpose laboratory equipment designed for a variety of applications. It is a compact and versatile device that can be utilized in various research and testing environments. The core function of the S2101 is to provide a controlled environment for conducting experiments and analyses. The specific details and intended use of this product are not available.

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Lab products found in correlation

7 protocols using s2101

Epigenetic Modulators: Inhibitor Evaluation

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The H3K4 methyltransferase LSD1 inhibitor S2101 was purchased from Merck Millipore (Burlington, MA, USA). The LSD1 inhibitor GSK2879552, H3K27 methyltransferase EZH2 inhibitor GSK126, and H3K79 methyltransferase DOT1L inhibitor EPZ-5676 were all purchased from Chemietek (Indianapolis, IN, USA). The H3K9 methyltransferase G9a inhibitor UNC0638, H3K27 demethylase JMJD3/UTX inhibitor GSKJ1, DOT1L inhibitor SGC0946, and MYC inhibitor 10058-F4 were all purchased from Sigma-Aldrich (St. Louis, MO, USA).

Ishiguro K., Kitajima H., Niinuma T., Ishida T., Maruyama R., Ikeda H., Hayashi T., Sasaki H., Wakasugi H., Nishiyama K., Shindo T., Yamamoto E., Kai M., Sasaki Y., Tokino T., Nakase H, & Suzuki H. (2019). DOT1L inhibition blocks multiple myeloma cell proliferation by suppressing IRF4-MYC signaling. Haematologica, 104(1), 155-165.

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Cell Viability Assay with Chemotherapeutics

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Cells were seeded (2.0 Â 10 3 ) in 96-well microtiter plates with or without various concentrations of chemotherapeutic agents, including CDDP (Sigma-Aldrich), RN-1 (EMD-Millipore), and S2101 (EMD-Millipore), after shLSD1 or shNT infection or treatment with 4-hydroxy-tamoxifen (4-OHT), if applicable. After 72 hours, 10 mL of WST-8 (cell counting kit-8, Dojindo Laboratories) was added to each well, and the optical density was measured at 450 nm using a microplate reader (Bio-Rad Laboratories) 4 hours later. Results are expressed as a percentage of cell viability.

Wirawan A., Tajima K., Takahashi F., Mitsuishi Y., Winardi W., Hidayat M., Hayakawa D., Matsumoto N., Izumi K., Asao T., Ko R., Shimada N., Takamochi K., Suzuki K., Abe M., Hino O., Sekido Y, & Takahashi K. (2022). A Novel Therapeutic Strategy Targeting the Mesenchymal Phenotype of Malignant Pleural Mesothelioma by Suppressing LSD1. Molecular cancer research : MCR, 20(1).

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RGC Isolation and Optic Nerve Crush in Rats

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The present study utilized tranylcypromine, which is also known as 2-phenylcyclopropylamine hydrochloride (Sigma-Aldrich Corp., St Louis, MO, USA), and S2101, which is also known as LSD1 Inhibitor II (no. 489477; Merck Millipore, Billerica, MA, USA). The isolation of RGCs was performed using 2-day-old Sprague-Dawley (SD) rats (Kyudo Co., Ltd., Kumamoto, Japan), and 8-week-old male Slc:SD rats (Japan SLC, Inc., Shizuoka, Japan) were used for optic nerve crush experiments. All experimental procedures were performed in accordance with the ARVO Statement for the Use of Animals in Ophthalmic and Vision Research, and all experimental procedures were approved by the Animal Care Committee of Kumamoto University.

Tsutsumi T., Iwao K., Hayashi H., Kirihara T., Kawaji T., Inoue T., Hino S., Nakao M, & Tanihara H. (2016). Potential Neuroprotective Effects of an LSD1 Inhibitor in Retinal Ganglion Cells via p38 MAPK Activity. Investigative ophthalmology & visual science, 57(14).

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Pharmacokinetics of LSD1 Inhibitor Derivatives

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LSD1 inhibitors used in this study include RN-1 (Calbiochem, San Diego, CA), ORY-1001 (Cayman Chemical, Ann Arbor, MI), OG-L002 (Selleck Chemicals, Houston, TX), S2101 (Millipore, Temecula, CA) and two N-alkylated derivatives of S2101, S2116 and S2157 (synthesized by Tokyo Chemical Industry, Tokyo, Japan) (15 (link)). A pharmacokinetic study was conducted with a single intraperitoneal injection of either S2116 or S2157 at 50 mg/kg to nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mice (Charles River Laboratories, Wilmington, MA), followed by serial sampling of blood at 1, 2, 4, 8 and 24 hours after administration. Brain tissues were harvested at 0.5 hour and homogenized in deionized water. Plasma and brain samples were subjected to LC-MS/MS analysis to determine the concentrations of each drug.

Saito S., Kikuchi J., Koyama D., Sato S., Koyama H., Osada N., Kuroda Y., Akahane K., Inukai T., Umehara T, & Furukawa Y. (2018). Eradication of central nervous system leukemia of T-cell origin with a brain-permeable LSD1 inhibitor. Clinical cancer research : an official journal of the American Association for Cancer Research, 25(5), 1601-1611.

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Pharmacokinetic Analysis of S2157

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The drugs used in this study were tubastatin A (Enzo Life Science, Am Arbor, MI), panobinostat, bortezomib, OG-L002, GSK2879552 (Selleck Chemicals, Houston, TX), and S2101 (Millipore, Temecula, CA). S2116 and S2157 were synthesized by Tokyo Chemical Industry Co., Ltd. (TCI), and the syntheses will be described elsewhere (Niwa et al., manuscript in preparation). All drugs were dissolved in dimethyl sulfoxide at appropriate concentrations. A pharmacokinetic analysis was performed following a single intraperitoneal (i.p.) dose of S2157 (50 mg/kg), and serial blood samples were collected at 0.5, 1, 2, 4 and 8 hrs after administration. Blood samples were centrifuged, and the plasma samples were deproteinized with acetonitrile. The supernatants were subjected to LC-MS/MS analysis to determine the plasma S2157 concentrations.

Osada N., Kikuchi J., Umehara T., Sato S., Urabe M., Abe T., Hayashi N., Sugitani M., Hanazono Y, & Furukawa Y. (2018). Lysine-specific demethylase 1 inhibitors prevent teratoma development from human induced pluripotent stem cells. Oncotarget, 9(5), 6450-6462.

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Epigenetic Regulation in Cancer Cell Lines

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YB5, MCF7, and HL60 cells were cultured in L-15 medium with 10% FBS, DMEM with 10% FBS, and IMDM with 20% FBS, respectively. Cell lines were obtained from ATCC (2005–2007) and were authenticated at MD Anderson Cancer Center genomic core facility by DNA fingerprinting in 2011. Cells were treated daily with 100 nM decitabine (5-aza-CdR, Sigma-Aldrich), 10 µM S2101 (Millipore), 1 µM UNC0638 (Sigma-Aldrich), and 1 µM GSK343 (Sigma-Aldrich) for 96 hours, or 20 nM depsipeptide (Romidepsin, Sigma-Aldrich) was added for 24 hours. Primary normal breast epithelial cells were isolated as and cultured as described previously (31 (link)). RNA isolation, DNA isolation, qPCR, western blot, and pyrosequencing were carried out as described previously (6 (link)). Primer sequences are listed in Table S3.

Sato T., Cesaroni M., Chung W., Panjarian S., Tran A., Madzo J., Okamoto Y., Zhang H., Chen X., Jelinek J, & Issa J.P. (2016). Transcriptional Selectivity of Epigenetic Therapy in Cancer. Cancer research, 77(2), 470-481.

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Muscle Differentiation Regulation Dynamics

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Tranylcypromine hydrochloride, dexamethasone, insulin (bovine pancreas), testosterone, 3,3′,5-triiodo-L-thyronine, MG132 and cycloheximide were from Sigma-Aldrich. S2101 was from Millipore. 17-β-Estradiol was from Wako. The antibodies used were anti-LSD1 (Abcam, ab17721), anti-mono-methylated histone H3K4 (Abcam, ab8895), anti-di-methylated histone H3K4 (Millipore, 07-030), anti-tri-methylated histone H3K4 (Millipore, 07-473), anti-pan histone H3 (Abcam, ab1791), anti-myosin heavy chain (Santa Cruz, sc-20641), anti-slow-myosin (Sigma-Aldrich, M8421), anti-glucocorticoid receptor (Santa Cruz, sc-8992) and anti-PHF15 (JADE-2) (Sigma-Aldrich, HPA025959).

Anan K., Hino S., Shimizu N., Sakamoto A., Nagaoka K., Takase R., Kohrogi K., Araki H., Hino Y., Usuki S., Oki S., Tanaka H., Nakamura K., Endo F, & Nakao M. (2018). LSD1 mediates metabolic reprogramming by glucocorticoids during myogenic differentiation. Nucleic Acids Research, 46(11), 5441-5454.

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