HONE1, HK1, CNE1, CNE2, SUNE1, C666-1, and NPC43 NPC cell lines, and immortalized nasopharyngeal epithelial cell lines NP69 and NP460 were cultured as previously described [4 (link),18 (link)]. Cell lines were authenticated by and obtained from the Hong Kong NPC AoE Cell Line Repository. HK11.19 is a HONE1/chromosome 11 microcell hybrid cell line (MCH) that was established by the transfer of an additional intact human chromosome 11 into HONE1 and expressed physiological levels of THY1 (in the recipient HONE1 cells, THY1 expression is downregulated by promoter hymermethylation, and human THY1 maps to chromosome 11q22.3) [4 (link),19 (link)]. Recombinant human PDGF-BB was obtained from PeproTech (PeproTech, Rocky Hill, NJ, USA, #100-14B-10). KX2-391 (Selleckchem, Houston, TX, USA, #S2700), bosutinib (Selleckchem, Houston, TX, USA, #S1014), and saracatinib (Selleckchem, Houston, TX, USA, #1006) were prepared in DMSO at a concentration of 10 mM for an in vitro assay. For the in vivo assay, KX2-391 was first dissolved in DMSO to a concentration of 85 mg/mL, then formulated with PEG-300 (Sigma-Aldrich, St. Louis, MI, USA, #202371) and PBS before injection following the manufacturer’s instructions (the injection solution contains 4% DMSO, 30% PEG-300, and 66% PBS).
Peg300
Manufactured by Merck Group
Sourced in United States, Germany
PEG300 is a polyethylene glycol with an average molecular weight of 300 g/mol. It is a clear, colorless, and odorless liquid. PEG300 is commonly used as a solvent, plasticizer, and surfactant in various pharmaceutical, cosmetic, and industrial applications.
Automatically generated - may contain errors
Lab products found in correlation
Dimethyl sulfoxide (dmso), by Merck Group (11 mentions)
Tween 80, by Merck Group (11 mentions)
Peg400, by Merck Group (7 mentions)
N methyl pyrrolidone (nmp), by Merck Group (5 mentions)
Cremophor el, by Merck Group (4 mentions)
Matrigel, by Corning (3 mentions)
Methylcellulose, by Merck Group (3 mentions)
Hydroxypropyl β cyclodextrin, by Merck Group (3 mentions)
Paclitaxel, by Merck Group (2 mentions)
4 oht, by Merck Group (2 mentions)
Matrigel, by BD (2 mentions)
Ketoconazole, by MedChemExpress (2 mentions)
Corn oil, by Merck Group (2 mentions)
Anti btk, by Cell Signaling Technology (2 mentions)
Polysorbate 80 tween 80, by Merck Group (2 mentions)
Fvb wild type mice, by Taconic Biosciences (2 mentions)
Cobicistat, by MedChemExpress (2 mentions)
Propylene glycol, by Merck Group (2 mentions)
N methyl 2 pyrrolidone, by Merck Group (2 mentions)
Oxaliplatin, by Merck Group (2 mentions)
82 protocols using peg300
1
Establishing and Characterizing NPC Cell Lines
2
Drug Formulation and Preparation Protocol
3
Generating Colon Carcinoma and Metastasis Models
4
Sodium Acetate, Propionate, and Butyrate in Endometriosis
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From day 0 to day 21 after endometriosis induction, mice were provided drinking water containing 300 mM sodium acetate (36 (link)), sodium propionate (36 (link)), or sodium butyrate (19 (link)) (all from Sigma-Aldrich) (36 (link)). These solutions were changed every week. The GPR43 antagonist GLPG0974 (10 mg/kg) and GPR109A inhibitor MB (10 mg/kg) were dissolved in dimethyl sulfoxide (vehicle) with 30% PEG-300 (Sigma-Aldrich) and administered via daily intra-peritoneal injection. Trichostatin-A (1 mg/kg), SAHA (25 mg/kg), MS-275 (20 mg/kg), valproic acid (500 mg/kg), and RGFP0966 (25 mg/kg) (all from Sigma-Aldrich) were dissolved in dimethyl sulfoxide with 30% PEG-300 and administered from day 0 to day 21 via daily intra-peritoneal injection. Similar amount of dimethyl sulfoxide with 30% PEG-300 was administered as vehicle.
5
Epigenetic Modulation in Mice
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The class II HDAC inhibitor TMP269 was purchased from Selleckchem (S7324), the DNMT inhibitor 5-Aza was from Sigma-Aldrich (A3656), PEG300 was from Merck (8.17019), NMP was from Sigma-Aldrich (328634). Intraperitoneal injections (30-gauge needle) started at the sixth week of age and continued daily for 10–15 weeks. Mice received vehicle (PEG300 and NMP), TMP269 (25 mg/kg), 5-Aza (0.05 mg/kg), a combination of the two compounds (TMP26 + 5-Aza, 25 mg/kg and 0.05 mg/kg, respectively). TMP269 and 5-Aza were diluted in PEG300 (500 µl/kg) and NMP (250 µl/kg). The final volume of drug or vehicle injected per mouse was 750 µl/kg body weight.
6
Evaluating Combination Therapy for Breast Cancer
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67NR cells were injected into the mammary fat pads of mice at day 0 as described [48 (link)]. The mice were treated 3x/week (up to six treatments) from day 7 with vehicle (97% polyethylene glycol 300 (PEG300, Merck) in DMSO (V/V), per oral (p.o), 0.15 mL, n=11), ATX-101 (6 mg/kg net peptide, intraperitoneal (i.p), 0.2 mL, n=11)(APIM Therapeutics, Trondheim, Norway), AEE788 (25 mg/kg, p.o, 0.15 mL, n=16) or APIM-peptide/AEE788 combination (n=16). Tumors were measured (3x/week, electronic Vernier Caliper) and volumes calculated using the formula for a spheroid: (2a=tumor width, 2b=tumor height). A subgroup of these mice were harvested 24 hours after the third treatment (n=6 in each treatment group). The tumors from these mice were used to study the kinome using the multiplexed-inhibitory bead (MIB)-assay. The remaining mice were used to follow tumor growth and overall survival (vehicle: n=5, ATX-101: n=5, AEE788: n=10, combination: n=10). Mice were euthanized using carbon dioxide (2L/min) and tumors harvested when they reached their humane end point (judged by tumor burden and health status). Treatments were stopped when tumors reached 900 mm3 or at day 19.
7
Evaluating Combination Therapy in Mice
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Mice with tumour volumes of ∼200–300 mm3 were divided across treatment arms and treated for up to 30 days. BYL719 (Selleckchem, S2814) was prepared in 5% DMSO (Sigma, 200‐664‐3) + 40% PEG300 (Merck, 25322‐68‐3) + 5% Tween80 (Merck, P4780‐500ML) + 50% ddH2O, according to manufacturer instructions. INK128 (Selleckchem, MLN0128) was resuspended in DMSO (Sigma, 200‐664‐3). Both components were diluted in .9% saline and administered daily via oral gavage (INK128, .3 mg/kg + BYL719, 25 mg/kg). Nivolumab (anti‐PD‐1) was provided by Bristol‐Myers Squibb (10 mg/mL solution for infusion), diluted in .9% saline and administered by intraperitoneal (i.p.) injection 2 times per week (10 mg/kg). Tumours were measured 3 times per week with a calipre and volume was calculated using the formula: length × width2 × π/6. Mice were euthanised after 30 days of treatment or before, whenever tumours reached a volume of 2000 mm3, or in case of any intolerable discomfort. Tumours were harvested and processed into formalin‐fixed, paraffin‐embedded (FFPE) blocks for immunohistochemistry (IHC) or multiplex immunofluorescence (mIF) stainings.
8
Venetoclax and Ruxolitinib in Allogeneic SCT
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The BCL2 inhibitor venetoclax and JAK1/2 inhibitor ruxolitinib (SelleckChem, Houston, TX) were used to treat C57BL/6 WT mice for two days prior to alloSCT. venetoclax (100 mg/kg) and its vehicle (60% phosal R 50 PG (Merck, Germany), 30% polyethylene glycol (PEG) 400 (Merck, Germany), 10% ethanol) were administered by oral gavage once daily for two days, with a cumulative total dose of 4 mg. ruxolitinib (180 mg/kg) and its vehicle (2% DMSO, 30% PEG 300 (Merck, Germany), ddH2O) were administered twice a day by oral gavage for two days, with a cumulative total dose of 14.4 mg.
9
Crizotinib Efficacy in ADK-VR2 Xenograft
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Crizotinib was formulated in 5% DMSO, 30% PEG300 (Merck) and 65% double distilled water. ADK-VR2 cell line was injected subcutaneously at the dose of 106 cells in NSG female mice (37-week-old) to assess tumor growth. The animals were randomized into control and treated group. Five mice were enrolled in each test group in order to have an 80% chance of showing, with a 5% significance, a 65% of success in the experimental group. Control group was not treated (n=5), treated mice received crizotinib 50 mg/kg daily per os by gavage starting from 12 days after cell injection (5 mice were enrolled but a censored mouse at 6 week from cell injection was not included in tumor growth analysis; n=4). Animals were checked weekly, and tumors were measured with calipers. Tumor volume was calculated as described in the previous section and mice were sacrificed as previously described. Blinding to assess the outcome of in vivo experiments was not done. To minimize potential confounders, we used labelled cages. Labels had a different colour for each group.
10
Preparation of Inhibitors for In Vivo and In Vitro Experiments
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The compound 33i (2-{3-(3-fluorophenethyloxy)phenylamino}benzamide) was gently provided by Dr. Suzuki and prepared in saline with 5% dimethyl sulfoxide (DMSO; Sigma-Aldrich, Saint Louis, MO, USA) and 18% Tween 80 (Sigma-Aldrich) for in vivo experiments. For in vitro studies, 33i was dissolved in DMSO. The SIRT2-peripheral inhibitor AGK-2 (2-cyano-3-[5-(2,5-dichlorophenyl)-2-furanyl]-N-5-quinolinyl-2-propenamide) was purchased from Selleck Chemicals (Houston, TX, USA) and prepared in saline with 5% DMSO (Sigma-Aldrich) and 30% PEG-300 (Merck KGaA, Darmstadt, Germany).
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