Methyl cellulose 400 solution

Manufactured by Fujifilm

Sourced in Japan

Methyl Cellulose 400 Solution is a viscous, clear liquid product manufactured by Fujifilm. It is primarily used as a laboratory reagent and excipient in various applications. The solution provides a consistent viscosity to aid in experimental procedures and formulations.

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Lab products found in correlation

13 protocols using methyl cellulose 400 solution

Antiviral Efficacy of AMNV and VACV

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AMNV (Maruho Co., Ltd., Kyoto, Japan) was suspended in 0.5 % (w/v) Methyl Cellulose 400 Solution (Fujifilm Wako Pure Chemical Corporation, Osaka, Japan) containing 1 % (w/v) Tween 80 (Nacalai Tesque, Inc., Kyoto, Japan). VACV (Fujifilm Wako Pure Chemical Corporation) was suspended in 0.5 % (w/v) Methyl Cellulose 400 Solution. The dosing volume was 10 mL/kg body weight and the test drugs were orally administered twice daily for 5 days from 3, 4, or 5 days after HSV-1 infection. The detailed administration schedule in each experiment is shown in Fig. 1A and3 A.

Ueda Y., Uta D., Tanbo S., Kawabata A., Kanayama S., Osaki M., Nozawa N., Matsumoto T, & Andoh T. (2020). Inhibitory effect of amenamevir on acute herpetic pain and postherpetic neuralgia in mice infected with herpes simplex virus-1. Journal of dermatological science, 98(1).

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Corticosterone Oral Administration Protocol

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Corticosterone (Fujifilm Wako, Japan) at 0.2 mg/body was dissolved in 0.1 ml of 0.5 w v⁻¹% methylcellulose 400 solution (Fujifilm Wako, Japan) and administered orally. In the control group, only 0.1 ml of vehicle was administered.

Chihara I., Negoro H., Kono J., Nagumo Y., Tsuchiya H., Kojo K., Shiga M., Tanaka K., Kandori S., Mathis B.J, & Nishiyama H. (2023). Glucocorticoids coordinate the bladder peripheral clock and diurnal micturition pattern in mice. Communications Biology, 6, 81.

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Xenograft Tumor Growth Inhibition by DS-7423

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Specific pathogen-free female nude mice (BALB/cAJcl-nu/nu), 6 weeks old, were purchased from CLEA Japan, Inc (Tokyo, Japan). Subcutaneous xenograft tumors in the mice were established by the injection of a 100-μL suspension containing 5×10⁶ cells of the TOV-21, RMG-I, or ES-2 lines in PBS. Tumors were removed after exponential growth, cut into 3-mm pieces, and transplanted subcutaneously into other mice for RMG-I cells. DS-7423 was suspended in 0.5 w/v% Methyl Cellulose 400 solution (Wako Pure Chemical Industries, Ltd.) Oral daily administration of DS-7423 started 8–22 days later, following the injection of the cells (5–6×10⁶ cells/0.1 mL). One week after tumor transplantation, mice were assigned randomly to one of the three treatment regimens: (1) non-treated control, (2) DS-7423 (1.5 mg/kg), (3) DS-7423 (3 mg/kg), and (4) DS-7423 (6 mg/kg). Each treatment group consisted of five mice. DS-7423 was injected orally (p.o.) once a day. Tumor volumes (in mm³) were calculated by the formula: ([major axis] × [minor axis]²/2). After the treatment, the tumors were removed and analyzed by western blotting. Tumor weight (wet weight) was measured, and the average weight was calculated for each group.

Kashiyama T., Oda K., Ikeda Y., Shiose Y., Hirota Y., Inaba K., Makii C., Kurikawa R., Miyasaka A., Koso T., Fukuda T., Tanikawa M., Shoji K., Sone K., Arimoto T., Wada-Hiraike O., Kawana K., Nakagawa S., Matsuda K., McCormick F., Aburatani H., Yano T., Osuga Y, & Fujii T. (2014). Antitumor Activity and Induction of TP53-Dependent Apoptosis toward Ovarian Clear Cell Adenocarcinoma by the Dual PI3K/mTOR Inhibitor DS-7423. PLoS ONE, 9(2), e87220.

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Opioid Receptor Agonist Pharmacokinetics

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For the in vitro assays, salt-free UD-030 (gift from UBE Corporation, Yamaguchi, Japan), DAMGO (MOP-selective agonist), and U-69593 (a KOP-selective agonist; Sigma Aldrich, St. Louis, MO, USA) were dissolved in dimethylsulfoxide. DADLE, DPDPE (DOP agonists; Sigma Aldrich), and nociceptin (NOP endogenous agonist; Enzo Life Sciences, Farmingdale, NY, USA) were dissolved in each assay buffer that is described below.
For the pharmacokinetic and pharmacological studies, morphine hydrochloride (Takeda Pharma, Osaka, Japan) was dissolved and diluted in saline and administered intraperitoneally (i.p.) in a volume of 10 mL/kg body weight. UD-030 and naltrexone hydrochloride (Tocris Bioscience, Bristol, UK) were dissolved and diluted in sterilized 0.5 w/v% Methyl Cellulose 400 Solution (FUJIFILM Wako Pure Chemical Co., Osaka, Japan) and administered orally (p.o.) in a volume of 10 mL/kg body weight. All experiments were conducted with a dose of morphine (10 mg/kg) that is sufficient to elicit CPP.

Ide S., Iwase N., Arai K., Kojima M., Ushiyama S., Taniko K, & Ikeda K. (2023). Inhibitory Effects of a Novel μ-Opioid Receptor Nonpeptide Antagonist, UD-030, on Morphine-Induced Conditioned Place Preference. International Journal of Molecular Sciences, 24(4), 3351.

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Breast Cancer Xenograft Model Establishment and Drug Evaluation

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Animal studies were approved by the IACUC and MD Anderson Animal Care and Use Committee. Female athymic homozygous nu/nu mice, age 4–6 weeks old, were purchased from MD Anderson’s Department of Experimental Radiation Oncology for the SUM190PT, SUM149PT, and MDA-MB-231 xenograft experiments. Mice were housed under pathogen-free conditions and treated in accordance with NIH guidelines. To establish breast cancer xenografts, SUM190PT (2x10⁶ cells/100 μL), SUM149PT (5x10⁶ cells/100 μL), or MDA-MB-231 (5x10⁶ cells/100 μL) cell suspensions were injected into one site in the abdominal mammary fat pad of each mouse. We observed 100% tumor incidence for all three cell lines. Drug treatments via daily oral gavage started when the tumors were approximately 100–150 mm³. We used 0.5% (w/v) methyl cellulose 400 solution (Wako Pure Chemical Industries, Ltd., Osaka, Japan) plus 0.25% Tween 20 as drugs vehicle. Tumor volume [V = 0.5 x (L x W²)] and body weight were measured twice weekly. Drug treatment continued for 28 days (SUM190PT), 56 days (SUM149PT), or 42 days (MDA-MB-231), and then mice were euthanized. Tumor samples were collected at biopsy, and sections preserved both by freezing and paraffin block embedding for downstream applications.

Torres-Adorno A.M., Lee J., Kogawa T., Ordentlich P., Tripathy D., Lim B, & Ueno N.T. (2017). Histone deacetylase inhibitor enhances the efficacy of MEK inhibitor through NOXA-mediated MCL1 degradation in triple-negative and inflammatory breast cancer. Clinical cancer research : an official journal of the American Association for Cancer Research, 23(16), 4780-4792.

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Pharmacokinetics of Cpd-7 in Mice

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Cpd-7 was orally administered to 35-week-old female NZB/W F1 mice at 100 mg kg⁻¹ dissolved in 0.5 w/v% Methyl Cellulose 400 Solution (WAKO, Japan). Blood was collected over 24 h from the isoflurane-anesthetized mice via the jugular vein. The plasma samples were separated by centrifugation. Cpd-7 was extracted from the plasma samples by protein precipitation with methanol and measured using LC/MS/MS (HPLC: SHIMADZU CORPORATION, Japan; MS: AB Sciex Pte. Ltd., Japan). The lower limit of quantification was set at 5 ng/mL.

Tojo S., Zhang Z., Matsui H., Tahara M., Ikeguchi M., Kochi M., Kamada M., Shigematsu H., Tsutsumi A., Adachi N., Shibata T., Yamamoto M., Kikkawa M., Senda T., Isobe Y., Ohto U, & Shimizu T. (2020). Structural analysis reveals TLR7 dynamics underlying antagonism. Nature Communications, 11, 5204.

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Analgesic Drug Evaluation in SNL Rat Model

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Five drugs were tested in this study: duloxetine, celecoxib (Tokyo Chemical Industry Co., Ltd, Tokyo, Japan), pregabalin (ChemFaces, Hubei, China), venlafaxine, and tramadol (Sigma-Aldrich, St. Louis, MO, USA). All drugs were dissolved in distilled water (Otsuka Pharmaceutical Factory Inc, Tokushima, Japan) containing 0.5% w/v methylcellulose 400 solution (Fujifilm Wako Pure Chemical Corporation, Osaka, Japan) and administered orally (5 mL/kg) on Day 7 after SNL.

Nozawa K., Karasawa Y., Shidahara Y, & Ushida T. (2022). Efficacy of Combination Therapy with Pregabalin in Neuropathic Pain: A Preclinical Study in the Rat L5 Spinal Nerve Ligation Model. Journal of Pain Research, 15, 3469-3478.

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Pesticide Preparation and Dosing

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Acephate (O,S‐dimethyl N‐acetylphosphoramidothioate), chlorpyrifos (O,O‐diethyl O‐3,5,6‐trichloro‐2‐pyridyl phosphorothioate), fenobucarb (O‐sec‐butylphenyl methylcarbamate) and molinate (S‐ethyl perhydroazepin‐1‐carbothioate) were purchased from Wako Pure Chemical Industries (Osaka, Japan); all were 99% pure. Acephate was dissolved in saline, and other chemicals were suspended in 0.5% w/v methyl cellulose 400 solution (Wako). Control experiments were conducted with appropriate vehicles. All dosing solutions were prepared immediately before use.

Suemizu H., Kawai K., Murayama N., Nakamura M, & Yamazaki H. (2018). Chimeric mice with humanized liver as a model for testing organophosphate and carbamate pesticide exposure. Pest Management Science, 74(6), 1424-1430.

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Acetaminophen and MDMA-Induced Liver Injury

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To induce liver injury, acetaminophen (H0190, Tokyo Chemical Industry Co., Tokyo, Japan) or 4,4′-methylene dianiline (M0220, Tokyo Chemical Industry Co.) was administered at 3 g/kg or 300 mg/kg, respectively by gavage. As a vehicle control group, 0.5 (w/v)% methylcellulose 400 solution (133-17815, Fujifilm Wako Pure Chemical Corporation, Osaka, Japan) was given at 10 µl/g. Only those rats in the experimental groups that were subjected to RNA sequencing had fasted between 21:00 and 9:00, which was the administration time.

Morita K., Mizuno T., Azuma I., Suzuki Y, & Kusuhara H. (2023). Rat deconvolution as knowledge miner for immune cell trafficking from toxicogenomics databases. Toxicological Sciences, 197(2), 121-131.

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Synthesis and Suspension Preparation

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BXM was synthesized at Shionogi & Co., Ltd. (Osaka, Japan) [16 ]. OSP was purchased from Sequoia Research Products (Oxford, UK). Suspensions of BXM and solution of OSP were prepared with 0.5% methylcellulose 400 solution (MC, FUJIFILM Wako Pure Chemical Corporation, Osaka, Japan). The administration dose was determined by body weight (1mL per 100 g body weight).

Fukao K., Ando Y., Noshi T., Kitano M., Noda T., Kawai M., Yoshida R., Sato A., Shishido T, & Naito A. (2019). Baloxavir marboxil, a novel cap-dependent endonuclease inhibitor potently suppresses influenza virus replication and represents therapeutic effects in both immunocompetent and immunocompromised mouse models. PLoS ONE, 14(5), e0217307.

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