Cmc na

Manufactured by Selleck Chemicals

Sourced in China

CMC-Na is a water-soluble polymer compound that serves as a thickening and suspending agent in various pharmaceutical and industrial applications. It functions by increasing the viscosity of aqueous solutions, allowing for the suspension and stabilization of solid particles or other ingredients. The core property of CMC-Na is its ability to modify the rheological characteristics of formulations.

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Lab products found in correlation

9 protocols using cmc na

In Vivo CRISPR Screening in Leukemia

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MOLM-13 luciferase-expressing cells were transduced with the lentiCRISPRV2-GFP construct with either nontargeting control or LZTR1 sgRNAs. GFP⁺ cells were sorted by FACS 2 days after transduction. One hundred thousand GFP⁺ cells with either sgNTC or sgLZTR1 were intravenously injected into sublethally irradiated (225 cGy) 8-week-old NSG mice. All whole-body bioluminescent imaging was performed by the intraperitoneal injection of Luciferin (Goldbio) at a 50 mg/kg concentration, and imaging was performed after 10 minutes using an IVIS imager. Engraftment was confirmed, and treatment began at day 10 after inoculation. Bioluminescent signals (radiance) were quantified using Living Image software with standard regions of interest rectangles.
For FLT3 inhibitor treatment, gilteritinib (Selleck Chemicals, S7754) was dissolved in 0.5% CMC-NA (Selleck Chemicals, S6703) to obtain a final concentration of 4 mg/mL. Upon disease onset as measured by bioluminescent imaging, mice were orally administrated with either 30 mg/kg gilteritinib or vehicle (0.5% CMC-NA) once daily for 5 days/week for 3 weeks.

Chen S., Vedula R.S., Cuevas-Navarro A., Lu B., Hogg S.J., Wang E., Benbarche S., Knorr K., Kim W.J., Stanley R.F., Cho H., Erickson C., Singer M., Cui D., Tittley S., Durham B.H., Pavletich T.S., Fiala E., Walsh M.F., Inoue D., Monette S., Taylor J., Rosen N., McCormick F., Lindsley R.C., Castel P, & Abdel-Wahab O. (2022). Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation. Cancer Discovery, 12(10), 2434-2453.

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Evaluating Sam68 knockdown on xenograft tumor growth

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Six‐week‐old female BALB/c nude mice were obtained from Beijing Vital River Laboratory Animal Technology Company (Beijing, China), randomized into two groups and anesthetized. NC‐65 cells (5 × 10⁶) transfected with control shRNA (sh‐Control) or Sam68 shRNA (sh‐Sam68) were subcutaneously injected into the rear back region of each mouse. When tumors reached 70‐100 mm³ at an average of 28 days later, each group of mice was randomized into two subgroups (n = 5 each) and treated with 0.5% carboxymethylcellulose sodium (CMC‐Na; Selleck, Shanghai, China; as placebo) or sunitinib (suspended in 0.5% CMC‐Na; 40 mg/kg/day) by gavage. Tumor volume was measured every 2–3 days and calculated as follows: volume = length×(width)²/2. The mice were euthanized 4 weeks after sunitinib treatment, and then tumors were resected and subsequently weighed. All animal experimental procedures were approved by the Laboratory Animal Ethics Committee of Sun Yat‐sen University Cancer Center.

Wu Z., Peng Y., Xiong L., Wang J., Li Z., Ning K., Deng M., Wang N., Wei W., Li Z., Dong P., Yu C., Zhou F, & Zhang Z. (2022). Role of Sam68 in Sunitinib induced renal cell carcinoma apoptosis. Cancer Medicine, 11(19), 3674-3686.

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LZTR1 Knockout Impacts AML Progression

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MOLM-13 luciferase-expressing cells were transduced with lentiCRISPRV2-GFP construct with either non-targeting control (NTC) or LZTR1 sgRNAs. GFP+ cells were sorted by FACS 2 days after transduction. 100,000 GFP+ cells with either sgNTC or sgLZTR1 were intravenously injected into sub-lethal irradiated (225 cGy) 8 week-old NOD scid gamma (NSG) mice respectively. All whole-body bioluminescent imaging was performed by intraperitoneally injection of Luciferin (Goldbio) at a 50 mg/kg concentration and imaging was performed after 10 mins using an IVIS imager. Engraftment was confirmed and treatment began at Day 10 post-inoculation. Bioluminescent signals (radiance) were quantified using Living Image software with standard regions of interests (ROI) rectangles.
For FLT3 inhibitor treatment, gilteritinib (Selleckchem, S7754) was dissolved in 0.5% CMC-NA (Selleckchem, S6703) to obtain a final concentration of 4 mg/ml. Upon disease onset as measured by bioluminescent imaging, mice were orally administrated with either 30 mg/kg gilteritinib or vehicle (0.5% CMC-NA) once daily for 5 days/week for 3 weeks.

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Preparation of Pharmacological Agents

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Ebosin (50 mg/ml), 1487B (20 mM) and Lipopolysaccharide (LPS, 1 mg/ml, Beyotime, China) were dissolved in Phosphate-Buffered Saline (PBS, Corning, Manassas, United States). Filtered through a 0.22 μm filter, they were stored at −80°C until use. Trichomicin (4 mM) and PMA (10 mM, Sigma, GER) were dissolved in DMSO, and were further diluted with medium (for cell assays). Sodium carboxymethyl cellulose (CMC-Na, Selleckchem, United States) was dissolved in double distilled water at 0.5 mg/ml and used as a solvent for animal experiments.

Chen Y., Zhuang Z., Yang J, & Bai L. (2021). Screening of Microbial Natural Products and Biological Evaluation of Trichomicin as Potential Anti-Cytokine Storm Agents. Frontiers in Pharmacology, 12, 770910.

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Investigating Protein Signaling Pathways

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Lapatinib (Selleck Chemicals, #S2111), alpelisib (BYL719, Selleck Chemicals, #S2814) and cobimetinib (GDC‐0973, Selleck Chemicals, #S8041) were dissolved in DMSO (Sigma, #D2650) for in vitro studies and in 0.5% CMC‐Na (Selleck Chemicals, #S6703) for in vivo studies. The primary antibodies used for western blotting included those against p‐HER2‐Tyr1221/1222 (Abcam, #ab131102, 1:500), HER2 (CST, #2242, 1:1000), pIGF‐1R (CST, #3021, 1:500), IGF‐1R (CST, #9750, 1:500), p‐AKT‐Ser473 (CST, #4060, 1:1000), p‐AKT‐Thr308 (CST, #13038, 1:1000), AKT (CST, #4691, 1:1000), p‐ERK‐Tyr202/204 (CST, #4370, 1:1000), ERK (CST, #4695, 1:1000), p‐MEK‐Ser217/221 (CST, #9154, 1:1000), MEK (CST, #9126, 1:1000), p‐S6‐Ser240/244 (CST, #5364, 1:1000), S6 (CST, #2217, 1:1000), HA‐tag (CST, #3724, 1:1000), p110α (CST, #4249, 1:1000) and vinculin (CST, #13901, 1:2000), and HRP‐conjugated goat‐anti‐rabbit secondary antibody (Invitrogen, #31460, 1:5000). Exposure time of each band depends on the saturation degree of chemiluminescent, generally no more than 1 min.

Guo L., Li X., Yang Y., Lu X., Han X., Lang G., Chen L., Shao Z, & Hu X. (2021). Large‐scale genomic sequencing reveals adaptive opportunity of targeting mutated‐PI3Kα in early and advanced HER2‐positive breast cancer. Clinical and Translational Medicine, 11(11), e589.

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Optimized Allopurinol and Cisplatin Protocol

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The FDA-approved drug library and allopurinol were purchased from Selleck Chemicals. allopurinol was dissolved with dimethyl sulfoxide (DMSO) for cell experiments. For animal study, allopurinol was dissolved in 0.5% sodium carboxymethyl cellulose (CMC-Na, purchased from Selleck Chemicals). Cisplatin was purchased from HANSON Pharma and dissolved in 0.9% sodium chloride.
The following antibodies were used in this study: The TMTC3 (sc-398137) and VEGFA (sc-152) antibodies were purchased from Santa Cruz. The β-actin (3700 S) and STAT3 (8768s) antibodies were purchased from Cell Signaling Technology. The HIF-1α (20960-1-AP), IMPDH2 (67663-1-Ig) antibodies were purchased from Proteintech. The p-STAT3 (bs-1658R) antibody was purchased from Bioss. The Flag (F3165) and β-tubulin (T5201) antibodies were purchased from Sigma. The p-JAK2 (ab32101) antibody was purchased from Abcam. The JAK2 (A19629) antibody was purchased from ABclonal Technology.
The siRNAs of IMPDH2 were synthesized by GenePharma (Suzhou, China). The siRNA sequences for IMPDH2 and primers for qPCR were listed in Supplementary Table 1.

Yuan H., Zhao Z., Xu J., Zhang R., Ma L., Han J., Zhao W., Guo M, & Song Y. (2023). Hypoxia-induced TMTC3 expression in esophageal squamous cell carcinoma potentiates tumor angiogenesis through Rho GTPase/STAT3/VEGFA pathway. Journal of Experimental & Clinical Cancer Research : CR, 42, 249.

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Signaling Pathway Profiling of LPS-Induced Inflammation

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Lipopolysaccharides (LPS) were purchased from Solarbio (Lot:L8880). Sorafenib (BAY 43-9006, CAS No.284461-73-0), and CMC-Na (Sodium carboxymethyl cellulose, CAS No. 9004-32-4) were purchased from Selleck. Abs specific for Phospho-Lyn (70926S), Lyn (4576S), Phospho-p38 (4631S), p38 (8690S), Phospho-Erk1/2 (9101S), Erk1/2 (9102S), Phospho-JNK (9255S), JNK (9252S), Phospho-Akt (4060S), Akt (4691S), Phospho-p65 (3033S), p65 (8642S), and Phospho-c-Jun (4691S) were obtained from Cell Signaling Technology. GAPDH (Cat No. 60004-1-Ig) was purchased from Proteintech.

Li X., Xu M., Shen J., Li Y., Lin S., Zhu M., Pang Q., Tan X, & Tang J. (2022). Sorafenib inhibits LPS-induced inflammation by regulating Lyn-MAPK-NF-kB/AP-1 pathway and TLR4 expression. Cell Death Discovery, 8, 281.

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Postnatal CSF1R Inhibitor Treatment

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CSF1R inhibitor PLX5622 (Selleck, China) was given to the CX3CR1-GFP mice. From P12, when the mice were taken back to room air, the natal mice were treated daily with oral gavage with 100 μL of solution (10 mg/mL) in CMC-Na (Selleck, China) per 10 g of body weight (at the dose of 100 mg/kg body weight).

Zhou Z., Jing Y., Niu Y., Chang T., Sun J., Guo C., Wang Y, & Dou G. (2022). Distinguished Functions of Microglia in the Two Stages of Oxygen-Induced Retinopathy: A Novel Target in the Treatment of Ischemic Retinopathy. Life, 12(10), 1676.

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Pharmacological Modulation of Cellular Pathways

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CHIR-99021 (S1263), IWP-2 (S7085), TEPP-46 (S7032), QX-77 (S6797), CMC-Na (S6703), MG-132 (S2619), leupeptin (S7380), Baf-A1 (S1413), E64d (S7393), cycloheximide (NSC-185) were purchased from Selleck. Phenylephrine hydrochloride (R815791) was purchased from MACKLIN.

Tang Y., Feng M., Su Y., Ma T., Zhang H., Wu H., Wang X., Shi S., Zhang Y., Xu Y., Hu S., Wei K, & Xu D. (2023). Jmjd4 Facilitates Pkm2 Degradation in Cardiomyocytes and Is Protective Against Dilated Cardiomyopathy. Circulation, 147(22).

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