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Vincristine sulfate

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Vincristine sulfate is a cytotoxic agent used in the treatment of various types of cancer. It is a sterile powder that is reconstituted and administered intravenously. The active ingredient is vincristine sulfate, which is derived from the periwinkle plant.

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Lab products found in correlation

Dimethyl sulfoxide (dmso), by Merck Group (6 mentions) Methanol, by Merck Group (3 mentions) N hexane, by Merck Group (3 mentions) Docetaxel, by Merck Group (2 mentions) Dexamethasone (dex), by Merck Group (2 mentions) Vincristine, by Merck Group (2 mentions) Doxorubicin, by Merck Group (2 mentions) Paclitaxel, by Merck Group (2 mentions) Ethyl acetate, by Merck Group (2 mentions) Chloroform, by Merck Group (2 mentions) Entinostat, by Selleck Chemicals (1 mentions) Osteocalcin antibody, by Santa Cruz Biotechnology (1 mentions) Horseradish peroxidase conjugated secondary antibody, by Cell Signaling Technology (1 mentions) Fitc conjugated anti mouse secondary antibody, by Jackson ImmunoResearch (1 mentions) β catenin, by BD (1 mentions) Semmes weinstein monofilaments, by Stoelting (1 mentions) Verapamil hydrochloride, by Merck Group (1 mentions) Fetal bovine serum (fbs), by HiMedia (1 mentions) Piperine, by Merck Group (1 mentions) Colchicine, by HiMedia (1 mentions)

Spelling variants of this product

Vincristine (167 citations) Vincristine sulfate salt (2 citations)

26 protocols using vincristine sulfate

1

Cytotoxicity Assessment of V. rotundfolia Leaves

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Cytotoxic activity of extract and fractions of V. rotundfolia (leaves) against breast cancer cell line, MCF-7, was determined using MTS assay (16 ). Cells were counted using CountessTM automated cell counter and cultured onto 96-well plates at a cell density of 6 × 103 cells/well and incubated at 37 °C in a humidified atmosphere of 5% (v/v) CO2 for 24 h. When the cell growth reached 80% confluency, the media was discarded and replaced with fresh media containing different concentrations of each sample and incubated for 24, 48, and 72 h individually. All dried fractions diluted in dimethyl sulfoxide (DMSO) (Sigma, USA) and in all cases the concentration of DMSO in every well was 1% (v/v). Vincristine sulfate (Sigma, USA) used as positive control in the cytotoxicity screening assay. After treatment, 20 μL of MTS reagent was added at each incubation period for 3 h at 37 °C. Finally, the absorbance was recorded at 490 nm using ELISA 96-well plate reader (Multiskan Thermofisher, USA).
Chaudhry G.E., Jan R., Mohamad H, & Tengku Muhammad T.S. (2019). Vitex rotundifolia fractions induce apoptosis in human breast cancer cell line, MCF-7, via extrinsic and intrinsic pathways. Research in Pharmaceutical Sciences, 14(3), 273-285.
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2

Evaluating HDAC Inhibitors in aRMS Cells

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The chemotherapy agent vincristine sulfate, used here in the treatment of Rh30 and U23674 cells, was obtained from Sigma (V8879). HDAC inhibitors (HDACi used in this study were were purchased from SelleckChem: entinostat (also known as MS-275, a class I HDACi; cat. no. S1053), panobinostat (a broad-spectrum HDACi; S1030), SAHA (suberoylanilide hydroxamic acid, a class and class II HDACi; S1047), CUDC-907 (a PI3K inhibitor and class I and II HDACi; S2759), and CUDC-101 (a class I and II HDACi and inhibitor of epidermal growth factor receptor family members EGFR and HER2; S1194). aRMS cell lines and primary tumor cell cultures were treated with these drugs at their clinically relevant Cmax (maximum plasma concentrations) or, where Cmax is not yet reported, their determined IC25 (25% inhibiting concentration).
Bharathy N., Berlow N.E., Wang E., Abraham J., Settelmeyer T.P., Hooper J.E., Svalina M.N., Ishikawa Y., Zientek K., Bajwa Z., Goros M.W., Hernandez B.S., Wolff J.E., Rudek M.A., Xu L., Anders N.M., Pal R., Harrold A.P., Davies A.M., Ashok A., Bushby D., Mancini M., Noakes C., Goodwin N.C., Ordentlich P., Keck J., Hawkins D.S., Rudzinski E.R., Chatterjee B., Bächinger H.P., Barr F.G., Liddle J., Garcia B.A., Mansoor A., Perkins T.J., Vakoc C.R., Michalek J.E, & Keller C. (2018). The HDAC3-SMARCA4-miR27a axis promotes expression of the PAX3:FOXO1 fusion oncogene in rhabdomyosarcoma. Science signaling, 11(557), eaau7632.
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3

Synthesis and Use of Disorazole C1 Compounds

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(−)-CP2-disorazole C1 (1) and 2 were synthesized as previously described (Figure 1) [21 (link)]. Vincristine sulfate and docetaxel were obtained from Sigma-Aldrich Co. (St. Louis, MO). For in vitro use, compounds were resuspended in dimethyl sulfoxide (DMSO; Sigma) and the DMSO concentration never exceeded 0.1% in any experiment.
Wu S., Guo Z., Hopkins C.D., Wei N., Chu E., Wipf P, & Schmitz J.C. (2015). Bis-cyclopropane analog of disorazole C1 is a microtubule-destabilizing agent active in abcb1-overexpressing human colon cancer cells. Oncotarget, 6(38), 40866-40879.
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4

Monoclonal Antibody Staining Reagents

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Mouse monoclonal antibodies against ANX2, p11 and β-catenin were obtained from BD Biosciences (San Jose, CA). Rabbit polyclonal GAPDH antibody and horseradish peroxidase conjugated secondary antibodies were from Cell Signaling Technology (Lexington, KY). FITC-conjugated anti-mouse secondary antibody was purchased from Jackson ImmunoResearch Laboratories (West Grove, PA). Alexa Flour 488 conjugated secondary antibody was from Life Technologies (Grand Island, NY). FITC-conjugated human CD45 and APC-conjugated mouse CD45 antibodies were obtained from eBioscience (San Diego, CA). Osteocalcin antibody was from Santa Cruz Biotechnology (Dallas, TX) and CD45 antibody was from Leica (Buffalo Grove, IL). Isotype-matched control IgG, dexamethasone and vincristine sulfate were obtained from Sigma-Aldrich (St. Louis, MO). 5-Benzyl-4-methyl-2-(toluene-4-sulfonylamino)-thiophene-3-carboxylic acid amide was purchased from Asinex (Winston-Salem, NC).
Gopalakrishnapillai A., Kolb E.A., Dhanan P., Mason R.W., Napper A, & Barwe S.P. (2015). Disruption of Annexin II /p11 Interaction Suppresses Leukemia Cell Binding, Homing and Engraftment, and Sensitizes the Leukemia Cells to Chemotherapy. PLoS ONE, 10(10), e0140564.
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5

Vincristine-Induced Neuropathy Model

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The vincristine-induced peripheral neuropathy model was used in this experiment. Baseline response to mechanical stimulation of the hind paw was established on day 1. Either vincristine sulfate (Sigma Aldrich Co., St. Louis, MO, USA) or saline was administered by injection to create the neuropathy model, as described previously.15 (link) In brief, 0.1 mg/kg/day vincristine was administered intraperitoneally for 5 days. Following cessation for 2 days, injection was continued for the next 5 days. On day 15, the paw withdrawal threshold (PWT) was measured with von Frey filaments (Semmes-Weinstein monofilaments, Stoelting Co., Wood Dale, IL, USA). If a foot withdrawal response occurred when a filament less than 0.6 g was applied to the hind paw, it was considered that mechanical allodynia had developed.
Lee J.Y., Sim W.S., Cho N.R., Kim B.W., Moon J.Y, & Park H.J. (2020). The Antiallodynic Effect of Nefopam on Vincristine-Induced Neuropathy in Mice. Journal of Pain Research, 13, 323-329.
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6

Investigating Multidrug Resistance Mechanisms

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Verapamil hydrochloride, piperine, vincristine sulfate, rhodamine 123 (Rho123), dimethyl sulfoxide (DMSO), RIPA buffer, and protease inhibitor cocktail were purchased from Sigma-Aldrich, USA. Colchicine, Dulbecco’s Modified Eagle Medium (DMEM), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), trypsin-ethylene diamine tetra acetic acid (Trypsin–EDTA) solution, penicillin–streptomycin solution, phosphate-buffered saline (PBS), acridine orange (AO), ethidium bromide (EB), 4′,6-Diamidino-2-Phenylindole, dihydrochloride (DAPI), Bradford reagent and fetal bovine serum (FBS) were obtained from HiMedia (Mumbai, India). Nitrocellulose membrane was purchased from GE healthcare, USA. Anti-P-gp (D-11), and anti-tubulin antibodies were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA).
Syed S.B., Arya H., Fu I.H., Yeh T.K., Periyasamy L., Hsieh H.P, & Coumar M.S. (2017). Targeting P-glycoprotein: Investigation of piperine analogs for overcoming drug resistance in cancer. Scientific Reports, 7, 7972.
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7

Multidrug Resistance Inhibitor Mechanisms

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MOX and the PGP inhibitors R(+)-verapamil monohydrochloride monohydrate, vincristine sulfate, doxorubicin, etoposide, actinomycin D, colchicine, vinblastine, rhodamine 123, quinidine, quinine and forskolin were purchased from Sigma Life Science. All compounds were dissolved in a final concentration of 0.25 v/v of dimethylsulfoxide (DMSO). The concentrations of MOX and inhibitors are indicated within each experiment. In addition to being inhibitors of PGP proteins, these inhibitors have an additional mechanism of action including targeting of ion channels (i.e., verapamil, quinidine, quinine), tubulin (i.e., vincristine, vinblastine, colchicine), DNA replication (i.e., actinomycin, doxorubicin, etoposide) and enzymes (i.e., rhodamine, forskolin) (Palmiera et al., 2012 (link)).
Bygarski E.E., Prichard R.K, & Ardelli B.F. (2014). Resistance to the macrocyclic lactone moxidectin is mediated in part by membrane transporter P-glycoproteins: Implications for control of drug resistant parasitic nematodes. International Journal for Parasitology: Drugs and Drug Resistance, 4(3), 143-151.
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8

Cytotoxicity Assay with Chemotherapeutics

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Tiopronin, N-Acetylcysteine, vincristine sulfate, and paclitaxel were obtained from Sigma Chemical, (St. Louis, MO). Mycoplasma Removal Agent (MRA) was obtained from BioRad, (Hercules, CA). Cell Titer Glo reagent was purchased from Promega Corporation (Madison, WI).
Huff L.M., Horibata S., Robey R.W., Hall M.D, & Gottesman M.M. (2020). Mycoplasma Infection Mediates Sensitivity of Multidrug-Resistant Cell Lines to Tiopronin: A Cautionary Tale. Journal of medicinal chemistry, 63(3), 1434-1439.
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9

Culturing B-cell Lymphoma Cell Lines

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Established human cell lines derived from germinal center B-cell (GCB) (SU-DHL-10),
activated B-cell (ABC) (HBL1) diffuse large B-cell lymphoma (DLBCL), mantle cell
lymphoma (MCL) (MINO), splenic marginal zone lymphoma (SMZL) (parental VL51, VL51
idelalisib resistant clone, VL51 ibrutinib resistant clone) were cultured in culture
RPMI-1640 media supplemented with fetal bovine serum (10%),
penicillin–streptomycin–neomycin (∼5,000 units of penicillin, 5 mg
of streptomycinm and 10 mg of neomycin/mL, Sigma), and l-glutamine (1%).
Vincristine sulfate was purchased from Sigma-Aldrich. Cell line identities were
confirmed by CellCheck test (IDEXX, BioResearch, Ludwigsburg, Germany). All compounds
were dissolved in dimethyl sulfoxide to obtain a stock concentration of 10 mM.
Spanò V., Rocca R., Barreca M., Giallombardo D., Montalbano A., Carbone A., Raimondi M.V., Gaudio E., Bortolozzi R., Bai R., Tassone P., Alcaro S., Hamel E., Viola G., Bertoni F, & Barraja P. (2020). Pyrrolo[2′,3′:3,4]cyclohepta[1,2-d][1,2]oxazoles, a New Class of Antimitotic Agents Active against Multiple Malignant Cell Types. Journal of Medicinal Chemistry, 63(20), 12023-12042.
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10

Anticancer Drug Library Screening

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A custom‐arrayed anticancer library was used (Bezu et al, 2018). In addition, bortezomib (5043140001); cisplatin (C2210000); crizotinib (PZ0191); dactinomycin (A1410); daunorubicin (D0125000); docetaxel (01885); doxorubicin (D1515); epirubicin (E9406); flavopiridol (F30055); ISRIB (SML0843); β‐lapachone (L2037); mitoxantrone (M6545); mycophenolate mofetil (SML0284); nonoxynol‐9 (542334); paclitaxel (T7191); thapsigargin (T9033); tunicamycin (T7765); vinblastine sulfate (V1377); and vincristine sulfate (V0400000) have been bought from Sigma‐Aldrich. Dactolisib (BEZ235) (sc‐364429) came from Santa Cruz biotechnology (Dallas, TX, USA). Oxaliplatin came from Accord Healthcare (Ahmedabad, India). Topotecan (609699), 7‐hydroxystausporine (UCN‐01) (72271), becatecarin (101524), 5‐fluorodeoxycytidine (B86) (515328), and RH‐1 (394347) were kindly provided by the National Cancer Institute (NCI). Lurbinectedin (PM01183) came from PharmaMar (Madrid, Spain).
Humeau J., Sauvat A., Cerrato G., Xie W., Loos F., Iannantuoni F., Bezu L., Lévesque S., Paillet J., Pol J., Leduc M., Zitvogel L., de Thé H., Kepp O, & Kroemer G. (2020). Inhibition of transcription by dactinomycin reveals a new characteristic of immunogenic cell stress. EMBO Molecular Medicine, 12(5), e11622.
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