Vincristine sulfate

Catalog No.S1241 Batch:S124110

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Technical Data

Formula

C46H58N4O14S
Molecular Weight 923.04 CAS No. 2068-78-2
Solubility (25°C)* In vitro DMSO 100 mg/mL (108.33 mM)
Water 100 mg/mL (108.33 mM)
Ethanol Insoluble
In vivo (Add solvents to the product individually and in order)
Homogeneous suspension
CMC-NA
≥5mg/ml Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description Vincristine sulfate is an inhibitor of polymerization of microtubules by binding to tubulin with IC50 of 32 μM in a cell-free assay. Vincristine sulfate induces apoptosis.
Targets
Microtubules [1]
(Cell-free assay)
32 μM
In vitro Vincristine inhibits net addition of tubulin dimers at assembly ends of steady-state microtubules with Ki of 85 nM. [1] At low concentrations, Vincristine stabilizes the spindle apparatus resulting in failure of the chromosomes to segregate leading to metaphase arrest and inhibition of mitosis. At higher concentrations, Vincristine may disrupt and induce total depolymerization of microtubules. [2] Vincristine induces apoptosis in tumor cells and inhibits SH-SY5Y cell proliferation with IC50 of 0.1 μM. Vincristine induces mitotic arrest and promots the expression of caspase-3 and -9 and cyclin B, while decreasing the expression of cyclin D. [4] Vincristine induced neurotoxicity is caused by interference with microtubule function, which results in blockage of axonal transport and thus in axonal degeneration. [5]
In vivo Vincristine (3 mg/kg) administrated by a single i.p. injection to mice bearing bilateral subcutaneous xenografts Rh12 or Rh18, induces mean growth delay of >120 and >52 day, and repopulating fractions of 0.06% and 5%, respectively. [6] Vincristine acts on subcutaneous colon 38 tumors in mice by host cell-mediated vascular effects as well as by direct tubulin-mediated cytotoxicity. Vincristine (5 mg/kg) reduces tumor blood flow of tumors by nearly 75% . [7]

Protocol (from reference)

Cell Assay:[1]
  • Cell lines

    B16 melanoma cell

  • Concentrations

    10 nM

  • Incubation Time

    3 days

  • Method

    Cells are plated in 2 mL of medium in 35-mm plates at a concentration of about 5 × 104 cells/mL and grow for 24 h at 37 ℃ in an atmosphere of 5% CO2 and 95% air. Then medium is replaced with fresh medium lacking or containing 4 nM drug and proliferation is continued for 3 days. Cell counts are done each day in a Coulter Counter after detaching the cells with trypsin and EDTA.
Animal Study:[6]
  • Animal Models

    Human rhabdomyosarcoma xenografts Rh12

  • Dosages

    3 mg/kg

  • Administration

    A single i.p. administration

References

  • https://pubmed.ncbi.nlm.nih.gov/3986806/
  • https://pubmed.ncbi.nlm.nih.gov/10226730/
  • https://pubmed.ncbi.nlm.nih.gov/23129065/
  • https://pubmed.ncbi.nlm.nih.gov/558047/
  • https://pubmed.ncbi.nlm.nih.gov/3190743/
  • https://pubmed.ncbi.nlm.nih.gov/1827725/

Customer Product Validation

<p>for HXO-RB44 cells, IC50 values for VCR were changed in the different SG600 treatment groups. The results are representative of three independent  experiments and of f our replicates in each experiment.</p>

Data from [ Int J Mol Sci , 2012 , 13, 10736-10749 ]

Plk inhibitor cooperates with chemotherapeutic agents. Conditional patched mutant tumor cells were treated with increasing concentrations of the chemotherapeutic agents vincristine alone or in combination with 10 nMol/L BI-2536. Cells were cultured for 48 hours, pulsed with 3H-Td, and harvested for analysis of 3H-Td incorporation at 66 hours.

Data from [ , , Cancer Research, 2013, 73(20): 6310-22 ]

Determination of mutation frequencies in cells treated with chemotherapy drugs following caspase inhibition. TK6 cells were incubated with no inhibitor or 10 μM QVD then treated with the following drug doses: 300 ng/ml TRAIL, 0.7 μM cisplatin, 0.5 μM temozolomide, 3 nM doxorubicin, 0.5 nM SN38 or 0.07 nM vincristine. (a) Caspase activity was assessed by luminescent detection of Caspase-3/-7 Glo reagent after 5 h. After 24- h treatment, (b) clonogenicity assays were performed to determine the proportion of cells maintaining clonogenic competency after treatment, whereas (c) surviving cells were grown in 6TG to select for the emergence of any HPRT mutants. (d) Clonogenicity and (e) HPRT mutation assays were repeated in CASP3/7 DKO lines in the same manner. Error bars represent mean±S.E.M. from at least three independent experiments. Two-sided T-tests were used to calculate P-values.

Data from [ , , Cell Death & Disease, 2017, doi:10.1038/cddis.2017.454 ]

Discrimination of micronuclei induced by EMS and VCR in V79-hCYP2E1-hSULT1A1 cells as CENP-B negative or positive. The cells were treated with EMS (5 mM) or VCR (5 nM) for 6 h, followed by a recovery period of 18 h. They were stained for CENP-B (green) and β-tubulin (red) by the immunofluorescence assays, as described in Section 2.5. DNA was stained with DAPI (blue). The vertical and horizontal arrows indicate CENP-B-negative and CENP-B-positive micronuclei, respectively.

Data from [ , , Chemosphere, 2018, 210:467-475 ]

Selleck's Vincristine sulfate has been cited by 128 publications

Molecular mechanisms of unique therapeutic potential of CUDC-907 for MEF2D fusion-driven BCP-ALL [ Signal Transduct Target Ther, 2025, 10(1):230] PubMed: 40695793
SOD2 is a regulator of proteasomal degradation promoting an adaptive cellular starvation response [ Cell Rep, 2025, 44(4):115434] PubMed: 40131931
Mitochondrial dysfunction fuels drug resistance in adult T-cell acute lymphoblastic leukemia [ J Transl Med, 2025, 23(1):542] PubMed: 40369632
N-glycosylation of ephrin B1 modulates its function and confers therapeutic potential in B-cell lymphoma [ J Biol Chem, 2025, S0021-9258(25)00076-6] PubMed: 39864628
Targeting RPLP2 Triggers DLBCL Ferroptosis by Decreasing FXN Expression [ Biomedicines, 2025, 13(6)1320] PubMed: 40564039
Small nuclear ribonucleoprotein polypeptide B2 regulated by SNHG4/miR-204-5p axis inhibits ferroptosis to aggravate the progression of hepatocellular carcinoma [ Discov Oncol, 2025, 16(1):1349] PubMed: 40670855
Preclinical efficacy of combinatorial B7-H3 CAR T cells and ONC206 against diffuse intrinsic pontine glioma [ bioRxiv, 2025, 2025.09.01.673023] PubMed: 40950080
Proteomic analysis of the urothelial cancer landscape [ Nat Commun, 2024, 15(1):4513] PubMed: 38802361
Orthogonal proteogenomic analysis identifies the druggable PA2G4-MYC axis in 3q26 AML [ Nat Commun, 2024, 15(1):4739] PubMed: 38834613
EFNB1 levels determine distinct drug response patterns guiding precision therapy for B-cell neoplasms [ iScience, 2024, 27(1):108667] PubMed: 38155773

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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

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