Vincristine sulfate  (Synonyms: Leurocristine sulfate; NSC-67574 sulfate; 22-Oxovincaleukoblastine sulfate)

Vincristine (Leurocristine; NSC-67574; 22-Oxovincaleukoblastine) sulfate is a microtubule inhibitor that disrupts microtubule polymerization by binding to β-tubulin (with a K_i of 85 nM in bovine), arrests the cell cycle and induces apoptosis. Vincristine sulfate inhibits cell replication, tumor blood flow and the proliferation of various cancer cells, while triggering effects such as oxidative stress, inflammation, calcium overload, epithelial-mesenchymal transition and peripheral neuropathic pain. Vincristine sulfate upregulates the expression of various transporters and nuclear receptors, and enriches gastric cancer stem-like cells. Vincristine sulfate is used in research related to various tumors including acute lymphoblastic leukemia, lymphoma, melanoma, gastric cancer, solid tumors and sarcomas^{[1][2][3][4][5][6][7][8]}.

Vincristine sulfate (100 nM; 0-48 h) induces apoptosis in G1-phase enriched ALL-2 and ALL-5 cells without mitotic arrest (no MPM2 staining); it also induces apoptosis in G2-M phase enriched ALL-2 and ALL-5 cells in the presence of mitotic arrest (enhanced MPM2 staining)^[2].
Acute treatment with Vincristine sulfate (1 μM; 2 h) inhibits the proliferation of B16 melanoma cells, and its potency is lower than that of vinblastine (HY-13780) and vindesine (HY-16514)^[4].
Vincristine sulfate (5-2000 nM; 24-48 h) induces mRNA expression of ABCC2, ABCC3, PXR and CYP3A4 (10 nM, 48 h) in LS174T and A549 cells, and regulates the expression of ABCB1 and ABCC2 in Caco2 cells in a concentration- and time-dependent manner^[5].
Treatment of SGC7901 cells with Vincristine sulfate (0.5-1.5 μg/mL) upregulates the mRNA expression of Snail, Twist, MRP and Pgp, indicating that the epithelial-mesenchymal transition and multidrug resistance pathways are activated^[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Vincristine (5-10 mg/kg; i.v.) sulfate induces significant tumor necrosis and reduces tumor blood flow in mice subcutaneously implanted with colon 38 adenocarcinoma^[3].
Vincristine (10 mg/kg; i.p.) sulfate induces significant tumor necrosis in subcutaneous multidrug-resistant P388 leukemia subline xenografts in mice^[3].
Vincristine (75 μg/kg; i.p.; daily; 10 days) sulfate induces peripheral neuropathic pain in mice, which is characterized by behavioral, electrophysiological, histopathological, oxidative stress and inflammatory changes^[7].
Vincristine (0.1 mg/kg; i.p.; daily; 7 days) sulfate induces dose- and duration-dependent peripheral neuropathic pain and oxidative stress in mice^[8].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

923.04

C₄₆H₅₈N₄O₁₄S

2068-78-2

Solid

White to off-white

CC[C@@]1(C=CCN2CC3)[C@@]2([H])[C@@]3(C4=CC([C@](C5=C6C7=CC=CC=C7N5)(C[C@](C[C@](CC)(O)C8)([H])C[N@@]8CC6)C(OC)=O)=C(OC)C=C4N9C=O)[C@]9([H])[C@](C(OC)=O)(O)[C@@H]1OC(C)=O.O=S(O)(O)=O

Room temperature in continental US; may vary elsewhere.

4°C, sealed storage, away from moisture and light

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

• [1]. Douer D, et al. Efficacy and Safety of Vincristine Sulfate Liposome Injection in the Treatment of Adult Acute Lymphocytic Leukemia. Oncologist. 2016;21(7):840-847.  [Content Brief]

  [2]. Kothari A, et al. Cell Cycle-Dependent Mechanisms Underlie Vincristine-Induced Death of Primary Acute Lymphoblastic Leukemia Cells. Cancer Res. 2016;76(12):3553-3561.  [Content Brief]

  [3]. Baguley BC, et al. Inhibition of growth of colon 38 adenocarcinoma by vinblastine and colchicine: evidence for a vascular mechanism. Eur J Cancer. 1991;27(4):482-487.  [Content Brief]

  [4]. Jordan MA, et al. Comparison of the effects of vinblastine, vincristine, vindesine, and vinepidine on microtubule dynamics and cell proliferation in vitro. Cancer Res. 1985;45(6):2741-2747.  [Content Brief]

  [5]. Huang R, et al. Vincristine transcriptional regulation of efflux drug transporters in carcinoma cell lines. Biochem Pharmacol. 2006;71(12):1695-1704.  [Content Brief]

  [6]. Xue Z, et al. Identification of cancer stem cells in vincristine preconditioned SGC7901 gastric cancer cell line. J Cell Biochem. 2012;113(1):302-312.  [Content Brief]

  [7]. Gong SS, et al. Neuroprotective Effect of Matrine in Mouse Model of Vincristine-Induced Neuropathic Pain. Neurochem Res. 2016;41(11):3147-3159.  [Content Brief]

  [8]. Babu A, et al. Effect of curcumin in mice model of vincristine-induced neuropathy. Pharm Biol. 2015;53(6):838-848.  [Content Brief]