Vincristine binds to tubulin and inhibits the formation of microtubules, thereby inhibiting mitosis of the cancer cell. Vincristine can be used as a microtubule-destabilizing agent for research on the treatment of hematologic cancers, such as leukemia and

METHODS: Neuroblastoma cells SH-SY5Y were treated with Vincristine (0.001-10 µM) for 24-72 h. Cell viability was measured by MTT assay.
RESULTS: Vincristine inhibited the proliferation of SH-SY5Y cells in a dose- and time-dependent manner, with IC50s of 0.113 µM, 0.078 µM, and 0.051 µM at 24, 48, and 72 h, respectively. [1]
METHODS: Human leukemia cells MOLT-4 were treated with Vincristine (0.3-3 µM) and SAHA (500 nM) for 24-48 h. Cell cycle was detected using Flow cytometry.
RESULTS: Vincristine treatment induced an increase in the G2/M phase of the cell cycle compared to SAHA. the combination of Vincristine plus SAHA resulted in almost complete cell arrest in the G2/M phase after short-term treatment (24 h), followed by induction of the cells into the sub-G1 phase after long-term treatment (48 h). the combination of Vincristine and SAHA resulted in an increase in the G2/M phase of the cell cycle compared to SAHA. [2]

METHODS: To assay antitumor activity in vivo, Vincristine (0.025 mg/kg, intravenously, once weekly) and SAHA (200 mg/kg, orally, once daily) were administered to SCID mice bearing MOLT-4 xenografts for 24 days.
RESULTS: TGD did not improve in mice treated with Vincristine or SAHA alone. However, log-rank analysis showed that co-treatment exhibited significant anti-tumor activity in the MOLT-4 xenograft model. [2]

DMSO: 12 mg/mL (14.55 mM), Sonication is recommended.

10% DMSO+40% PEG300+5% Tween-80+45% Saline: 1 mg/mL (1.21 mM), Sonication is recommended.