Vinblastine inhibits microtubule formation and suppresses nAChR activity with IC50 of 8.9 μM, used to treat certain kinds of cancer.

nAChR:8.9 μM

Vinblastine does not depolymerize spindle microtubules, yet it powerfully blocks mitosis (for example, IC50 0.8 nM in HeLa cells) and cells die by apoptosis[2]. In NB4 cells, vinblastine produces alteration of p53 and DNA fragmentation. Vinblastine treatment has an antiproliferative effect via the induction of apoptosis producing Bax/Bcl-2 imbalance. Vinblastine treatment suppresses NFκB expression and depresses NFκB-DNA binding activity while maintaining JNK activation that subsequently results in apoptotic response through caspase-dependent pathway[3]. Vinblastine is found to trigger apoptosis as evidenced by the loss of mitochondrial membrane potential, the release of both cytochrome c and apoptosis inducing factor, activation of caspase-9 and 3, and cleavage of Poly (ADP-ribose)-Polymerase[4].

Vinblastine is a widely used anticancer drug with undesired side effects. Its conjugation with carrier molecules could be an efficient strategy to reduce these side effects[5].

Six-well treatment plates are set up that contained 5 × 104 cells/mL in each well, suspended in 3 mL culture medium, and these are treated with vinblastine for 3 h followed by 21 h growth. (Only for Reference)

Ethanol: 6 mg/mL (7.4 mM), Sonication is recommended.

DMSO: 42 mg/mL (51.79 mM), Sonication is recommended.