Nocodazole

Nocodazole (Oncodazole) is a rapidly-reversible inhibitor of microtubule. Nocodazole binds to β-tubulin and disrupts microtubule assembly/disassembly dynamics, which prevents mitosis and induces apoptosis in tumor cells. Nocodazole inhibits Bcr-Abl. IC50 & Target:IC50: 0.21 μM (ABL), 0.53 μM (ABL E255K), 0.64 μM (ABL T315I)^[1]
Microtubule^[2], CRISPR/Cas9^[6] In Vitro:Nocodazole exhibits good affinity toward c-KIT, with a K_d value of 1.6 μM in highly malignant human cancer cells. Nocodazole displays good binding affinity toward the components of the mitogen-activated protein kinase (MAPK) pathway, such as BRAF (K_d=1.8 μM), BRAF(V600E) (K_d=1.1 μM), MEK1 (K_d=1.7 μM), and MEK2 (K_d=1.6 μM)^[1]. Nocodazole has the highest affinity for αβ_IV and the lowest affinity for αβ_III^[2].
Nocodazole (1 nM) induces apoptosis of COLO 205 cancer cells^[3].
Nocodazole (≥ 30 μg/mL) significantly increases the percentage of annexin-V-binding cells without significantly modifying average forward scatter of human erythrocytes^[4].
In CHO cells, the addition of 1 nM Nocodazole, a concentration that suppresses microtubule dynamics, slows migration and increases the frequency and duration of resting states, but the directionality of the cells is maintained. In contrast to the effects of the low drug concentration, the addition of 70 nM Nocodazole, a concentration that eliminates the microtubule network, causes cells to move much more randomly, i.e., the directionality of the cells toward the wound is lost^[6]. In Vivo:Nocodazole (5 mg/kg/three times per week, i.p.) has antitumor effects in athymic mice bearing COLO 205 tumor xenografts. Nocodazole (1 nM) + R-41400 dramatically increase the levels of p21/CIP1 and p27/KIP1 protein in the tumor tissues^[3].