tcsc1893 Nocodazole

Nocodazole is a rapidly-reversible inhibitor of microtubule polymerization, which exhibits good potency against ABL, ABL(E255K), and ABL(T315I) with IC₅₀ values of 0.21 μM, 0.53 μM, and 0.64 μM, respectively, and increases CRISPR/Cas9-mediated editing frequencies.

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]. After release from the nocodazole block, cells synchronized in mitosis remaine sensitive to very low concentrations of paclitaxel for < 30 min, the time required for spindle formation, yet remains sensitive to vinblastine for > 90 min^[3]. Nocodazole (1 nM) induces apoptosis of COLO 205 cancer cells^[4]. Nocodazole (≥ 30 µg/mL) significantly increases the percentage of annexin-V-binding cells without significantly modifying average forward scatter of human erythrocytes^[5].

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) + ketoconazole dramatically increase the levels of p21/CIP1 and p27/KIP1 protein in the tumor tissues^[4].