tubulin β

Thiabendazole (2-(4-Thiazolyl)benzimidazole) is a benzimidazole derivative with anthelminthic property.

Combretastatin A4 (CA4) is a microtubule-targeting agent that binds β-tubulin (Kd: 0.4 μM).

Batabulin (T138067) is an antitumor compound that binds covalently and selectively to a subset of the β-tubulin isotypes, disrupting microtubule polymerization. This disruption affects cell morphology, induces cell-cycle arrest, and ultimately leads to apoptotic cell death.

Entasobulin is an inhibitor of β-tubulin polymerization. It has a potential anticancer activity.

Tubulin inhibitor 24 is a potent compound that inhibits tubulin polymerization.

Tubulin inhibitor 6 (iHAP1) is an inhibitor of tubulin and a potent inhibitor of multiple cancer cell lines.

Tubulin inhibitor 1 is an inhibitor of tubulin, inhibits tubulin polymerization, with potent anti-tumor activity, induces cellular apoptosis causes and cellular mitotic arrest in the G2/M phase.

Tubulin Inhibitor 11 is a potent, orally active agent that inhibits tubulin by targeting the Colchicine binding site. It impedes tubulin polymerization, leading to mitotic blockade and apoptosis.

Tubulin inhibitor 35 (Tubulin IN 35) is a potent dual inhibitor of topoisomerase I and microtubule protein polymerization with antitumor activity, inhibits migration and invasion of MGC-803 and RKO cell lines, interrupts the cell cycle and induces apoptosis.

Tubulin inhibitor 32 is an orally active novel microtubule inhibitor with antiproliferative and antitumor activity, inhibits microtubule polymerization, induces apoptosis and cell cycle arrest in G2/M phase.

Tubulin polymerization-IN-47 is a tubulin polymerization inhibitor and mitotic inhibitor with antitumor activity and inhibitory effects on neuroblastoma cancer cell proliferation, with IC50s of 7 and 12 nM for Chp-134 and Kelly cell lines, respectively. Tubulin polymerization-IN-47 is a candidate compound for the treatment of hepatocellular carcinoma, colon cancer, lung cancer and breast cancer.

Tubulin polymerization-IN-55 is a potent Tubulin Polymerization inhibitor with potential anti-angiogenic and anti-tumor activity, demonstrating anti-proliferative effects against A549, K562, HepG2, MDA-MB-231, and HFL-1.

Tubulin polymerization-IN-62 (Compound 14b) is a microtubule polymerization inhibitor (IC50 of 7.5 μM) that also functions as a degradation agent for α-/β-tubulin. This compound suppresses the proliferation of cancer cells MCF-7, A549, and HCT-116 with IC50 values of 32, 60, and 29 nM, respectively. It induces G2/M phase cell cycle arrest and inhibits the migration of MCF-7 cells. In a 4T1 syngeneic mouse model, Tubulin polymerization-IN-62 demonstrates antitumor efficacy with a tumor growth inhibition rate (TGI) of 74.27%.

Tubulin polymerization-IN-83 (Compound A23) is a flavonol derivative with antifungal activity against various plant pathogenic fungi. It has an EC50 of 0.338 μg/mL against Botrytis cinerea. The compound works by targeting β-tubulin, disrupting hyphal morphology, and affecting cell membrane permeability, while posing low ecological risk.

Tubulin Polymerization-IN-2 is a powerful anticancer agent that targets β-tubulin, exhibiting an IC 50 of 0.92 μM. It demonstrates promising efficacy against a range of cancer cell lines including leukemia, non-small cell lung, renal, prostate, and breast cancers [1].

Tubulin polymerization-IN-53 (compound 4b) inhibits β-tubulin polymerization, arrests the cell cycle at the G2/M stage, and demonstrates antiproliferative efficacy against the MDA-MB-231 cell line, with an IC50 value of 3.24 μM [1].

Tubulin inhibitor 43 exhibits significant antitumor activity by impeding the proliferation and growth of cancer cells through the inhibition of β-microtubulin activity, ultimately inducing apoptosis [1].

Tubulin inhibitor 7 is an inhibitor of tubulin and a potent inhibitor of multiple cancer cell lines (tubulin polymerization (IC50: 0.52 μM), K562 cell growth (IC50: 11 nM)).

Tubulin polymerization-IN-68 (compound 32) serves as a tubulin inhibitor, disrupting cellular microtubule networks by hindering tubulin polymerization. It also upregulates PARP-1 and caspase-3 expression, thereby inducing apoptosis and exhibiting anticancer properties. Notably, Tubulin polymerization-IN-68 effectively suppresses HepG2 cells with an IC50 of 93 nM and markedly reduces the growth of HepG2 xenograft tumors in nude mice through oral administration.

Tubulin inhibitor 48 (compound 16) is an anticancer agent targeting microtubules. It exhibits IC50 values of 0.1 μM and 0.07 μM against LN-229 and Capan-1 cells, respectively.

Tubulin Polymerization-IN-1 prodrug (Compound 2b) is a microtubule polymerization inhibitor prodrug mediated by Pd. Developed from colchicine-binding site inhibitors (CBSIs), it aims to reduce toxicity and enhance targeted release. Compared to the parent compound, its cytotoxicity is decreased by 68.3 times, but can be in situ restored in the presence of Pd resin. Mechanistic studies show it retains the same antitumor activity as CBSIs. In vivo tests demonstrate that, once activated by Pd resin, it significantly suppresses tumor growth (63.2% inhibition rate). Tubulin Polymerization-IN-1 prodrug is a promising candidate for cancer research.

Tubulin polymerization-IN-71 (Compound 4k) is an inhibitor of tubulin polymerization with an IC50 of 3.06 μM. It suppresses the proliferation of cancer cells MG-63 and U2OS, with an IC50 ranging from 0.08 to 0.14 μM. Additionally, Tubulin polymerization-IN-71 induces cell cycle arrest at the G2/M phase and triggers apoptosis in MG-63 cells.

Tubulinpolymerization IN-59 ((R) -9k) is an effective inhibitor of CBSI (colchicine binding site).

Tubulin/MMP-IN-3 (Compound 15j) is a dual inhibitor of tubulin polymerization and MMP, effectively inhibiting MMP-2 and MMP-9 with IC50 values of 21.13 μM and 19.24 μM, respectively. It disrupts the NF-κB signaling pathway, leading to mitochondrial dysfunction and mitochondrial-dependent apoptosis. Tubulin/MMP-IN-3 shows antiproliferative activity in various cancer cells by causing cell cycle arrest at the G2/M phase and demonstrates antitumor effects in mouse models.