colchicine-binding

Crolibulin (EPC2407) 是一种微管蛋白聚合抑制剂，具有诱导凋亡和抑制细胞生长的作用。它有抗肿瘤活性，还具有心血管毒性和神经毒性。

Tartaric acid disodium dihydrate (Disodium L-(＋)-Tartrate Dihydrate) 常用来制作分子生物学和细胞培养中的缓冲液,。Tartaric acid disodium dihydrate 是酸性磷酸酶抑制剂, 可增加秋水仙碱结合 tubulin1的概率。

Colchicine 是一种具有口服活性的天然生物碱，通过抑制微管蛋白聚合（IC50=3 nM）及作为α3甘氨酸受体的竞争性拮抗剂，具有广泛的抗炎、免疫抑制和抗纤维化活性，能抑制NLRP3炎症小体激活预防NSAID引起的小肠损伤，具备用于痛风性关节炎和风湿病研究的潜力，且常用于构建阿尔茨海默症模型。

3-Demethylthiocolchicine, 一种Colchicine衍生物, 显示出强大的抗肿瘤活性。与Colchicine相比, 该化合物在阻止酪蛋白诱导的淀粉样变性、微管结合和抗炎作用方面表现出相似的效能，但其毒性更低。

Tubulin polymerization-IN-70（compound Q19）是一种高效的tubulin polymerization抑制剂，可以靶向微管蛋白的秋水仙碱结合位点，并阻断微管蛋白的聚合。这种化合物不仅具有抗增殖作用，还能诱导细胞凋亡(apoptosis)与细胞周期在G2 M期的停滞。此外，Tubulin polymerization-IN-70通过降低线粒体膜电位并提升reactive oxygen species(ROS)水平来发挥作用。它同时还显示出抗血管生成和抗癌的活性。

Tubulin Polymerization-IN-1 prodrug (Compound 2b) 是一种通过Pd-介导的微管蛋白聚合抑制剂前药。它基于秋水仙碱结合位点抑制剂 (CBSIs) 设计，通过降低毒性和提升靶向释放性能。相较于母体化合物，Tubulin Polymerization-IN-1 prodrug 的细胞毒性减少了68.3倍，但在存在Pd树脂时，可原位恢复其细胞毒性。机制研究显示，其抗肿瘤活性与CBSIs一致。在体内实验中，经Pd树脂激活后，Tubulin Polymerization-IN-1 prodrug 能明显抑制肿瘤生长（抑制率63.2%）。该化合物在抗癌研究中展现出潜在应用前景。

Tubulinpolymerization-IN-59 ((R)-9k) 是 CBSI（秋水仙碱结合位点） 的有效抑制剂。

Tubulin polymerization-IN-72 (Compound 4a4) 是一种抗癌微管合成抑制剂。其通过与秋水仙碱位点结合抑制微管蛋白聚合，导致癌细胞在 G2 M 期被阻滞，并诱导凋亡 (Apoptosis)。对癌细胞的IC50范围为 0.4-2.7 nM。

Tubulin polymerization-IN-76（compound 20b）是一种强效且口服活性的微管蛋白聚合抑制剂。它通过干扰秋水仙碱结合位点，以IC50值2.505 μM抑制微管蛋白的聚合，破坏细胞内的微管网络并干扰细胞有丝分裂。Tubulin polymerization-IN-76 对MGC-803和HGC-27细胞展现显著抑制，IC50值分别为1.61和1.82 nM。该化合物有效抑制MGC-803和HGC-27细胞的集落形成及迁移，并诱导G2 M期细胞周期阻滞和细胞凋亡（Apoptosis）。此外，Tubulin polymerization-IN-76 展示出广谱抗增殖活性。

BKS3031A 是一种抑制剂，特异性结合于 αβ-微管蛋白 (αβ-tubulin) 的秋水仙碱结合位点，抑制微管的组装动力学。

Plinabulin (NPI-2358) 是一种抗微管蛋白解聚肿瘤细胞的血管破坏剂，选择性地靶向并结合到微管蛋白的秋水仙碱结合位点，从而中断微管动力学的平衡。它对人肿瘤细胞系具有抑制作用，对 HT-29 细胞系的IC50值为 9.8 nM。

DAT1 is an antimitotic and antiangiogenic that acts by binding to the colchicine binding site of tubulin.

Mivobulin is a tubulin inhibitor potentially for the treatment of glioma, malignant melanoma, prostate, ovarian cancer. CI-980 acts at the colchicine-binding site.

Combretastatin A-1 phosphate (OXi-4503) tetrasodium, a prodrug of Combretastatin A-1, is a tubulin-binding microtubule polymerization inhibitor that targets the colchicine-binding site. By inducing tubulin depolymerization, Combretastatin A-1 phosphate tetrasodium inhibits the Wnt β-catenin pathway and leads to the deactivation of AKT. It possesses both anti-tumor and anti-vascular properties.

Tubulin inhibitor 29 (compound 3c) 是一种有效的微管抑制剂，可抑制微管聚合并与秋水仙碱位点结合 (IC 50 = 1.2 μM)。Tubulin inhibitor 29 具有抗增殖作用，对人乳腺癌细胞 MCF-7 细胞的 IC50值为 7.5 μM。

Tubulin polymerization-IN-36 可用于癌症研究，例如淋巴癌。Tubulin polymerization-IN-36 结合微管蛋白的秋水仙碱位点并且抑制秋水碱结合，是一种微管蛋白聚合的抑制剂，IC50值为 2.8 μM。

Tubulin polymerization-IN-37 is a potent inhibitor (IC50: 2.3 μΜ) of tubulin polymerization by binding specifically to the colchicine site of tubulin and preventing colchicine binding. It has potential applications in cancer research, notably for lymphomas [1].

MY-875 is a potent microtubulin polymerization inhibitor that competes at colchicine binding sites, exhibiting an IC50 value of 0.92 μM. It effectively suppresses microtubulin polymerization, exerting its inhibitory effect. Additionally, MY-875 exerts its biological impact by activating the Hippo pathway, inducing apoptosis, and displaying commendable anticancer activity [1].

Tubulin polymerization-IN-26 (compound 12h) is a chemical compound that inhibits the polymerization of microtubulin. It achieves this by binding to the colchicine binding site of microtubulin, with an IC50 value of 4.64 μM. Additionally, Tubulin polymerization-IN-26 has the ability to induce apoptosis and inhibit cell metastasis or migration. Due to these properties, it holds potential as a valuable compound for researching lung cancer [1].

Tubulin inhibitor 11 是一种口服活性的有效微管蛋白抑制剂。它通过靶向秋水仙碱结合位点，抑制tubulin聚合，进而促进有丝分裂阻断和apoptosis。

IRC-083927 HCl is novel and potent microtubule inhibitor with potential anticancer activity. IRC-083927 inhibits the tubulin polymerization by a binding to the colchicine site. IRC-083927 inhibits in vitro cell growth of human cancer cell lines in the low nanomolar range. More interesting, it remains highly active against cell lines resistant to microtubule-interacting agents (taxanes, Vinca alkaloids, or epothilones). Chronic oral treatment with IRC-083927 (5 mg kg) inhibits the growth of two human tumor xenografts in nude mice (C33-A, human cervical cancer and MDA-MB-231, human hormone-independent breast cancer). Together, the antitumor effects induced by IRC-083927 on tumor models resistant to tubulin agents support further investigations to fully evaluate its potential for the treatment of advanced cancers, particularly those resistant to current clinically available drugs.

IG-105 is a potent microtubule inhibitor with potential anticancer activity. IG-105 inhibits microtubule assembly by binding at colchicine pocket. IG-105 shows a potent anticancer activity in vitro and in vivo and has good safety in mice. IG-105 showed a potent activity against human leukemia and solid tumors in breast, liver, prostate, lung, skin, colon, and pancreas with IC(50) values between 0.012 and 0.298 mumol L. It was also active in drug-resistant tumor cells and not a P-glycoprotein substrate. It inhibited microtubule assembly followed by M-phase arrest, Bcl-2 inactivation, and then apoptosis through caspase pathways.

Cornigerine is a natural product analog of colchicine produced by Colchicum cornigerum that inhibited tubulin polymerization both with and without microtubule-associated proteins, inhibited the binding of radiolabeled colchicine to tubulin, and stimulated tubulin-dependent GTP hydrolysis.

ABI-231 is a potent, orally bioavailable tubulin inhibitor that interacts with the colchicine binding site and is currently undergoing clinical trials for prostate cancer. ABI-231, has an average IC50 = 5.2 nM against panels of melanoma and prostate cancer cell lines, is orally bioavailable, and strongly suppress melanoma tumors in vivo. ABI-231 holds great promise as a new generation of orally available tubulin inhibitor.