Colchicine, deacetamido-5,6-didehydro- is a biochemical.

Colchicine, N-deacetyl-10-thio- is a biochemical.

Colchicine-d6 is a deuterated compound of Colchicine. Colchicine has a CAS number of 64-86-8. Colchicine is a tubulin inhibitor (IC50: 3 nM) and blocks polymerization of microtubules by binding to tubulin.

Colchicine (Colcin) is a natural product that is an inhibitor of microtubule polymerization (IC50=3 nM) and blocks microtubule polymerization by binding to microtubule proteins. Colchicine can be used in the treatment of ventilation and rheumatic diseases.

Thiocolchicine is an effective inhibitor of tubulin polymerization with an IC50 of 2.5 µM and a Ki of 0.7 µM. Thiocolchicine induces cell apoptosis. Thiocolchicine can be used as an ADC cytotoxin in ADC technology.

Lumicolchicine is a bioactive chemical.

Tubulin polymerization-IN-43 is an inhibitor of tubulin polymerisation.Tubulin polymerization-IN-43 has multiple effects, disrupting the cellular microtubule network by targeting the colchicine locus and promoting cell cycle arrest and apoptosis in leukaemia cells. Tubulin polymerisation-IN-43 has multiple effects, promoting leukaemia cell cycle arrest in G2/M phase and apoptosis by targeting Colchicine sites to disrupt the cellular microtubule network.

Tubulin inhibitor 24 is a potent inhibitor that can inhibit tubulin polymerization.

N-Acetaminophen (N-Methylcolchicine) is a methylated form of Colchicine.

Suprafenacine (N'-[(E)-(4-methylphenyl)methylidene]-4,5,6,7-tetrahydro-1H-indazole-3-carbohydrazide) is a cell-permeable microtubule destabilizer that induces cell cycle arrest and apoptosis in G2/M phase. Suprafenacine binds to microtubules and inhibits aggregation at the colchicine junction. Suprafenacine is selective for cancer cells, including drug-resistant cancer cells.

gamma-Lumicolchicine is three, alpha, beta, and gamma isomers of ultraviolet degradation products of colchicine that lack many of the physiological actions of the parent; used as experimental control for colchicine actions.

3-demethylcolchicine is a natural product isolated from Gloriosa superba.Inhibitory effect on the polymerization of purified bovine brain tubulin.

Deacetylisocolchicine is a biochemical.

4-Formylcolchicine, a potent anticancer agent, demonstrates cytotoxicity with IC 50 values of 1.007 µM for A549 cells, 0.128 µM for HT-29 cells, and 0.054 µM for HCT116 cells.

Deacetylthiocolchicine hydrochloride is a biochemical.

Trimethylcolchicinic acid methyl ether (HAN 76504), an antimitotic agent, blocks microtubule assembly by attaching to tubulin and inhibiting its polymerization. It enhances tubulin's intrinsic GTPase activity, induces apoptosis across various normal and tumor cell lines, and activates the JNK/SAPK pathway. Currently unnamed, it is referred to by a provisional code name in line with MedKoo Chemical Nomenclature (https://www.medkoo.com/page/naming) for ease of communication.

LP-261 is a novel tubulin targeting anticancer agent that binds at the colchicine site on tubulin, inducing G2/M arrest.

Tubulin Polymerization-IN-56 (compound 8l), an indazole derivative, potently inhibits tubulin polymerization by targeting the colchicine site, which induces cell cycle arrest and apoptosis. Additionally, this compound diminishes cell migration and significantly inhibits tumor growth in vivo [1].

YS-370 is an orally active inhibitor of P-gp and shows moderate inhibition against CYP3A4. YS-370 effectively reverses multidrug resistance to paclitaxel and colchicine and exhibits stronger antitumor activity in combination with paclitaxel.

Tubulin polymerization-IN-45, a tubulin-targeting agent, acts as a tubulin polymerization inhibitor by binding to the tubulin's colchicine site. It induces apoptotic cell death in hepatocellular cancer (HCC) cells [1].

Tubulin polymerization-IN-39, a tubulin polymerization inhibitor with an IC50 of 4.9 μM, targets the colchicine-binding site to hinder tubulin polymerization. This compound effectively suppresses cancer cell proliferation.

Malformin C is a natural fungus-derived bicyclic pentapeptide that has antibacterial properties, particularly against species of Bacillus. Malformin C potently blocks the ability of bleomycin to induce G2 arrest in human T-cell leukemia-derived Jurkat cells (IC50 = 0.9 nM). It less potently abrogates colchicine-induced M phase arrest in Jurkat cells (IC50 = 24 nM). Malformin C inhibits cell growth dose-dependently in Colon 38 and HCT 115 cancer cells (IC50s = 0.27 and 0.18 μM, respectively) but has a low therapeutic index against cancer xenografts when tested in mice.

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].

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.

ABI-274 is a novel potent colchicine binding site inhibitor (CBSI) and tubulin inhibitor.

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) is a potent tubulin inhibitor that inhibits tubulin assembly and bounds in the colchicine site (IC 50 = 1.2 μM). Tubulin inhibitor 29 exhibits antiproliferative effects with an IC 50 value of 7.5 μM for MCF-7 cells. [1].

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

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.

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.

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.

Tartaric acid disodium dihydrate (Disodium L-(＋)-Tartrate Dihydrate) is commonly used as a buffer in molecular biology and cell culture.Tartaric acid disodium dihydrate is an acid phosphatase inhibitor that increases the probability of colchicine binding to tubulin1.

MPT0B214 is a novel and potent microtubule inhibitor with potential anticancer activity. MPT0B214 inhibited tubulin polymerization through strongly binding to the tubulin's colchicine-binding site and had cytotoxic activity in a variety of human tumor cell lines. After treatment with MPT0B214, KB cells were arrested in the G2-M phase before cell death occurred, which were associated with upregulation of cyclin B1, dephosphorylation of Cdc2, phosphorylation of Cdc25C and elevated expression of the mitotic marker MPM-2. Furthermore, the compound induced apoptotic cell death through mitochondria/caspase 9-dependent pathway. Notably, several KB-derived multidrug-resistant cancer cell lines were also sensitive to MPT0B214 treatment. ( PLoS One. 2013;8(3):e58953).

Torilin is an inhibitor of testosterone 5 alpha-reductase, it (IC50 = 31.7 +/- 4.23 microM) shows a stronger inhibition of 5 alpha-reductase than alpha-linolenic acid (IC50 = 160.3 +/- 24.62 microM) but is weaker than finasteride (IC50 = 0.38 +/- 0.06 microM). Torilin has immunomodulatory, hepatoprotective, and anti-inflammatory properties, it inhibits inflammation by limiting TAK1-mediated MAP kinase and NF-κB activation, it can attenuate arthritis severity, modify leukocyte activations in dLNs or joints, and restore serum and splenocyte cytokine imbalances. Torilin inhibits melanin production in alpha-melanocyte stimulating hormone-activated B16 melanoma cells, with an IC(50) value of 25 microM. Torilin shows excellent antimicrobial activity against Bacillus subtilis ATCC 6633 spores and vegetative cells. Torilin has a potent anti-angiogenic activity both in vivo and in vitro, and it may have a strong activity to suppress tumorigenesis by inhibition of tumor invasion, it reverses multidrug-resistance in cancer cells, it can potentiate the cytotoxicities of adriamycin, vinblastine, taxol and colchicine against multidrug-resistant KB-V1 and MCF7/ADR cells.

MPT0B098 is a potent microtubule inhibitor through binding to the colchicine-binding site of tubulin. MPT0B098 is active against the growth of various human cancer cells, including chemoresistant cells with IC50 values ranging from 70 to 150 nmol/L. MPT0B098 arrests cells in the G2–M phase and subsequently induces cell apoptosis. In addition, MPT0B098 effectively suppresses VEGF-induced cell migration and capillary-like tube formation of HUVECs. Distinguished from other microtubule inhibitors, MPT0B098 not only inhibited the expression levels of HIF-1α protein but also destabilized HIF-1α mRNA. The mechanism of causing unstable of HIF-1α mRNA by MPT0B098 is through decreasing RNA-binding protein, HuR, translocation from the nucleus to the cytoplasm. Notably, MPT0B098 effectively suppresses tumor growth and microvessel density of tumor specimens in vivo. Taken together, our results provide a novel mechanism of inhibiting HIF-1α of a microtubule inhibitor MPT0B098. MPT0B098 is......

33-BCRP inhibitor is a compound that blocks the action of breast cancer resistance protein (BCRP), enhancing the susceptibility of mitoxantrone-resistant H460/MX20 lung cancer cells to the cytotoxic effects of mitoxantrone, both individually and when combined with UV radiation. Additionally, it enhances the sensitivity of KB-C2 epidermal carcinoma cells, which overexpress P-glycoprotein (P-gp) or multidrug resistance protein (MDR), to colchicine-induced apoptosis. Furthermore, at a concentration of 5 µM, it boosts the intracellular accumulation of mitoxantrone in H460/MX20 cells.

MY-673, a colchicine binding site inhibitor (CBSI), impedes tubulin polymerization and disrupts the ERK signaling pathway, consequently modulating SMAD4 protein expression in the TGF-β/SMAD pathway. This compound effectively reduces cell proliferation and migration while inducing apoptosis in both in vivo and in vitro settings [1].

Tubulin polymerization-IN-36 is able to be used in cancer research, for example, lymphomas. Tubulin polymerization-IN-36 binds to the colchicine site of tubulin and inhibits colchicine binding, that is an inhibitor of tubulin polymerization with IC50 of 2.8 μΜ[1].

Plinabulin (NPI-2358) (NPI-2358) is a vascular disrupting agent (VDA) against tubulin-depolymerizing tumor cells ( IC50: 9.8-18 nM). Plinabulin selectively targets and binds to the colchicine-binding site of tubulin, thereby interrupting equilibrium of microtubule dynamics. This disrupts mitotic spindle assembly leading to cell cycle arrest at M phase and blockage of cell division.

Avanbulin is a potent inhibitor of tubulin polymerization with antitumor activity. It elicits a unique microtubule (MT) phenotype, distinct from colchicine, paclitaxel, and vinblastine has broad in vitro anti-proliferative activity against a diverse range

Tubulin polymerization-IN-49 (compound 12d), a potent inhibitor of tubulin polymerization, binds to the colchicine site on tubulin, subsequently inducing cell cycle arrest at the G2/M phase and triggering apoptosis. This compound exhibits anticancer activity by preventing tumor generation and inhibiting tumor proliferation and angiogenesis [1].

EHT-6706 is a novel microtubule-disrupting agent that targets the colchicine-binding site to inhibit tubulin polymerization. At low nM concentrations, EHT 6706 exhibits highly potent antiproliferative activity on more than 60 human tumor cell lines, even those described as being drug resistant. EHT 6706 also shows strong efficacy as a vascular-disrupting agent, since it prevents endothelial cell tube formation and disrupts pre-established vessels, changes the permeability of endothelial cell monolayers and inhibits endothelial cell migration. Genome-wide transcriptomic analysis of EHT 6706 effects on human endothelial cells shows that the antiangiogenic activity elicits gene deregulations of antiangiogenic pathways. These findings indicate that EHT 6706 is a promising tubulin-binding compound with potentially broad clinical antitumor efficacy.

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

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].

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.

Crolibulin (EPC2407) is an inhibitor of small molecule tubulin polymerization.