| Size | Price | Stock | Qty |
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| 200mg |
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| 500mg |
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Purity: ≥98%
Colchicine (Colchicina; Condylon; Colsaloid; Colchicinum) is a mitotic/tubulin inhibitor that inhibits microtubule polymerization (also called microtubule disrupting agent or tubulin inhibitor) with potential anticancer and anti-inflammatory effects. Its IC50 is less than 10 nM, which means it inhibits the growth of cancer cells. A medication called colchicine, which is approved to treat gout, is also being studied for possible anticancer properties. Microtubule destabilizers, such as colchicine, encourage the depolymerization of microtubules. Colchicum autumnale L., a poisonous meadow saffron, yielded colchicine, the first tubulin destabilizing compound. Colchicine was authorized in 2009 for the management of familial Mediterranean fever and gout. Strong antimitotic and anticancer properties were also shown by colchicine. Colchicine's severe side effects, which include anemia, gastrointestinal distress, bone marrow damage, and neutropenia, prevented it from being developed clinically as an anticancer treatment.
| Targets |
Microtubule/Tubulin
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| ln Vitro |
Experiencing 1μM The microtubule disrupting agent colchicine caused rat cerebellar granule cells (CGC) to undergo apoptosis. A moderate but progressive increase in the resting intracellular Ca2+ concentration is also brought on by colchicine treatment[1], as well as changes in the Ca2+ responses to chemical depolarization. Colchicine binds to the main structural element of microtubules, the soluble tubulin heterodimer, to initiate its biological actions. The mechanism of Colchicine binding to brain tubulin is thoroughly examined, and the capacities of tubulins to bind Colchicine from diverse sources are enumerated. Colchicine's high affinity binding to tubulin is attributed to its colchicinoid structure, which is reviewed in relation to its analogues in the Colchicine series. This relationship also sheds light on the structural characteristics of Colchicine. The association's kinetic and thermodynamic features are discussed and assessed in relation to the binding mechanism. Colchicine's low energy electronic spectra exhibit peculiar changes upon binding to tubulin. The nature of the Colchicine-tubulin complex is discussed in relation to the spectroscopic characteristics of Colchicine bound to tubulin. There are attempts to identify the high affinity Colchicine binding site on tubulin[2]. The lesion index measured 24 hours after indomethacin administration shows that colchicine treatment inhibits small intestinal injury caused by indomethacin by 86% (1 mg/kg) and 94% (3 mg/kg). Colchicine suppresses the expression of mature IL-1β and cleaved caspase-1 proteins, but has no effect on NLRP3 or IL-1β mRNA expression[3].
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| ln Vivo |
Vehicle or Colchicine (1 mg/kg) is put on the tongue half an hour before indomethacin. Within 24 hours of indomethacin administration, mice treated with Colchicine had smaller lesions in their small intestine when stained with Evans blue as compared to mice treated with vehicle. Furthermore, compared to mice treated with a vehicle, Colchicine-treated mice exhibit decreased mucosal inflammation and ulceration as well as a reduction in the size and quantity of lesions. This was revealed by histological examination. When administered at doses of 1 mg/kg and 3 mg/kg (by 86% and 94%, respectively), colchicine treatment dramatically lowers the lesion index in comparison to vehicle treatment. Treatment with colchicine markedly reduces the protein levels of mature IL-1β by 56% and 69%, respectively, at doses of 1 mg/kg and 3 mg/kg, without changing pro-IL-1β levels.
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| Enzyme Assay |
Spending time in 1μM In rat cerebellar granule cells (CGC), the microtubule disrupting agent colchicine caused apoptosis. In addition, administering colchicine results in a gradual but moderate rise in the resting intracellular Ca2+concentration as well as changes in the Ca2+ responses to chemical depolarization [...]. By binding to the soluble tubulin heterodimer, which is the main building block of the microtubule, colchicine has its biological effects. An extensive examination of the mechanism of Colchicine binding to brain tubulin is conducted, along with a summary of the tubulins' capacity to bind Colchicine from all sources. Insight into the structural characteristics of Colchicine that enable its high affinity binding to tubulin is gained from the correlation between the structure of the colchicinoid and tubulin binding activity. This relationship is also examined for Colchicine series analogs. The association's kinetic and thermodynamic features are discussed and assessed in relation to the binding mechanism. Colchicine's low energy electronic spectra exhibit peculiar changes upon binding to tubulin. The nature of the Colchicine-tubulin complex is discussed in relation to the spectroscopic characteristics of Colchicine bound to tubulin. There are attempts to identify the tubulin's high affinity Colchicine binding site[2]. The lesion index 24 hours after indomethacin administration shows that colchicine treatment inhibits 86% (1 mg/kg) and 94% (3 mg/kg) of indomethacin-induced small intestinal injury. Without influencing the mRNA expression of NLRP3 and IL-1β, colchicine suppresses the protein expression of mature IL-1β and cleaved caspase-1.
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| Cell Assay |
HeLa cells are grown in 6-well plates, and after two hours, they are treated with 100 μM EBI. After that, they are treated with KXO1, vinblastine, or colchicine at varying concentrations. After using radioimmuno_x005fprecipitation assay buffer to extract the total protein, β~-tubulin is analyzed using Western blot analysis. The loading control is GAPDH. The process of Western blotting is carried out.
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| Animal Protocol |
Mice: Male 8-week-old mice that are free of specific pathogens are used. Both NLRP3?/? mice and wild-type C57BL/6 mice on a C57BL/6 background are employed. 30 minutes before indomethacin is given, either a vehicle or 1 or 3 mg/kg of Colchicine is given orally to investigate the impact of Colchicine on NSAID-induced small intestinal damage. Three hours after being treated with indomethacin, mice were given intraperitoneal injections of either mouse recombinant IL-1β (0.1 μg/kg) or sterilized phosphate buffered saline. Before indomethacin is given to NLRP3?/? mice, vehicle or colchicine (1 or 3 mg/kg) is also given. 24 hours after indomethacin is administered, the lesion index is assessed, and 6 hours later, the mRNA and protein expression of inflammasome components is investigated.
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| References |
| Molecular Formula |
C22H25NO6
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| Molecular Weight |
399.44
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| Exact Mass |
399.17
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| Elemental Analysis |
C, 66.15; H, 6.31; N, 3.51; O, 24.03
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| CAS # |
64-86-8
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| Related CAS # |
Colchicine-d6;1217651-73-4;Colchicine-d3;1217625-62-1
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| Appearance |
Solid powder
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| SMILES |
CC(=O)N[C@H]1CCC2=CC(=C(C(=C2C3=CC=C(C(=O)C=C13)OC)OC)OC)OC
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| InChi Key |
IAKHMKGGTNLKSZ-INIZCTEOSA-N
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| InChi Code |
InChI=1S/C22H25NO6/c1-12(24)23-16-8-6-13-10-19(27-3)21(28-4)22(29-5)20(13)14-7-9-18(26-2)17(25)11-15(14)16/h7,9-11,16H,6,8H2,1-5H3,(H,23,24)/t16-/m0/s1
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| Chemical Name |
N-[(7S)-1,2,3,10-tetramethoxy-9-oxo-6,7-dihydro-5H-benzo[a]heptalen-7-yl]acetamide
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| Synonyms |
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
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| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: 2.78 mg/mL (6.96 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication (<60°C).
(Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.5035 mL | 12.5175 mL | 25.0350 mL | |
| 5 mM | 0.5007 mL | 2.5035 mL | 5.0070 mL | |
| 10 mM | 0.2504 mL | 1.2518 mL | 2.5035 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT04818489 | Active Recruiting |
Other: the standard protocol only Drug: Colchicine 0.5 MG |
Pulmonary Fibrosis Interstitial Covid19 |
ClinAmygate | March 25, 2021 | Phase 4 |
| NCT05472337 | Recruiting | Drug: Colchicine | Acute Coronary Syndrome | Pontificia Universidad Catolica de Chile |
August 1, 2022 | Phase 2 |
| NCT06095765 | Not yet recruiting | Drug: Colchicine 0.5 MG Oral Tablet Drug: Placebo |
Coronary Artery Disease | AZ Sint-Jan AV | February 1, 2024 | Phase 3 |
| NCT05279690 | Recruiting | Drug: Colchicine | Metastatic Solid Tumor Urothelial Cancer |
Icahn School of Medicine at Mount Sinai |
February 14, 2022 | Phase 1 |
| NCT05618353 | Recruiting | Drug: Colchicine Drug: Placebo |
Coronary Artery Disease | VA Office of Research and Development |
August 1, 2023 | Phase 4 |
Preventive effects of colchicine treatment on indomethacin-induced small intestinal injury.Sci Rep. 2016; 6: 32587. |
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Effect of exogenous IL-1β and colchicine treatment on indomethacin-induced small intestinal injury.Sci Rep. 2016; 6: 32587. |
Preventive effects of colchicine treatment are mediated by suppression of the NLRP3 inflammasome.Sci Rep. 2016; 6: 32587. |
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