Colchicine, a toxic plant-derived alkaloid extracted from plants of the genus Colchicum, inhibits microtubule polymerization (IC50 = 3.2 μM). It inhibits the growth of MCF-7 human breast carcinoma cells and has anti-inflammatory activity. Colchicine can lower body temperature, inhibit the respiratory center, enhance the effect of sympathomimetic drugs, constrict blood vessels, and raise blood pressure.
Catalog Number | Size | Price | Quantity | ||
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BADC-00004 | 1 g | $298 | Inquiry |
NCT Number | Title | Condition Or Disease | Phase | Start Date | Sponsor | Status |
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NCT00000577 | Asthma Clinical Research Network (ACRN) | Asthma | Phase 3 | September 1993 | Milton S. Hershey Medical Center | Withdrawn |
NCT00004368 | Phase I Study of Colchicine Therapy in Childhood Hepatic Cirrhosis | Cirrhosis | Phase 1 | May 1990 | National Center for Research Resources (NCRR) | Unknown status |
NCT00004748 | Low-Dose Oral Methotrexate Versus Colchicine for Primary Biliary Cirrhosis | Liver Cirrhosis, Biliary | Phase 3 | November 1989 | National Center for Research Resources (NCRR) | Completed |
NCT00128414 | Study of Colchicine to Treat and Prevent Recurrent Pericarditis (First Episode) | Pericarditis | Phase 3 | August 2005 | Azienda Sanitaria Locale 3, Torino | Completed |
NCT00128427 | Study of Colchicine to Prevent the Postpericardiotomy Syndrome | Postpericardiotomy Syndrome | Phase 3 | June 2005 | Azienda Sanitaria Locale 3, Torino | Completed |
Colchicine is a natural alkaloid compound primarily extracted from plants of the genus Colchicum, such as the autumn crocus. It has been used for centuries for its medicinal properties, most notably in the treatment of gout. The compound is known for its anti-inflammatory characteristics, which arise from its ability to disrupt microtubule polymerization. This disruption affects various cellular processes, including cell division, motility, and secretion, rendering colchicine a critical agent in treating inflammatory diseases. Its application in gout therapy is largely due to its capacity to prevent neutrophil-mediated inflammation, thereby alleviating the pain and swelling associated with gout attacks.
Recent advances in drug discovery have highlighted colchicine’s potential beyond gout management. Its ability to inhibit microtubule formation has made it an attractive candidate for cancer research, where it is being studied for its potential to impede the growth and proliferation of cancer cells. Colchicine’s mechanism of binding to tubulin, a key protein in microtubule assembly, allows it to interrupt the mitotic process, potentially leading to cell cycle arrest and apoptosis in rapidly dividing cancer cells. This mechanism has sparked interest in developing colchicine derivatives and analogs that might offer better efficacy and reduced toxicity for oncological applications.
In addition to its emerging applications in oncology, colchicine has been investigated for its role in cardiovascular conditions. Studies have shown promising results in using colchicine to manage pericarditis, a swelling and irritation of the pericardium, as well as to prevent post-operative atrial fibrillation, a common complication following heart surgery. The anti-inflammatory properties of colchicine play a crucial role here by modulating the inflammatory response associated with these cardiovascular issues, which could lead to a reduction in complication rates and improved patient outcomes.
Despite its promising applications, colchicine’s toxicity remains a significant challenge in its therapeutic use. The therapeutic index of colchicine is narrow, meaning the range between effective and toxic doses is small. Overdose can lead to severe consequences including multi-organ failure. Thus, drug development involving colchicine requires careful consideration of dosing regimens and delivery methods to maximize therapeutic benefits while minimizing side effects. Research is ongoing to engineer new forms of colchicine with enhanced safety profiles, which include targeted delivery systems or novel formulations that mitigate systemic exposure.
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