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Restrict the search for
colchicine
to a specific field?
Status:
Possibly Marketed Outside US
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Demecolcine, also called Colcemid, was isolated from the autumn crocus in 1950 and commercialized by Ciba. Initially, it was explored as a cancer drug due to its low toxicity. Demecolcine depolymerizes microtubules and limits microtubule formation (inactivates spindle fiber formation), thus arresting cells in metaphase and allowing cell harvest and karyotyping to be performed. Today, it is only used as a research tool mainly to overcome limitations of colchicine due to its very slow association and dissociation rate constants. It binds to tubulin at the same site as colchicine, but ~10-fold faster, and it also dissociates faster. Demecolcine main use has been to arrest cells in mitosis for cytogenetic analysis, though to our knowledge it offers no special advantages over other drugs in this application.
Status:
US Approved Rx
(2013)
First approved in 1958
Class:
MIXTURE
Status:
US Approved Rx
(2019)
Source:
ANDA209470
(2019)
Source URL:
First marketed in 1921
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Colchicine is an alkaloid obtained from the plant colchicum autumnale (also known as "meadow saffron"). Colchicine is an alternative medication for those unable to tolerate NSAIDs in gout. Mechanism of action of colchicine is inhibition of microtubule polymerization by binding to tubulin. Availability of tubulin is essential to mitosis, so colchicine effectively unctions as a "mitotic poison" or spindle poison.
Status:
US Approved Rx
(2019)
Source:
ANDA209470
(2019)
Source URL:
First marketed in 1921
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Colchicine is an alkaloid obtained from the plant colchicum autumnale (also known as "meadow saffron"). Colchicine is an alternative medication for those unable to tolerate NSAIDs in gout. Mechanism of action of colchicine is inhibition of microtubule polymerization by binding to tubulin. Availability of tubulin is essential to mitosis, so colchicine effectively unctions as a "mitotic poison" or spindle poison.
Status:
Investigational
Source:
NCT02132468: Phase 2 Interventional Completed Neuroendocrine Tumors
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Combretastatin A4 is a vascular disrupting agent (VDA) that targets tumor vasculature to inhibit angiogenesis. Combretastatin A4 is a tubulin-binding agent that binds at or near the colchicine binding site of β-tubulin and inhibits tubulin assembly. This tubulin-binding agent was originally isolated from an African shrub, Combretum caffrum. Combretastatin A4 is cytotoxic to umbilical-vein endothelial cells (HUVECs) and to a range of cells derived from primary tumors and these cytotoxicity profiles have been used to assess several novel analogs of the drug for future development. Combretastatin A4 has antitumor activity by inhibiting AKT function. The inhibited AKT activation causes decreased cell proliferation, cell cycle arrest, and reduced in vitro migration/invasiveness and in vivo metastatic ability. Several studies in mice have shown that a single administration of combretastatin A4 (100
mg/kg) does not significantly affect primary tumor growth. However, repeated administration (12.5 – 25.0mg/kg twice daily) for periods of 10 – 20 days resulted in approximately 50% retardation of growth of ectopic Lewis lung carcinoma and substantial growth delay of T138 spontaneous murine breast tumors. In clinical studies, Combretastatin A4 has been well tolerated in patients at doses up to 56 mg/m2, following a protocol of five daily 10-minute intravenous infusions every 21 days. The disodium combretastatin A4 phosphate prodrug is currently undergoing clinical trials in the UK and USA.
Status:
Investigational
Source:
NCT00003359: Phase 1 Interventional Completed Unspecified Adult Solid Tumor, Protocol Specific
(1998)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Batabulin or T138067 (2-fluoro-1-methoxy-4-pentafluorophenylsulfonamidobenzene) covalently and selectively modifies the beta1, beta2, and beta4 isotypes of beta-tubulin at a conserved cysteine residue, thereby disrupting microtubule polymerization. Cells exposed to batabulin become altered in shape, indicating a collapse of the cytoskeleton, and show an increase in chromosomal ploidy. Batabulin is equally efficacious in inhibiting the growth of sensitive and multidrug-resistant human tumor xenografts in athymic nude mice. Batabulin has been in clinical trials for the treatment of cancers (breast cancer, colorectal cancer, glioma, hepatocellular carcinoma, non-small cell lung cancer). It does not have clinical activity in the treatment of colorectal cancer and glioma. Batabulin development was discontinued.
