combretastatin

For more information about this drug and its actions, see combretastatin.

A variety of possible routes to the combretastatin skeleton are possible.

Except those factors, one of the disadvantage of combretastatin is the low water solubility.

Members of the combretastatin family possess varying ability to cause vascular disruption in tumors.

In vivo, it is dephosphorylated to its active metabolite, combretastatin A-4.

Combretastatin A-1 is also a potent cytotoxic agent.

This plant contains combretastatin A-4.

It is a derivative of combretastatin.

Of the natural products presently known combretastatin A-4 is the most potent in regards to both tubulin binding ability and cytotoxicity.

Combretastatin A-4 phosphate is a prodrug.

Combretastatin B-1 is a combretastatin and a dihydrostilbenoid.

Ombrabulin is a combretastatin A-4 derivative that exerts its antitumor effect by disrupting the formation of blood vessels needed for tumor growth.

Endothelial cells treated with combretastatin rapidly balloon in shape causing a variety of effects which result in necrosis of the tumor core.

Additionally, derivatives have been made of phenolic compound, combretastatin A-4, an anticancer molecule, including nitrogen or halogens atoms to increase the efficacy of the treatment.

Combretastatin binds to the β-subunit of tubulin at what is called the colchicine site, referring to the previously discovered vascular disrupting agent colchicine.

Combretastatin and combretastatin B-1 are two dihydrostilbenoids found in Combretum caffrum, an African tree.

A variety of different natural combretastatin molecules are present in the bark of Combretum caffrum, commonly known as South African Bush Willow.

Currently designated an orphan drug by the FDA, combretastatin A1 diphosphate (OXi4503) is in Phase I clinical trials.

One synthetic derivative, fosbretabulin disodium (combretastatin A4 phosphate), underwent preliminary study for the treatment of anaplastic thyroid cancer, but it was not effective enough to progress to more advanced trials.

Combretastatin A-4 is the active component of combretastatin A-4 phosphate, a prodrug designed to damage the vasculature (blood vessels) of cancer tumors causing central necrosis.

In 2011, CXCL12 was shown to be responsible for recruiting macrophages to breast tumours in mice in response to the experimental anti-cancer drug combretastatin A-4 phosphate, which damages tumour blood vessels.

Blocking CXCR4, the receptor for CXCL12, with Plerixafor (AMD-3100) increased the effectiveness of combretastatin in a mouse model of breast cancer, it is presumed by preventing macrophages from being recruited to tumours.

However, with today's technology, new drugs, such as fosbretabulin (a type of combretastatin), bortezomib and TNF-Related Apoptosis Induced Ligand (TRAIL), are being introduced and trialed in clinical labs and human clinical studies.

Combretastatin A-4, the most potent naturally occurring combretastatin known, its phosphate prodrug (CA-4-P), and other analogs of CA-4 such as ombrabulin are currently being investigated in a number of clinical trials.

Molecules that fall into the combretastatin family generally share 3 common structural features: a trimethoxy "A"-ring, a "B"-ring containing substitutents often at C3' and C4', and an ethene bridge between the two rings which provides necessary structural rigidity.