Tuesday 20 September 2011

Development of "Smart Bomb" (DRUG) against cancer.


Scientists have come up with what they claim is a cancer-busting “smart bomb” which can destroy all solid tumors in single jab.
A team at University of Bradford says the revolutionary drug, ICT2588, “detonates” and becomes active on reaching its target; it circulates in the bloodstream, destroying cancers which have spread, while leaving healthy tissue unharmed.
The jab is to be tested on patients in Britain, possibly as soon as 2013, a media report said.
In tests on mice, half the animals appeared to be free of disease after one injection. Just one injection, lung, breast, bowel and prostate cancers in the rodents have been completely eradicated.
Prof Laurence Patterson, who is leading the team, said: “Sometimes the treatment is so effective that you actually remove the tumor's ability to grow. We were able to cure, in some studies, half the mice of their cancer. These mice no longer had any tumors growing in them, and they remained healthy.”
The secret is the way the drug is activated by an enzyme which tumors use to invade surrounding tissue. Once activated, it destroys vital blood vessels which feed the cancer tumor, starving it to death.
AddICT2588 is selectively activated by MMPs. A, structure of ICT2588 and ICT2552, indicating the MT-MMP–selective scissile bond. B, metabolism of ICT2588 by HT1080 and MCF7 tumors relative to mouse liver and mouse plasma. Metabolites detected by LC-MS and expressed as concentration of ICT2588 remaining. C, metabolism of ICT2588 in the presence of a pan-MMP inhibitor, ilomastat (GM-6001). Points, mean of three independent experiments; bars, SD. caption
Prof Patterson said: “What we've designed is, effectively, a smart bomb that can be targeted at any solid tumor to kill it without appearing to harm healthy tissue.”
A, ICT2588 (peptide conjugate) induces a significantly greater inhibition of HT1080 tumor growth compared with (B) the authentic metabolite (ICT2552) at equimolar concentrations. Mice were treated with a single i.p. dose of ICT2588 (A) or ICT2552 (B) and tumor size determined daily (*, one animal in the ICT2588 62.5 mg/kg treatment group showed complete tumor remission). C, combination of ICT2588 with doxorubicin resulted in significantly greater antitumor potency relative to single-agent doxorubicin or ICT2588 administration. Mice were administered 75 mg/kg of ICT2588 (i.p.) 24 h prior to 5 mg/kg of doxorubicin (i.v.) and tumor size determined daily (C). Four out of eight mice showed complete tumor remission with the coadministration schedule; therefore, results in this group are the summary of four remaining mice. The tumor growth delay is defined as the time taken for doubling of tumor volume relative to control, denoted in parentheses in the key for each figure panel.       

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