Cancer market getting crowded?
Some seem to think that the cancer market is getting crowded. They're right, but as Dr. Jay pointed out, this crowding is a good thing for patients. Targeted therapies don't have huge margins of success. Some work in as little as 25% of patients. Therefore more options = better chances of success.
There is also some new evidence that Avastin is effective in treating renal cancer, which is huge news, because renal cancer has been incredibly difficult to treat, even with all of our advances in cancer treatment. Now Sutent looks to be getting in on the renal game, even beating Avastin in several trials (which were funded by Pfizer, the makers of Sutent).
These new targeted drugs are great news for cancer patients, but will require lots of keeping up on the part of oncologists. This is certainly an exciting time in the field of oncology — it looks like we're seeing the beginnings of a revolution similar to the one that occurred with the development of chemotherapy.
As usual, it will be up to the docs to sort the wheat from the bologna:
This big study should make Pfizer’s Sutent a clear choice for initial treatment of advanced metastatic kidney cancer, says Memorial Sloan Kettering Cancer Center oncologist Robert Motzer, who led the big Sutent study. He says most of his patients will now get Sutent first. "It is the most complete, most definitive study," he says.
But Wyeth contends its drug should be the clear favorite.
"It is the first compound to show significant improvement in overall survival in kidney cancer," says Lee Allen, a Wyeth vice president. "It is positioned to become the first-line therapy standard for renal cell cancer patients."
Allen says the company plans to file for approval of Temsirolimus in the fourth quarter of this year.
Let's hope it's sorted out quickly so patients can benefit from real, hard findings. I think it is likely that we'll begin to see cancer drug cocktails, in much the same way that HIV is treated. Forbes seems to be thinking along similar lines. I wonder how the analysts and investors are going to react to all the exciting happenings.
[tags]medicine, pharmacy, cancer, oncology, ASCO, Avastin, Sutent, Wyeth, Pfizer, temsirolimus[/tags]
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[...] The FDA has fast-tracked an Onyx/Bayer drug on the fast-track for approval following Stage III trials. Nexavar looks like it'll be a competitor to Pfizer's Sutent — a drug which is showing promise in treating hithertofore untreatable renal cancer, and Wyeth's new experimental drug, Temsirolimus. [...]
Pingback by OnThePharm » FDA fast-tracks Nexavar for liver cancer — June 13, 2006 @ 3:55 pm
[...] I hate to keep beating the cancer therapy drum, but these new, targeted treatments popping up left and right are great for patients for the reasons outlined above. I hope that Big Pharma starts to figure out that there can be big money in new antibiotics as well, even drugs that don't work in 90-100% of cases. [...]
Pingback by OnThePharm » Drug resistant cancer cells — June 17, 2006 @ 11:44 am
Sutent, One of the New 'Targeted' Drugs
The new "smart" drugs are a really exciting element of cancer medicine. One of the new molecularly-targeted cancer drugs is Sutent. It is a "multi-targeted kinase inhibitor." A drug that inhibits several proteins involved in triggering replication in cancer cells. Basically, inhibits various kinases, a type of enzyme that transfers phosphate groups from high-energy donor molecules to specific target molecules.
Sutent (sunitinib) is an inhibitor of multiple protein kinases, platelet-derived growth factor (PDGFR), vascular endothelial growth factor receptors (VEGFR), stem cell factor receptor (KIT), FMS-like tyrosine kinase (Flt3), colony stimulating factor (CSF-1R), and the neurotrophic factor receptor (RET). Because these proteins are involved in both tumor proliferation and angiogenesis, Sutent has both anti-tumor as well as anti-angiogenic properties. In addition, because Sutent inhibits multiple kinases, it possesses activity against multiple types of tumors.
Sutent can be used as a second-line drug for tumors that are non-responsive to Gleevec. The proto-oncogene KIT, a tyrosine kinase that is inhibited by Gleevec, is overexpressed in a majority of GISTs. Some patients have suffered relapses due to acquired point mutations in KIT, which prevents Gleevec from binding to the protein. Similar mutations have been characterized in EGFR from Iressa-resistant lung cancer patients.
The largest group of kinases are Protein kinases, which act on and modify the activity of specific proteins. So people will try and get some sort of gene-based test to measure the expression-mutation of these kinases. But something more elemental is going on. Does the drug even enter the cell? Once entered, does it immediately get metabolized or pumped out, or does it accumulate?
Sutent is conveniently pigmented. Brilliant yellow. Easy to see which cells have taken it up. In photomicrographs (two magnifications), it is fairly easy to see that some clones of tumor cells don't accumulate the drug. These cells won't get killed by it. But you wouldn't pick this up with an assay which only measured the kinases themselves. The new EGFRx (TM) Assay measures the net effect of everthing which goes on (Whole Cell Profiling). Are the cells ultimately killed, or aren't they?
Normal chemotherapy kills both cancer cells and healthy normal cells (mainly rapidly-dividing cells). Oncologists try to minimize damage to normal cells and to enhance the cell-killing effect on cancer cells. Too often, this delicate balance is not achieved.
Targeted therapy drugs interfere with specific molecules (receptors and enzymes inside and outside a cancer cell). By focusing on these molecular and cellular changes, targeted cancer drugs go after the "target" in these cells, rather than just all cells. Because of this, "targeted" drugs may be more effective than current treatments, and may be less harmful to normal cells.
Whole cell profiling can discriminate between the activity of different "targeted" drugs and identify situations in which it is advantageous to combine the "targeted" drugs with other types of cancer drugs. Because these new "smart" drugs will work for "some" but not "all" cancer patients who receive them, whole cell profiling can accurately identify patients who would benefit from treatment with molecularly-targeted anti-cancer therapies.
Not only is this an important predictive test that is available, but it is also a unique tool that can help to identify newer and better drugs, evaluate promising drug combinations, and serve as a "gold standard" correlative model with which to develop new DNA, RNA, and protein-based tests that better predict for drug activity.
This kind of technique exists, and might be very valuable, especially when active chemoagents are limited in a particular disease; it makes more sense than ever to test the tumor first. Afterall, cutting-edge techniques can often provide superior results over tried-and-true methods that have been around for many years.
The EGFRx (TM) Assay is the only assay that involves direct "visualization" of the cancer cells at endpoint. This allows for accurate assessment of drug activity, discriminates tumor from non-tumor cells, and provides a permanent archival record, which improves quality, serves as control, and assesses dose response in vitro.
Comment by Gregory D. Pawelski — November 21, 2006 @ 3:21 am