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Old Mon Mar 5, 2012, 11:51 PM
Greg H Greg H is offline
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Join Date: Sep 2010
Location: North Carolina
Posts: 660
Hey Ann!

As I understand it, Vidaza and Dacogen both work in pretty much the same way. They are both "hypomethylating agents," which means they affect important processes at the level of DNA. I'd like to be more specific than that, but the point in Biology 201 where you start understanding the inner workings of DNA is about the point that I decided to major in Religion.

I believe the testing that won Vidaza its FDA approval produced better results than similar testing for Dacogen, which is why folks typically go with Vidaza first. The test design may have had something to do with the less impressive Dacogen performance.

It's not uncommon for folks who try one of these drugs without success, or relapse after some period of success, to try the other one.

Both tend to lower counts initially before improving them. When they work, they can make folks less transfusion dependent, lower blast counts, and sometimes get rid of chromosomal abnormalities.

These drugs won FDA approval after being tested in higher risk MDS patients, those with IPSS scores that put them in the INT-2 or High Risk categories. They are much less effective in lower risk patients. For example, Vidaza can produce improvement in perhaps two-thirds of higher risk patients, but is likely to help only a quarter of lower risk folks. So they are generally reserved for later in the course of the disease.

That's the narrative version. Birgitta has way more actual data at her fingertips, so I hope she'll jump in and correct me or back me up with some data.

Take care!

Greg
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Greg, 59, dx MDS RCMD Int-1 03/10, 8+ & Dup1(q21q31). NIH Campath 11/2010. Non-responder. Tiny telomeres. TERT mutation. Danazol at NIH 12/11. TX independent 7/12. Pancreatitis 4/15. 15% blasts 4/16. DX RAEB-2. Beginning Vidaza to prep for MUD STC. Check out my blog at www.greghankins.com
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