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docbanker

03/07/08 12:58 PM

#3702 RE: iwfal #3701


Proellex® did not induce, however, the blood vessel wall thickening and latticed capillary patterns seen with some other progesterone receptor modulators.

? Anyone have an explanation for that? Why one would be better than another? Unlike, say, statins which seem to operate through several mechanisms, Progesterone modulation would seem to be something that should be pretty straight forward. (I say that knowing that mif also affects the HPA axis - but that seems far distant from the endometrium.). Probably a question for which it is unreasonable to expect a complete answer - but in the current FDA environment it may be useful to have some possible explanations.

******This is what we have been saying all along. Proellex is a pure antagonist. Asoprisnol is a mixed agonist/antagonist. Asoprisnol saw induced blood vessel formation which Proellex is not seeing. This is why people on asoprisnol bled and got D+C's after 2 yrs. Proellex does not have this. This is what is most problematic. What is not problematic is the thickening (which is not cancer for the n-th time) and to make this benign finding a non-issue, the holiday period was developed.

People are confusing the above.
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io_io

03/07/08 4:38 PM

#3713 RE: iwfal #3701

<"an area of research I still need to understand - the competition">


Historically the board never found much. For a start, look for "Clinical / SPRM rivals – Asoprisnil, RU-486, etc" in the i_Box above.

I think there was also a NIH program on another drug in UF, but it was well behind Proellex. Nothing else.