Replies to post #265224 on Amarin Corp Plc (AMRN)

[bidmark]

How did Mori arrive at the 4g of 96% pure EPA? Did he take that from other studies previously done? What was his source? And how does the product he used compare to Amarin's EPA? Did Amarin lift the 4g/96% dose from Mori or were there other identical dosing studies done along the way that just confirmed it for Amarin? And then Amarin just took the ball and ran to the USPTO for the patent?

[HDGabor]

r-

Now if you want to claim DHA raises LDL more than EPA, you have to do a direct comparison. When this is done, there is no statistically significant increase.

So IMO, Mori ALONE does not teach, in an obvious way that EPA raises LDL levels less than DHA. But why not?

Agree … IF you claim "DHA raises LDL more than EPA" but the claim (null hypothesis) is (e.g. … Excerpts from the U.S. Patent No. 8,293,728)

without substantially increasing LDL-C compared to second subject having fasting baseline triglyceride level of 500 mg/dl to about 1500 mg/dl who has not received the pharmaceutical composition and concurrent lipid altering therapy

and Mori "teach" it. (Please note: Some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to modify the prior art reference or to combine prior art reference teachings to arrive at the claimed invention.)

In case of Apo-B, the claim (null hypothesis) is "reduction in fasting apolipoprotein compared to second subject having fasting triglyceride of 500 mgldl to about 1500 level who has not received the pharmaceutical composition and concurrent lipid altering therapy"

Kurabayashi definitely did not teach, suggest or motivate since between the groups different was statistically non/significant.

Kurabayashi shows (only) that "reduction in fasting apolipoprotein in subject who has received the pharmaceutical composition" (change compared to the baseline) …. but it is not … could not be … a basis of any teaching, suggestion, or motivation (meanwhile Mori could).

Best,
G

[rmitra]

Kura and Mori, Part II.

1. Mori does not teach that DHA raises LDL levels MORE than EPA.
2. Mori does teach that DHA raises LDL level relative to a placebo group with greater than 95% probability. (or more precisely, you can reject the null with >95% percent probability, which is a slightly different, but more accurate statement).

Does Mori teach that EPA DOES NOT raise LDL levels relative to a placebo group? No. It teaches there is not 95% confidence that EPA raises LDL levels relative to placebo.

What is the probability, given the DATA in Mori that EPA raises LDL levels? One can easily compute this since they report the mean and SEM.

The answer is 87.38%

Or conversely there is a ~12.6% chance that EPA does NOT raise LDL levels given the data in Mori.

These probabilities can be changed by looking at data outside of Mori, of which there is some. But not in the right Tg populations. Nor is Mori the right triglyceride population. So is it obvious? Well trying to be unbiased, w.r.t. LDL, I can maaaybee see an argument, though I tend not to agree. But with regards to ApoB and Kura, I do not see it. Combined, I do not see it.

[alm2]

Please send to amarin /Covington -vital they have-Alm

[alm2]

Please send to amarin /Covington -vital they have-Alm