Amarin Corp Plc (AMRN)

[HinduKush]

sts
A claim was made by the generics and accepted/discussed extensively by Judge Du in her epihanic judgement; this claim was of EPA being demonstrated to not elevate LDL as opposed to DHA and was therefore THE basis for Du's entire prima facie obviousness construct and Du used the Mori 2000 Am J Nutr data to justify it. Everything else in terms of legal procedure (relegating secondary indices, weighing objective indicia versus each other etc..) follows one step after another from this ONE singular assumption...it is our source of the Nile. Remove this absurd claim and every part of Du's construct falls like the walls of Jericho.Interpretation of Mori was and remains a CLEAR factual error (as was the interpretation of the Kuryabashi paper table statistics--which incidentally goes to incorrect METHOD of assessing the published prior art). Furthermore, IF the assessment of the prior art was based entirely on this fallacious interpretation ofthe 2000 Mori data, what then remains? Du's sequence of logic in accepting MORI's data relevance to the MARINE patents with TG>500 mg/dl was based on the idea that EPA would work in the SAME way above or below TG=500mg/dl which every bit of scientific literature says it doesn't. I will present some of this evidence below as post-script. Bays the lead author of the MARINE trial, and a true POSA amongst PHOSITA's summarized POSA prior art knowledge completely in 2008 (vide infra). Lastly the eror in Kuryabashi and Mori are not just evidence of incompetent assessment of key data in a trial. Kuryabashi supports directly the Apob Claim in patent 715 which I cite below.
HK

The ’715 Patent
The ’715 patent issued on November 27, 2012 to the Inventors. The patent issued from Application No. 13/282,145 (“the ’145 application”). (ECF No. 324 at 4.) Claim 14 of the ’715 patent is asserted. The asserted claims of the ’715 patent, and any claims from which they depend, are reproduced below. 13. A method of reducing triglycerides in a subject having a fasting baseline triglyceride level of 500 mg/dl to about 1500 mg/dl, who does not receive concurrent lipid altering therapy, comprising administering orally to the subject about 4 g per day of a pharmaceutical composition comprising at least about 96% by weight, ethyl eicosapentaenoate (ethyl-EPA) and substantially no docosahexaenoic acid (DHA) or its esters for a period of at least 12 weeks to effect a statistically significant reduction in triglycerides without effecting a statistically significant increase in LDLC or apolipoprotein B in the subject. The method of claim 13 comprising administering to the subject about 4 g per day of the pharmaceutical composition to effect a statistically significant reduction in triglycerides and apolipoprotein B without effecting a statistically significant increase of LDL-C in the subject.

BAYS published a summary of POSA thought circa 2008-it was peer reviewed:Bays HE, Tighe AP, Sadovsky R, Davidson MH. Expert Rev. Cardiovas. Ther. 2008

We can trace the line of thought regarding EPA and DHA effects on lipids as follows between 1997-2008:EVERY EXPECTATION WAS FOR OMEGA3'S TO INCREASE LDL WHEN ADMINITERED ALONE FOR SEVERE HYPERTRIGLYCERIDEMIA--ONLY WHEN BAYS PUBLISHED MARINE TRIAL DATA DID THE THINKING CCHANGE ON EPA
1999:


2006:


2008: