Amarin Corp Plc (AMRN)

[HinduKush]

on the topic of inflammation diabetes and triglycerides:
Triglyceride rich remnants are clearly a marker for CV risk but R-IT and likely EVAPORATE will show the key is the AA:EPA levels that correlate much better with clinical benefit than mere LDL apoB or even TG lowering. Paul Ridker showed the way with his seminal trial work on CRP, inflammation, CV risk and statin's role in reducing risk through CRP via JUPITER and then later also CANTOS using IL-1 inhibition.
What causes what is not as important as the interrelationships and their consequences for therapy.
All this was known before the MARINE patents were applied for and received:

9. Ridker PM, Rifai N, Clearfield M, Downs JR, Weis SE, Miles JS,
et al. Air Force/Texas coronary atherosclerosis prevention study
investigators. Measurement of C-reactive protein for the
targeting of statin therapy in the primary prevention of acute
coronary events. N Engl J Med 2001; 344: 1959-65.
10. Pradhan AD, Manson JE, Rifai N, Buring JE, Ridker PM.
C-reactive protein, interleukin 6, and risk of developing type 2
diabetes mellitus. JAMA 2001; 286:327-34.
11. Nesto R. C-reactive protein, its role in inflammation, type 2
diabetes and cardiovascular disease, and the effects of insulinsensitizing treatment with thiazolidinediones. Diabet Med 2004;
21:810-17.
12. Rhee EJ, Kim YC, Lee WY, Jung CH, Sung KC, Ryu SH, et al.
Comparison of insulin resistance and serum high-sensitivity Creactive protein levels according to the fasting blood glucose
subgroups divided by the newly recommended criteria for
fasting hyperglycemia in 10059 healthy Koreans. Metabolism
2006; 55:183-7.

The CRP data was available for ANCHOR not sure about MARINE...a construct that lowered TG's, neutral to LDL lowered apoB and lowered CRP would not be obvious in 2008.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3572383/pdf/40256_2012_Article_2.pdf

Here is a good review onthe interelationships:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4465984/pdf/nihms509119.pdf

HK