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Do the volume play
Try to make it OTC if possible
So somebody else makes Vascepa for amarin
Cancel that and hire Apotex or teva to do both brand and generic for amarin.
No. You are wrong
As a medication prescriber i can tell you it will not fly.
No insurance will cover it :)
It is the same molecule so...the answer is no
Once generic is out, can amarin examine their pill to look for other patent infringements?
How come nobody mentions Vascepa in Australia and New Zealand?
Does amarin get the same profit per bottle as in US?
My understanding is Amarin makes only crumbs in Canada? Correct?
That would be awesome
It is way better than cancer drug given population size
From ST
AMRN needs to go to Teva and workout a buyout deal... Why this would be good.. A.)Teva is a generics monster and will mop the floor with those penny-ante Generics like Dr. Buttheads and Hikima in the USA and beat them at their own game .B.) Teva has a heavy presence in Europe and will be able to sell the crap out of Vascepa there. They win on both ends. $20 a share gets it done
Type hikma stock in google
Can vascepa be sold at pharmacies without prescription?
Hkmpf
Hikma stock up 320 percent
I agree the dick did not read briefs
Generics do not advertise.
The expert’s expertise is invalidating patents for good of public. He is a director of such organization. Google his name
You cannot make such assumptions based on plaque reduction only. FDA will not allow this inference.
Thanks to Vascepa and other medical therapy (statins, beta blockers, imdur, aspirin, plavix/brilinta), the field of interventional cardiology abd bypass surgery will be less busy.
Ischemia study is one example but there were other studies before that one.
In general, stents are useful and decrease mortality in acute MI (STEMI and NSTEMI) and for reduction of angina (mortality still not decreased over medical therapy)
Fro uptodate
Revascularization versus medical therapy for stable angina — In the broad population of patients with diabetes, risk of death and future myocardial infarction are similar between revascularization and optimal medical therapy [6-9]. Patients at high angiographic or clinical risk may benefit from revascularization [10].
The best available evidence regarding a comparison of revascularization and optimal medical therapy comes from the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI) 2D trial [6,7]. In BARI 2D, 2368 patients with type 2 diabetes mellitus and nonacute ischemic heart disease (defined as either a ≥50 percent stenosis of a major epicardial coronary artery associated with a positive stress test or ≥70 percent stenosis and classic angina) were randomly assigned to either prompt revascularization (PCI or CABG) plus medical therapy or medical therapy only. The most appropriate mode of revascularization (PCI or CABG) was determined by the investigator prior to randomization. At five years, the primary end points of the rates of survival or freedom from major cardiovascular events (eg, death, myocardial infarction [MI], or stroke) did not differ significantly between the prompt revascularization group and the intensive medical therapy alone group (88.3 versus 87.8 percent and 77.2 versus 75.9 percent, respectively). However, in subgroup analysis, the rate of freedom from major cardiovascular events was significantly higher with CABG (77.6 versus 69.5 percent), predominantly attributable to a reduction in nonfatal MI. In the PCI stratum, there were no differences in major adverse cardiovascular events with prompt revascularization, when compared with intensive medical therapy alone (77.0 versus 78.9 percent).
In the COURAGE trial, an initial revascularization strategy with PCI did not reduce the risk of death or MI when compared with an initial trial of medical therapy in a broad group of patients (see "Chronic coronary syndrome: Indications for revascularization", section on 'Indications'). However, patients treated with initial revascularization were more likely to be free from angina at one year (66 versus 58 percent). In the subgroup of patients with diabetes (n=766), patients treated with initial medical therapy had similar cardiovascular outcomes as patients treated with revascularization (HR 0.99; 95% CI 0.73-1.32) [8,9].
In an attempt to understand further which patients might benefit from CABG, a risk score was developed from baseline angiographic (myocardial jeopardy index, total number of coronary lesions, prior coronary revascularization, and LVEF) and clinical variables (Framingham Risk Score) [10]. Patients were then stratified into high- and low-risk subgroups using either angiographic or clinical variables or both. The composite endpoint of death, MI, or stroke occurred significantly less often in the CABG stratum than in the intensive medical therapy group (24.8 versus 36.8 percent) among those in the highest angiographic risk tertile, and this effect was even more pronounced in patients with both high angiographic and high clinical risk (27.1 versus 47.3 percent; hazard ratio 2.10, p = 0.0051). Although this analysis is limited by small sample size in subgroups and lack of validation of the angiographic risk score used, it suggests that in patients with diabetes, those at highest angiographic and clinical risk benefit the most from revascularization with CABG. In the 381 patients from the CABG stratum that were considered high risk, the rates of death, MI, or stroke at five years were 24.8 percent in the CABG arm and 36.8 percent in the medical therapy arm. In contrast, there were no differences between PCI and medical therapy in the high-risk PCI stratum (29.7 versus 29.9 percent).
My point is since the compound is different from Vascepa they would need to run a CVOT. Otherwise they can just treat triglycerides, which is fine.
We know that all fish oil CVOT trials have failed except RI trial.
I disagree. Without CVOT it will not work.
Putting stents in people without MI doesn’t do anything in terms of survival.
So stents in stable CAD failed CVOT.
The numbers are correct. Why do untrained people think they know better then JACC or ESC editors and biostatisticians?
There are two types of cardiologists
Those that follow up with new science, monitor conferences and literature and change their practice habits based on new findings. There will be several articles coming our next week. I can think of “cardiology today” article, a weekly magazine that all cardiologists receive. Some probably will throw it in the garbage and some will read it, or at least skim through it.
The second group is not interested in updating their practice. Not sure what their motive is ($$$? Money? ). They don’t read any literature and not updating their knowledge.
2 years post Reduce-it, there is no excuse for any cardiologists to ignore Reduce-it findings and not to apply it to their practices.
I still think the major problem is the insurance coverage and all the hassle that physicians have to go through in order to prescribe Vascepa. It should get better in 2021. Hopefully the patents go back to Amarin.
I can do it
Sent you a text message
No
That reasoning is incorrect. Sorry.
The statement is correct. 17 percent compared to baseline. Nothing to do with placebo group. Your thinking about this is incorrect.
Yes it is easier for patients to accept Vascepa if you tell them that their 60 percent lesion will not only not progress but regress.
“Hey this medication will reduce your blockages so you don’t need to operate on your carotids or put stents in your heart. “.
“Ok doc. That sounds great”
Patients understand such language better.
I think Evaporate results complement Reduce-it results perfectly. Amazing result.
Yes everyone in my family has antibodies except me.
The biggest obstacles to more Vascepa scripts are quite simple:
1. Insurances, insurances, insurances
2. High copay even if insurance covers it (usually tier 4)
Soft plaque (more prone to rupture and cause STEMI) vs calcified plaque.
Both are bad but calcified is more stable.
Had a patient with 0 calcium score but 99 percent left main stenosis (soft plaque not detected by calcium score).
I think Vascepa should reduce calcium score. I am sure they will do studies on that. Easy to do.
Cardiovascular studies are the best studies done in all medicine
Another impressive study
Amazing
https://www.nejm.org/doi/full/10.1056/NEJMoa2022190
Only crestor does it (that’s why i am on it).
It causes regression
https://pubmed.ncbi.nlm.nih.gov/17384434/
We can make conclusion that if you are on a statin, the plaque will progress.
More to do with insurance companies not approving Vascepa and doctors accepting “substitute@ as recommended by insurance companies and pharmacists. I always say no but most doctors say yes.
The study population in evaporate has less severe CAD and CABG is excluded.
Yes there is no no statin group, but the patients on statins progressed by 0.9 mm
So i can say statins may cause slowing of progression but don’t cause regression.
Both placebo and treatment group was 100 percent on statins
Placebo group progressed 0.9 mm and treatment group regressed 0.3 mm
Two conclusions:
1. Statins cause no plaque regression
The placebo group on statin progressed by 0.9mm
2. Vascepa benefit has nothing to do with triglycerides. Niacin, fenofibrates lower triglycerides without clinical benefit.