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Congrats. What about ldl?
That part I don't understand. If the effect is mainly anti-inflammatory, shouldn't EPA alone has some effect?
I don't think so. Comparators arms are used by pharmaceutical companies frequently to show superiority of their test drug. There is no benefit for the owner of the approved drug to allow for it and lots of risk as they could lose their current market. Therefore I don't think they need their approval.
They can show that in the study hi Epa/aa levels correlate with lower CVD.
Data is blinded as they don't know for sure is a given patient was on vascepa or changed his/her diet to sushi. But it would give the FDA the science it needs to be more comfortable with the idea as those with the higher epa/aa are more likely to be on vascepa.
Once said that. I am persuaded by other arguments in the board indicating that this scenario has likely not happened. I understand now why it is important to maintain all blinded including for the labs.
I think they get that data. For instance using that data they decided that they already had enough patients in the 150-200 TG group and decided to continue recruiting only patients with TG above 200
Maybe they showed this BLINDED data to the FDA to support label change before end of reduce it?
They report all that data to the central database. Company is still blinded (they don't know for sure if a patient with hi ratio is on V). They also know what is going on for each patient. So even if they are blinded they should know if lower event rate is happening on patients that have hi EPA/AA
I guess they know the EPA/AA ratio.
Hi AVII77,
What is DES?
Do you have any thoughts on my post #81561?
HD and others,
Provided that Reduce-it is successful, what additional studies would take for a EPA/statin combination to become a reality? As a reminder, amarin already conducted a phase-I (http://investor.amarincorp.com/releasedetail.cfm?ReleaseID=772903). So my question is what would be needed to built on that successful trial and secure regulatory approval for the combination.
Thanks
M
That sounds logical on the surface. However I believe it misses to explain the paradox of why the expected CVD rate in reduce-it is expected to be about 4 times higher than in Jellis.
It can hardly be explained by LDL levels only I think.
Thanks!
Got it. Thanks!
Thanks. So what you are implying is that the other 1M may be an insurance for edinpharm so Amarin do not brake the deal in case early stop? The speculative comment you made is what I am trying to understand.
Thanks so much for your great research. I read each of your posts!
Sorry I do not follow. Amarin received 1M when CTA was submitted as a milestone. What are you implying?
Did I Get this right?
This is what I understand. They recruited within that 2 years patient with a primary CV event. Then they followed up for 12 months and the 12% reflect secondary cardiovascular events. Did I understand it correctly?
Also secondary events are the one that are been tracked in R-it, correct?
My understanding is that it is a 12 month:
"Twelve months follow-up data were obtained
in a total of 325 patients; in 19 cases, statins were stopped,
and six cases of MACE occurred before 4 weeks, as determined
by inspection of"
See paper below.
Very small trial (only 325 patients) however they had a yearly CVD rate of 12%. See in particular patients with TG higher than 150.
What do you think? What are the chances that the rate in R-IT is actually much larger than 5.9%?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784976/pdf/kjim-24-330.pdf
HDgabor,
According to my calculations (conservative calculations), trial should end with a composite rate of 4.65% and worst case scenario of 4.95%
Do you get similar numbers?
OK this is very informative. Then do you have an estimation on what could be the composite rate if interim hits on March?
I think I answered my own question. In this trial the event rate/year is 3.8% approximately even when 73% of the patients had CVD. Study can be found online
Thanks AVII and JL for all the DD done in this. The rest of the board, including me appreciate it greatly.
I am glad to see (If I understand correctly from this study) that MACE could be as high as 7.4% and MACE+ could be as high as 12%? Is that correct? Were the patients on this trial on statins?
Also, AVII, considering all your research on the issue, do you have an estimation on the composite rate for reduce it if stopped in Feb, March or April?
Thanks so much!
Got it. Thanks so much for the clarification.
I am then still wondering whether there is a good way of modeling the composite score taking out the 967 first events
best
AVII, please ignore this post. Obviously this cannot be calculated correctly, as there is no way to know what is a FIRST vs subsequent event.
Pretty much I just realized we know a lot less than we would like about the chances of interim stop. We can still follow the TOTAL number of events. However we do not know whether any given composite rate (regardless of how low it is) may be enough for an early stop.
Happy to hear others thoughts
AVV, Have you (or anybody else here) modeled the trial taking out the FIRST EVENT? I would do it myself, but I am afraid that is beyond my math skills
That is helpful. Then the total number of FIRST EVENTs will be a lot less and therefore it is likely that the guidance of the company indicating they do not expect a stop at interim may be driven in part by this.
In other words, the trial may be going brilliantly, but due to the much lower number of FIRST EVENTS that drive the primary endpoint they may not reach the strong statistical significant that is required.
Thoughts
Also thanks AVII, raf, JL, HD and others for their very thoughtful posts
Maybe you have shown this before. How do you conclude the composite rate is 4.5-4.7% According to my calculations (967/20000) is about 4.8%
Thanks
Thanks
Can someone give a brief explanation of what this means to those like me with null financial background.
Does this mean reduction of debt? does this means more cash? does this affect in anyway chances of finishing reduce-it?
Thanks
Great numbers, thanks Sam81
Thanks so much for your estimates. Really appreciate it.
When would you expect a stop if cv events are larger let's say 6 or 7% and vascepa reduce them by 25%?
I took the trouble of doing some math on the Cherry data by amplifying the dot plot and manually counting dots. I divided that dot plot into 4 quadrants. I put de lines at 0 in the y axis (improvement vs no improvement in the plaque volume), and at 100 in the percent change for EPA/AA in the x-axis. The rationale for using this cut-off is that I believe most EPA treated patients should be above that level.
Not perfect, but using these cut-offs I got about 100 dots on the low EPA/AA and about 100 on the high EPA/AA indicating that this is likely to be a good way of distinguish treated vs untreated. Then I calculated the % of patients that get worse (increased plaque volume) in each of the groups. This is what I got:
-43% of patients got worse in the low EPA/AA ratio group.
-Only 9% of patients got worse in the high EPA/AA group.
I know this analysis have limitations but in my view, the chances of having a cardiovascular event would increase if plaque volume get worse. My conclusion is that a the very minimum, EPA stops or reduce plaque growth very efficiently.
I wonder what you all think
Can someone remind me the effect of vascepa on HDL-C?
Does it affect it in any way?
See below, this is extracted from the Amicus Curiae letter.
Wouldn't that mean that FDA must approve anchor. In other words, they need to expand label of vascepa as a drug that lowers triglycerides and that is safe for patients in the very high triglycerides (>500 mg/dL; or MARINE) to also include high triglycerides (200-500 mg/dl; ANCHOR). And it would be to the doctors to prescribe vascepa each time they feel they have to lower triglicerides, whether it is for pancreatitis (strong science behind it) or cardiovascular diseases (not completely proven but many doctors thinking that there are enough evidence to give such a safe drug to patients). Am I understanding this correctly?
"Although FDA determines the overall safety and efficacy of a drug as part of the drug approval
process, the Agency does not determine all the uses for which a drug may be safe and effective.
Thus, even if FDA had the authority, the Agency is in no position to overrule the medical
judgment of a healthcare professional regarding the benefits of a drug in treating his or her
patients. The prescribing physician is in the best position to understand the patient’s medical
history, condition, and potential responsiveness to a prescription drug."
"$15 million upfront payment which we received last week, together with development, regulatory and sales-based milestone payments of up to an additional $154 million"
They already got the payment....Can someone explain me why they would defer the recognition in revenues? This may be obvious but I do not have a background in finance.
how omega via can produce EPA500 without breaching amarin's patents.
My understanding is that it is a very similar product. Any comments?
Thanks so much!