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CYTK:
>So improving ejection fraction is not a good thing for heart function?<
Depends where you are on the scale
Going from 20% EF to 40% will likely make an impact, but 33 to 36%? 45% to 50%? Probably not so much. And in the latter two cases, I'm not sure anyone can say with reasonable certainty that the persons with 36 and 50% EF will live longer than the ones with 33 and 45% EF.
CYTK was at least realistic enough to know that finding the proper clinical scenario for CYTK may exceed their grasp at this time. I think we're on the same wavelength in this regard.
We'll see what type of endpoint Amgen decides to pursue.
Re: skeletal muscle drug
>If you increase the contraction strength for a set amount of signal couldn't that translate into conserving the muscle mass and thereby reducing the rate of decline?<
Perhaps. But if the root of the muscle wasting is the decrease in innervation, then by and large the decline in muscle performance is going to take place.
I don't dispute that it will help lessen the rate of muscle wasting, and I think we can agree that it won't prevent the wasting outright. However, thinking about it from an approval standpoint, what is a meaningful improvement for people with a chronically debilitating disease?
I can't answer that with a reasonable level of confidence. That's why I'm watching out of curiosity but not a vested financial interest.
CYTK:
My dosing concern is more a big picture one. The effect of this drug is very direct, and depending on the extent of myocardial dysfunction, different patients could have greatly different dosing requirements. Specifically, this drug aims to "activate" myosin, but what it is practically doing is increasing the attachment time of myosin on the actin filament (and thus increasing duration of the contraction). This increase in attachment time has to be well synchronized, because having regions of the heart with varied contraction durations is a good way to achieve arrhythmia and other issues during systole.
>The ph1 and ph2 trials used stroke volume, change in heart rate and change in lv ejection fraction as endpoints to correlate PK with activity, but I don't think that is what they plan on using for later stage trials. Publicly they have stated that they are going for reduction in death and/or hospital readmission as well improvements in exercise capability as potential indications targeting both acute patients that are candidates for LVAD and chronic patients.<
Right, so the connection between ejection fraction and survival / reduced readmissions is a murky one. I see little connection. As South Park put it: underpants + ??? = profit.
As for changes in exercise capability and such: patients with significantly reduced exercise capacity are generally looked at as (re)vascularization candidates. Patients who get on the treadmill and experience chest pain do so because of ischemia / low blood and oxygen supply to regions of the heart. This is a consequence of having one or more vessels with significant occlusion. As such, I don't see how increasing the force of the contraction helps these patients. You create more flow through a constricted pipe, increasing shear stress which is believed to be related to atherothrombosis.
So I'm on the sidelines until I have a clear view of how they intend to get this drug approved. The pathways that involve large pools of the CV patient population don't look like rational pathways to me at this stage.
>Are you thinking of the dystrophies when you mention skeletal muscle conditions in which the scaffold is disrupted? Yes, one would not expect the drug to show any effect in these indications. However, they are looking at ALS and myasthenia gravis in which the nerve impulses are disrupted resulting in poor muscle function with the idea of improving the quality of contractions. Does that make sense to you?<
Yes, I was primarily addressing dystrophies in the previous post. But I think the disconnect still applies to conditions like ALS and MG.
Consider a typical muscle activation pathway with 4 distinct states:
motor neuron innervation -> neurotransmitter release -> Ca2+ release inside muscle cell -> contraction
Conditions like ALS / MG involve defects in the first two states. CYTK's drug only impacts the fourth state. So if the first two steps continue to break down in these degenerative diseases, the muscle is never going to get activated to allow the CYTK drug to augment the strength of the contraction.
Dunno. Anyway I look at it, I can't make much sense of the skeletal muscle initiative.
Onyx / Proteolix:
Onyx's share price was taking a beating in part due to rumblings that the CEO Tony Coles would pull a Goddard. Perhaps the small rally in ONXX shares today, which is often unusual for the acquiring company, reflects a bit of relief by investors that Coles didn't, in the end, pull an outright Goddard.
Two things are somewhat surprising / concerning to me about this deal:
1) Why buy the company outright rather than set up a development collaboration? The purchase pretty much reads like a collaboration, and the other assets are quite immature and unlikely to be deal drivers.
2) This is a follow-up compound on bortezomib / Velcade, which was the much maligned Millennium's drug for multiple myeloma. Millennium was routinely the butt of jokes (deserved, to some extent) for their history of blowing money during the biotech craze. In my view, however, many people underestimate the acumen with which their clinical staff guided Velcade through the approval process and the label expansion process. It appears as if Onyx is counting on a similar treatment of carfilzomib by the FDA. There are pitfalls to this expectation, in part because Millennium did a very good job in shepherding Velcade to market, and because the "unmet need" status for multiple myeloma patients was much more acute then than it is now.
But at least it's no EYET... yet
* For those examining the loose relationship between performance of wall street executives and compensation, they should dedicate a chapter to Goddard. How he kept his job is difficult for anyone but his mother to explain.
For those interested in DNDN:
I will be attending a presentation by Urdal this Wednesday. If there are any scientific questions, please post them or PM me and I'll do my best to get answers.
Please do not forward me questions about marketing partners, Pazdur, FDA / big pharma conspiracies, and general profitability (how much will it cost, etc...) questions as I do not think they are appropriate for the upcoming forum.
I agree.
This stratification simply reflects the utility of LDH as a marker for prognosis. It provides no value whatsoever as to the efficacy of drug X. In other words, even if you only admit low LDH patients into a trial, you have no data in hand to suggest that your drug will show a differential benefit. But most companies make this mistaken leap by assuming that the LDH results in the first trial were indicative of drug activity itself.
CYTK:
For their cardiac drug, my concern way back when was that they wouldn't really be able to target the cardiac muscle myosin with enough selectivity. Myosin is one of the most abundant proteins in the body, and is present in all muscles as well as the vasculature. This concern has been somewhat alleviated, as the side effect profile is more benign than I had thought.
I have two remaining concerns. I think it will have a very narrow dosing window, and I'm not sure how that will play out in larger trials. Also, what indication are they going to go for? Increasing ejection fraction is not really a direct road to increased survival, so what do they do? Perhaps go for an acute indication where you dose the drug after thrombolytics with people who are experiencing MIs? Otherwise, the evidence suggests that cardio patients do well with rate control (beta-blocker / ca2+ channel blocker) that attenuates force output from the heart. The CYTK drug would do the opposite, so at first glance it seems the chronic population is not really in play here.
I've not followed it closely in the last year, but the hypotension side effect doesn't make much sense to me unless it is a secondary physiological response to increased ejection fraction.
As for the skeletal muscle version, this one has me a bit puzzled. Many of the skeletal muscle associated conditions present as weakness but it is because the contractile units of the muscles themselves don't make good contacts with the scaffolding around them to transmit the force. This eventually leads to the atrophy. If you cause the contractile units to create more force, it doesn't address the fact that the force is not well transmitted. So I don't really "get" the basis for this one. Maybe it will cause a short term increase in strength? But longer term? Almost seems like a way to exacerbate the condition and cause more tears within the muscle architecture.
I think you need to spend less time trying to make fun of me and my supposed "scientific" knowledge and more time analyzing the clinical data at hand.
A lone response in a single agent trial does not seem to me to be "amazing efficacy" and I would urge you to support your assertion with facts. Please provide some comparisons to demonstrate that the melanoma trial data recently reported by THLD provides evidence of "amazing efficacy" versus drugs currently used for melanoma.
Additionally, if we look at the 50 patient combination trial results they recently presented, the median survival time for those on this combination study was 3 months. Can you name an oncology indication at any line of defense that would benefit from a drug offering a 3 month median survival?
Even for the largest subgroup in that trial, NSCLC patients, the median survival is 4 months. The third line therapy in NSCLC is generally considered to be Tarceva. In its pivotal trial, Tarceva single agent showed a median survival of 6.7 months versus placebo at 4.7 months. Note that the placebo response in the Tarceva third line trial is arguably the same duration as the TH-302 combination data! Although I would never argue, based on the limited NSCLC subset, that placebo beat TH-302, I would argue that it is clearly not supportive of your "amazing efficacy" declaration.
The second largest subset in the recent TH-302 combination study is in pancreatic cancer, with TH-302 combinations showing a median survival of 4 months. In the pivotal Tarceva + gemcitabine versus gemcitabine trial in pancreatic cancer, the combination had a median survival of 6.4 months versus gemcitabine alone at 6.0 months. Th-302 + gemcitabine? 4 months. Again, I'm not saying gemcitabine alone beat gemcitabine + TH-302, but the data are not supportive of amazing efficacy.
So please, less declarations of amazing efficacy and more discussion of the data at hand, and how they stack up against the currents standards of care, be it first line or subsequent lines of therapy. Let's discuss the clinical trial data.
THLD:
>Wasn't much of a discussion<
I agree. A 13% response rate isn't much to write home about.
Adverse Events and PR reading:
As you correctly note, AEs "may or may not be considered related to the medical treatment or procedure."
I think a little PR dissection is useful.
"TH-302 continues to be tolerated and there have been no new unexpected adverse events. Fatigue was the most commonly reported adverse event and was reported in 5 (55%) patients. Severe (grade 3/4/5) adverse events were reported in 4 (44%) patients and there was one study drug related severe adverse event of grade 3 vaginal mucositis. Two serious adverse events (ascites and seizures from brain metastases) were reported but neither was considered related to TH-302. Hematologic toxicity was not dose-limiting. Skin toxicity is common with 8 of the 9 patients having at least one skin adverse event of grade 1 or 2. Approximately half of the patients have had a mucosal adverse event of grade 1 with the exception of the one patient with grade 3 vaginal mucositis."
So we have grade 3/4/5 adverse events reported in 4 patients. They note that one of them (grade 3 vaginal mucositis) was related to study drug. Then we have 2 (ascites and seizures) that they considered unrelated to study drug.
That leaves 1 patient who had a serious adverse event, and is likely the one who experienced the grade 5 AE*. But the PR, as written, excludes this adverse event from being related to study drug (they only pointed out one that was drug related), nor was it unrelated to study drug (they point out those two in the PR). So we're left with a difficult situation to reconcile: the grade 5 adverse event was neither related, nor unrelated to study drug.
I guess we can argue as to whether the omission is deliberate or not.
*Note that patient deaths due to progression of disease in clinical trials are, unfortunately, expected but are not reported as adverse events.
THLD:
>Severe (grade 3/4/5) adverse events were reported in 4 (44%) patients<
Although I generally dislike quizzes, anyone want to take a stab at what a Grade 5 adverse event is?
I agree. I appreciate his posts on entry / exit points.
THLD:
I'm not saying it's a scam.
I'm simply saying that the data they have provided are incomplete and cannot be reliably used to make the conclusions that you have.
THLD:
This is the beauty of how they wrote the PR!
"The partial response included both confirmed and unconfirmed partial responses. In a confirmed partial response, partial response was maintained through a subsequent response assessment at least 28 days later, and in an unconfirmed partial response, the partial response was reported at one assessment but was not maintained in a subsequent response assessment."
So what are they really saying here?
1) The "partial responses" we report are a blend of observations that are and are not partial responses.
2) They then define what they consider a partial response and what they consider no respon... er... unconfirmed partial response.
Note the beauty how the italicized sentence is constructed. They simply tell you what is and isn't a partial response, but give you absolutely no idea how many of their partial responses fell into either category. 90 / 10 split? 50 / 50?
Why make investors guess?
Objective responses:
>Also with THLD we'll know a lot more in a few months and I agree that when they mention initial recist PR's its misleading - but imo it's not their intention to be disingenuous, rather they are pointing out that initially they saw a % decrease in tumor size that would make it a PR based on the RECIST criteria - but the patient dropped out due to other reasons and they did not get a chance to do a followup and confirm it.<
Right, which by definition means it is not a partial response. So now when you're comparing objective responses across investigational drugs, the bar that THLD has set for themselves is lower than everyone else. So they *may* look good in comparison, but it is simply an illusion.
Also, by definition, it requires a single confirmatory scan to verify a partial response, and this scan is usually (but not less than) 4 weeks after the initial observation of a partial response. So if, as you say, some of these recent data are a continuation of some ASCO data, then how can it be that in 5-6 months they haven't been able to take a simple follow-up scan?
I agree with you that patients can drop out of trials for a variety of reasons. It is rare for patients who are seeing a continuation of their objective responses to drop out; therefore, these types of patients that don't have their PRs confirmed have either progressed symptomatically, or the follow up scan showed progression and they left the trial. Rarely do people who are having a true, robust response to the drug wander out of the trial. To build on the blond guy's gambling analogy, why would you leave the table midway through a hot streak?
It's all about disclosure. Companies don't hide or obfuscate great data. They do, however, dance around mediocre and poor data.
They're reporting unconfirmed PRs again.
GTCB:
>you were one of the most vocal and combative yahoo posters in the promotion of the goat stock...<
Oh really?
You may have enough fingers and toes to count the number of posts I made on the GTCB board. And if you go back to them, you'll note that they're primarily talking about science (as I've done for thld).
I did have a small position with GTCB and I believe i lost around 15% of my investment. Hardly my biggest biotech loser, and I've had a few that I'm sure people on this board can easily recite. For those following, I looked back on my records and they seem to come once every 3-4 years, so I'm due in the next 12-18 months
I will say again that I appreciate the trading tips that you and wallst post on the board. But when wading into the science there is utter ignorance being shown.
And I'm not really sure what your reply is about... are you saying i'm wrong on the scientific merits of THLD? Or the naivete of the "investor" who thinks it is "if" not "when" and peppers that with a beautifully irrelevant Las Vegas gambling scenario?
Well, this guy has mentioned two of the common observations made by the naive (or of those with the intent-to-deceive).
1. That all important single MD that is excited about the results.
2. That all important discussion and feeling that it is not "if" there will be approval, but "when."
If I only had a nickel for every time I've read an investor repeat these fallacies...
Post the new data and let's discuss them.
PPHM:
PPHM:
Well, I understand the PS premise, but I don't understand how the antibody adds to this equation.
Perhaps you can share from your DD.
PPHM:
>He also apparently understands the mechanism of action which you have struggled with...
Quote:
_________________________________________________
"Bavituximab's novel mechanism that enables the patient's immune system to attack tumors more effectively combined with its natural synergy with chemotherapy make it an intriguing and promising new approach to treating solid tumors," said Dr. Chabner. "The early clinical data on bavituximab is encouraging and I look forward to assisting Peregrine as they advance the bavituximab cancer program into later-stage trials in a number of indications."
______________________________________________________<
Let's put aside the insults. That spoonfed quote can be used for ANY drug that, in any way, targets or modulates the immune system. Change "bavituximab" to "drug x" and "Peregrine" to "maker of drug x" and voila, you've got an equally insightful commentary on the MOA of any drug.
>But you are correct in saying that he is not the only Oncologist who has spoken highly about Bavituximab.<
This centers on my main intended point: we are happy to deceive ourselves into thinking that, this time, it will be different!
By and large, human beings don't make rational economic choices and jump from one cognitive dissonance to another. There are obviously multiple reasons why, but this is an example of one of them.
Is Dr. Chabner the first MD to come aboard and talk supportively about PPHM's candidates?
I could have sworn that over the years, there were doctors with different names that generated the same response from investors.
INCY:
I think the financing was something that had to be done, and I'm unsure whether it can be painted clearly positive or negative. The negative perspective is as you stated: why didn't they monetize some of their assets through a partnership rather than dilute?
With both trials up and running for MF, my perspective is that the company gambled and decided that they would not gain from partnering before the trial outcomes; the reason being that a partner at this stage could not add to the MF development program (it's already set in stone), and they'd only get a lesser deal now versus after the trial results (obviously presuming they're positive). It's the Velcade approach to partnering.
As for the other drugs, my view is that they are all at least 2+ years behind the 424 MF program and won't bring in worthwhile $$$. For example, if you license the HSD or diabetes drug, you won't get enough upfront to fund the 424 MF program. So what's the point since you'll still have to dilute? And although it is often a claim made in CCs, I don't think companies can practically outlicense one indication of a drug and keep other indications for themselves, which ruled out the RA indication with 424 (at least in my book). The follow-on compound for RA doesn't have sufficient data yet to be worth partnering, and its existence discourages partners from looking at partnering 424 in RA.
I think the driving force behind this is that Friedman is in love with his drug. He spends the CCs talking about how great 424 is and how bad the other drugs are. This type of thinking can be fatal, but I think it can explain why he hasn't been able to partner his baby.
OT:
>For example, there were at two rounds of decimation at Goldman Sachs <
Just to make my point clearer, I do not think there is any incentive to fire underperforming MDs absent large external pressures. Firing a few MDs because the hospital has to cut payroll by 25% is not the same thing as routinely assessing MDs (especially early career) and firing them for poor performance despite adequate finances.
And you'll have to excuse me if I'm not super impressed by Goldman laying some people off imminent to the sharpest recession in decades
OT: MD admits
I agree that increasing the number of slots in US medical schools would decrease the quality. My small twist on this is that there are already too many slots. Plenty of dim people get in and are hand-held through the training. My small solution to this is to make an undergraduate science degree mandatory (no more humanity majors), and if a student can't get in after his/her undergraduate, then their admission to medical school in later years should almost require a Master's degree. My reasoning is that MDs need a thorough background in science, and if they couldn't get into med school after undergraduate, how are they any better a candidate 12 months later absent a documented accomplishment?
The problem as it relates to US graduates is two-fold: 1) the graduates all want to make significant salaries once they graduate, and 2) there is no incentive at any level to fire underperformers (i guess they learned this from Wall Street). Medical schools don't want to kick kids out because it lowers their graduation rate and they lose out on 30-50K tuition per year. Residency programs, especially ones in less glamorous areas, are filling slots out of necessity and can't afford to lose a doctor.
As for the apparent shortage, my bet is that there is a shortage *if* you're living in non-metropolitan areas. I have a friend here who did residency in NY for 45K per year but now won't go back there for a faculty job because it pays 140K. His reasons were that it wasn't enough to live in NY (despite pulling it off previously with 45K) and that he's trained too long to make that pittance. We then compared training durations, remuneration, and the discussion reached an awkward silence.
Now he's mulling an offer from a private practice in LA for ~500K per year.
Bottom line is that MDs are falling into the excessive salary trap now made famous by Wall Street. Whereas in the past advanced degrees gave you an advantage to compete against others in the job market, they're now a badge of entitlement. So if you go to NY and LA you'll find plenty of doctors. Scranton, PA? Not so much.
And I agree with microcap that the requirements placed on foreign trained MDs are ridiculous. I have many friends here that trained in Ireland and are under pressure to redo certain aspects of their training here in the US because... well, simply because the people running the qualifying tests need to get paid off. Otherwise, the only explanation is that there is some secret anatomy to US citizens that foreign doctors don't understand.
INCY:
I took some profits recently, and it's currently well below my sale price. Care to share some thoughts about support levels so that I can buy those shares back?
INCY:
This company was badly in need of cash, and the convertibles were looming. Others smarter than myself suggested that the company would look to sign a partner for their lead myelofibrosis drug, and use the proceeds to shore up their cash requirements.
However the company diluted without a partnership. Friedman does strike me as the kind of CEO who falls in love with his own drugs, so I wonder if he's being unreasonable on the partnership front.
That said, I still think their two phase III trials (US and Europe) are really great arrangements for the company. Perhaps he's trying to do what Millennium did with Velcade... announce approvable data and then strike the deal.
OT: Compensation
A small minority of people are now lamenting the supposed death of capitalism, purportedly at the hands of an administration that hates the concept.
The real irony of the situation is that capitalism is crushing itself. The progress of capitalism has completely dislocated the concepts of compensation and profit from innovation and production. I won't even bother opining on the obscene compensation of the Pepsi and Cheetos CEO, because arguing that you need to be innovative to sell junk food to bovine America should be difficult to do for any sane person.
I'm now curious as to how hard our society is going to protect "banks" like JP Morgan and Goldman Sachs who make hundreds of millions (and billions) every year through high frequency trading and other automated methods of churning stock. Maybe one day someone can explain to me how making money by trading 100K shares of GE for 0.25 cents per share profit in 18 seconds adds to "production."
tony / ARIA:
>I don't believe the market can be up forever. <
Agreed.
>I am definitely buying around ASH time, but have no intention to hold the stock though october and nov. To many things can happen. If the general market corrects as I expect in ocboter we can easily see sub 2s PPS.<
I don't disagree with you. However, at ARIA's stage, I do not think it is a bad idea to set some mental price targets (or event targets) and purchase fixed dollar amounts at these points. So perhaps it is going below 2 due to market conditions / rida failure; even if so, buying some at 2.25, 2, 1.50 etc... is not a bad play if you think 534 has merit.
Blade / ARIA
As far as management, I don't think too much of Berger. He's not a fraud of a CEO a la Bianco / CTIC, but I do believe he is the type that is in love with his company and the prestige derived from it. I see the CEO risk confined mainly to 534, since ridaforolimus has a partner (thus tempering Berger's involvement).
I think the preliminary data on 534 looked good, and if the company looks to license once again, today's share price will look good.
Shares outstanding doesn't bother me too much. It isn't great, but the dream of having a company with a phase 3 drug and 35 million shares outstanding is just that... a dream. I suspect companies with ARIA's financial situation are going to be the norm going forward.
Overall, having given it much thought over the last couple of years, I've subscribed *generally* to the theory that investing in phase I / early phase II drugs is a good way to go*. If you're diligent about doing the research into the drugs at this stage, then you stand a good chance of making profits as phase II data roll out. You can then keep a portion of the shares going into phase III if you so wish. ARIA fits this bill, as does my other (now lesser) holding INCY.
* Birchenough at Lehman (now Barclay?) articulated this a couple of years ago and I think it has merit.
ARIA:
>It is dead money now.<
I guess in the trader's sense, yes.
But if you're looking forward to seeing more data from 534 like I am, it is not a bad idea to average into the stock at opportune moments.
OT: IBD
Especially over the last year or so, Investor's Business Daily has become an over-the-top partisan rag.
I think their "ragness" peaked when they wrote a recent health care reform story meant to scare people... and Stephen Hawking especially. The story wrote that under a system like the one they have in Britain, brilliant scientists like Stephen Hawking would have been dead long ago.
THLD:
Yumm... nothing says crappy data like "partial response included both confirmed and unconfirmed partial responses."
OT: Scams
At the risk of enraging First Amendment die-hards, is it possible to ban talk of obvious scams like CVM?
I fear that the posts on it are simply doing what the pumpers want, which is to spread the ticker. And it's not like anyone who cares to follow this board is confused about what CVM is and isn't.
just a suggestion...
INCY:
From the presentation slides:
- 3 month, double blind, randomized, vehicle controlled study of 200 pts
- dosed once daily with vehicle, 0.5%, 1% or 1.5% formulation
- Primary endpoint: change in total lesion score (erythema + scaling + thickness)
- Secondary endpoints: percentage of patients achieving clear or almost clear lesions; change from baseline in the psoriasis area and sensitivity index (PASI)
Results:
- at 12 weeks, absolute change in lesion score was ~-1% for vehicle versus -2 to -2.5% for 0.5, 1 and 1.5% doses. All three were significantly different than vehicle with P < 0.05 for 0.5 and 1% and P < 0.01 for 1.5%.
- statistically significant change versus vehicle was observed beginning at two weeks for 1 and 1.5% formulations and 4 weeks for 0.5% formulation.
- can see some dose-response as the 0.5% formulation appears to have a more graded onset of activity than the 1 and 1.5% which are very similar.
- at week 12, 25% of patients in the 1% and 1.5% dose levels were clear or almost clear by PGA versus 6% in the vehicle group
- the webcast can be accessed from INCY's website... some nice, hand-picked pics can be viewed in the presentation.
Obesity Drugs:
10% weight loss in a year?
BFD.
Consider me on the side of people who hope the FDA takes these drugs to the woodshed. None of these results are impressive imo. I don't see how either company can charge a profitable price for a pill that will have a much less meaningful outcome in real world use.
If anything, these drugs should be entirely out of pocket expenses and not covered at all by insurance or medicare.
ARIA:
>I have no position right now but intend to buy in for the ASH meeting BTW.<
Apparently I was more invested in this interim analysis than you were...
My comments were merely to reflect my impression that the ratio of "successful" interim analyses to the number of succesful phase III trials is probably 100:1. No sense in jeopardizing hard earned money on a low accuracy signal.
ARIA:
>Is it not correct that the drug was showing some efficacy otherwise the trial would have been stopped already ?<
I hold ARIA as well, but let me ask a simple question: Can they get "some" approval if they show "some" efficacy?
My answer would be no. You need to show clear efficacy to get clear approval. All the interim analysis did was show that there was no clear disadvantage to being on the drug arm. Personally, that's not the type of information that would cause me to increase my position at all.
I know that you noted that this patient population has little in the way of treatment choices. However, that is an argument for approval in the face of a modest, but statistically significant efficacy demonstration. It would not be a convincing argument in the case of a numerical advantage for the rida arm without statistical confirmation / validation.
OT: Anyone else feeling like a genius in this market?
I think it's out of control.
Is this the real real one? Or just the real one?
Remember Taitz has shown us a "real" one before.
On that note, I'm outta here. I need to go confiscate some guns from second amendment activists.
Good luck guys! Don't let the news discourage any of you from your righteous paths.