it must not have occurred to you that being wrong is not something to be proud of. but in your case if you didn't take pride in what little consistency you have even if it's being consistently wrong, you would have nothing at all. So thump that chest and continue to tell use how you're going to win it big.
i'll even let you in on my position. i had about 300k at an average price of about 1.65. i recently sold 100k at around 2.5. i'm going to hold the remaining shares going into meteor readout since i expect the trial will not only meet it's primary endpoint but will exceed it by a wide margin. This success will elevate all debt concerns and the market cap for exel should pass 3 billion giving a stock price of at lease 15/share. At which point, i'm going to sell about 100k and will let the rest ride to see how much higher i'll go.
during all this excitement, i might just think back and wonder how can anyone miss such a great buying opportunity; at which point, i may think of you. If you're still around them, i'm sure i'll have a few good words to share with you.
seman, for some but not you, it is easy. for example, I'm already on the beach enjoying the spoils of my investments contrary to ignoring experts like you who only know how to fud. keep up the good work.
you sure is smart seman. I really like the result from the last time you said the stock price was definitely going under a dollar before the end of 2014. this time you should stick around when your prediction blows up in your face so we can try to comfort you.
regarding my comment on mydicar bystander effect, i was referring to what the company said at their analyst day. In their animal data (didn't say which animal models), they saw that 60 to 80 percent of the cells were infected by the drug and the uninfected cells performed better by nature of just being next to those that were.
i think the company still has a link to this presentation... if it's still up, just go to the Q&A section to hear what they said.
my comment about ogut was not based on the blog you referenced but on ogut's posts on investorshub. his alias there is poorgradstudent. in one of his post, he made a statement about "expression trumps persistence". inferring that not only does mydicar not increase persistence it also does not increase expression. it seems he's basing this opinion (in his mind, it's a fact) on proof from ONE preclinial large animal studies showing that delivery of drugs like mydicar was ineffective when given by intracoronary.
From having read post from ogut in the past, i've concluded that he's very opinionated and is extremely bias against any drugs (companies) that does not fit neatly into his theory or understanding of how things should work. needless to say, he has stated cupid 1 is a fluke and mydicar does not work. here's the quote from poorgradstudent regarding cupid 1 and mydicar, "Honestly, I think it's just one of those fluke results you get in small CV trials. I'm rather confident it's unrelated to their intended mechanism. Expression trumps persistence, and their pig model data demonstrated no meaningful increase in protein expression. "
As you can see, it seems he's aware of the study i've posted but according to him, the increase in expression is irrelevant b/c in his mind, it was not enough. never mind that this increase in expression restored SERCA2a back to normal level and that this increase resulted in meaningful improvements in the treatment group over control. he's an example of a person who only sees what he want's to see. never mind that the pig study showed "cardiac SERCA2a expression was significantly decreased in group 2 (control) whereas in group 1 (treatment) it was restored to normal levels." And that this observed increase in expression of SERCA2a was the result of an intracoronary infusion. This pig study basically disproved his argument but b/c the SERCA2a expression was not large enough (in his mind), it doesn't count.
the bear case for ogut hinges on the argument that preclinical data for large animal is questionable and does not support the drug's clinical efficacy. To support this argument, he only list on preclinical (Recirculating cardiac delivery of AAV2/1SERCA2a improves myocardial function in an experimental model of heart failure in large animals) study to support his narrow views.
Well, here's another preclincal study in large animal that supports the bull case. google "Reversal of Cardiac Dysfunction After Long-Term Expression of SERCA2a by Gene Transfer in a Pre-Clinical Model of Heart Failure". to read the full study select the link by onlinejacc.
i'm not sure the piece by ozgur ogut paints a complete picture. for example, in celladon analyst day, they said preclinical studies showed an infaction rate of btw 60 to 80 percent.
also, ogut only focused on one aspect of the preclinical studies, and seemed to have ignored all other data showing "significant improvements in cardiac function in pre-clinical models of heart failure in rodents, pigs, and sheep, even when the underlying pathophysiology or insult (e.g. mitral valve rupture or pacing induced heart failure) is not corrected"
as it turns out, it seems ozgur ogut is "poorgradstudent" from the investorshub. having seen some of poorgradstudent's posts on other companies in the past, he tends to be very narrow minded in his beliefs. if things don't fit nice and neat, he'll doubt and scream bloody mary until the cows come home(i.e. until the data proves him wrong.)
only fools invest based on analyst opinions. if all it took to be a successful biotech investor was to have a phd, then these analyst would be running their own hedge fund making millions or billions instead of working long hours for a few hundred thousand a year if even that.
for the record, I've been long cldn long before these analyst even started coverage.
i don't think the dose reduction is as big as people think. the design dose in the early stage RCC trail was 140 mg. however, dose reduction was common such that the median dose actually used was 75 mg. So, as a result of "extensive dose work across multiple indications", 60 mg was selected. also note 60 mg was used in the mCRPC trail and it basically duplicated the results seen in the earlier stage trail designed to used 100 mg. So, considering the cabo dose in meteor is only slightly less than the 75 mg used in the previous RCC trail, we can only trust the company is correct in it's choice of 60 mg.
I like our chances of success in RCC but i can't really wrap my head around it definitively enough to give it any odds. I can only say that i strongly believe it's much more likely to succeed than not based on two facts: 1) the earlier data in RCC and HCC were much better than what was seen in competing drug trails. 2) cabo as been very consistent in it's efficacy across multiple trials of different size and indications. i think it's very likely the earlier cabo results will be repeated in RCC. The question is will the control behave as expected and there's enough data to believe that it will.
the issue with the comet trials was they didn't have a clear understanding of what the benefits were for the control arm and to add insult to injury, they underestimated those benefits. The treatment arm for both comet trials did show some benefits; however, the benefits shown where not better than what was already achieve using the standard of care. The design of the comet trails had no margin for error; it was obvious they were swinging in the dark and hoping for a home run.
Unlike in mCRPC, the design for both RCC and HCC has a huge margin for error when you consider the threshold need for success for both the METEOR and CELESTIAL trails are significantly less than the results seen in the earlier clinical trials.
Also, data for cabo to date has been very consistent across multiple trials. Even for the failed comet trials, the treatment arms performed similar to those from the earlier trials. what doomed exel were that there were no control arms in their earlier mCRPC studies to show them that cabo only had limited efficacy in mCRPC and was not worth chasing. in fact, even without the control data, exel shouldn't have chased after mCRPC b/c there just wasn't enough data to design a good phase 3 trail but the company was too greedy to see clearly.
mj, you could be right, but since he has stated his position, real or not, he's gone on record and we can see how good a trader he is or not.
seman, i take what i say back, you're not gutless, though depending on how this pans out, you could still be a fool. got no problem with anyone talking their position since that's the game we all choose to play. i see your 10,000 short shares and raise you 300,000 long share. on top of that, i don't intend to sell any shares until meteor results are out. do you have the same conviction to be short going into the meteor result?
seman, you really are a fool... by investing aren't we all betting on the stocks outcome. if you want to bet the stock will go to sub 1 by 1/1/15, then just short or buy puts or sell calls. there's all these ways you can bet against us longs but here you are making this cowardly excuse to not place your money where you mouth is. stop making this stupid childish wager knowing that it will just get ignored; stop being so damn cowardly and just short exel until it hurts if you've got any balls. otherwise, you're just another fool trying to talk big but fooling no one.
the 8mm/qtr cash burn includes the cost of running the cupid 2 trial. so far, the company has been very conservative in the size and number of the trials they are running. now, if the fda requires them to run a large phase 3 trail after successful cupid 2 results, than no doubt the qtr burn rate will increase.
if you look at the cupid 1/2 trail, you will see that "MYDICAR is Administered on Top of Optimized Drug and Device Therapies" so, it will not replace pacemakers/ICDs anytime soon.
I've seen reports saying there are 400,000 devices install yearly in the US. cost for ICD is around 26k and pacemakers are around 7k. that's only for the device. the cost to implement the device adds another 10k to the bill.
as for the cost of MYDICAR, the company has not come out with a price yet b/c that would be like putting the cart ahead of the horse. however, they have mention 20k as an example when trying to size the market b/c that's usually how much it costs to treat a heart failure.
akanz2, 135mm? the company's burn is roughly 8MM/year and as of last qtr they had over 90MM. So, the company is currently well of financially. Now, if CUPID 2 is successful and is approved in the EU (not sure where the FDA stands with regards to cupid 2); i doubt any of us will be mad with them for raising capital to support the launch of MYDICAR.
ulingt, it's best to just ignore socialidiocies since nothing he says makes any sense. how can cabo be designed to "fixed Gefitinibs failure", when they don't even have the same target? another thing socialidiocies does is treat theories (pulled out of thin air) as accepted fact. you will note that his theories do not reflect what has been observed in clinical trials. e.g. he thinks RCC will fail but does not and can not explain why we saw such strong phase 1 cabo data in RCC. Here's what we have seen from the cabo RCC trail:
"Tumor Regression. Objective evidence of tumor regression was observed in 19 of 21 patients (90%) with ≥1 post-baseline assessment. Best overall response was determined per RECIST criteria with 7 of 25 patients (28%) showing a confirmed partial response (PR). Importantly, PRs were observed in heavily pretreated patients, including 3 patients with 2-4 prior systemic therapies, and 2 patients with 4 prior systemic therapies. Thirteen additional patients (52%) had stable disease (SD) as their best response, and only a single patient (4%) demonstrated evidence of primary refractoriness to cabozantinib with a best overall response of progressive disease. The rate of disease control (PR + SD) at week 16 for all 25 patients is 72%.
Progression-Free Survival, Overall Survival, and Treatment Duration. Kaplan Meier estimate of median progression-free survival (PFS) is 14.7 months (95% CI, lower limit 7.3 months – upper limit not reached). Median overall survival (OS) has not yet been reached after median follow-up of 14.7 months. The estimated 1-year survival rate is 60%. Seven patients remain on study and progression free with treatment durations ranging up to 21.8+ months."
Anyone can dream up theories... but only fools will continue to argue against empirical data. with socialidiocies, we have such a person. But it's your dollar so believe who you want.