The average price for a long before the recent run up in price is $53.75.
The market is currently up roughly 20% for the year.
20% to $53.75 is $64.50.
Let me put it together differently...
You are an institutional money manager and your job is to... and to retain your job that feeds your kids, pays your mortgage etc... - is to match or beat the broad market.
As baskets of capital are reallocated towards year end, where does Vertex stand? Right now we are up on an average basis.
Where does Vertex stand with institutional money if the price falls below $64.50?
So if you didn't heed my warnings a week ago... pay no attention to this one.
On a risk adjusted basis, Vertex is currently worth 10 billion in my opinion. Potentially worth more but I am discounting that due to the inept business management presently being hacked out by a bunch of lab researchers.
This is a precipice... and when big money starts to lose, they will get out quickly to limit their losses. I am guessing a $10 drop.
Been wrong before... wasn't wrong last week.
So I will say it again... This is going to fall to the $40 to $50 range. Take your profits before Wall Street does.
glad to see the market shares your enthusiasm - loss of 4billion in market cap in a week. Way to go Leiden!!
Q, you are right-on. There was an anecdotal story of weight gain of 5 pounds after 4 wks of 809/770 in the Ph II. Did you see the ClinicalTrial website on 809/770 trials? Vertex is apparently preparing for a huge (1100+ participants) rollover study of 809/770. They are not yet recruiting, but the trial eligibility requirement is that the participants must have gone thru Ph II or Ph III of 809/770. 1100+ strong rollover indicates to me that all of homozygous 508del who received 809/770 for 4 wks or longer. You CANNOT recruit so many if there were dropouts or dissatisfied participants. Vertex must be confident about the safety AND efficacy of TRAFFIC and TRANSPORT trials. Rojospan may be right about early reporting of preliminary results. Because of number of shorted shares we will see a huge spike in the share price when the results are announced earlier than expected.
Third, thank you for all of your analyses of the prior 809/770 Vertex data and the new emerging science using miRNA technologies to correct CFTR function disclosed at the NACF meeting last month. Regardless of the potency demonstrated using 809/770 in earlier clinical trials, analysts like Geoff Porges seem to believe 661 is superior to 809 in combination with 770, even when adjusting dosing of 770 to offset pK drug interactions between 809 and 770. Perhaps as most TRANSPORT AND TRAFFIC patients finish their six months of treatment in the first quarter of next year, investigators will be reporting that as their study patients go off 809/770 at the end of the 24 week treatment protocol, they will no longer have the benefit of the study drugs, and consequently, there will be having a noticeable decline in their health. This should prompt Vertex to report to the FDA the obvious benefit of the study drugs while the study is still underway. Under these circumstances, the FDA has in the past has allowed an earlier than scheduled unblinding of the data on a compassionate use basis, to allow study patients in the control group and those who went off treatment with study drugs after 24 weeks, the opportunity to resume study drugs in long term 'rollover' studies to maintain their health, and accelerate the approval process of these critically needed drugs by allowing earlier NDA submission.
particularly because CFTR “repair” at the RNA level is complementary to the CFTR “repair” at the protein level, and the two approaches can be added together to enhance the outcome.
Both miRNA-138 mimic and antisense technologies would have drug delivery problems to overcome. First, the RNA mimics have to be intravenously injected and then they have to cross the cell membranes without being degraded by cellular enzymes. Great technologies but clinically do not have the convenience of oral drugs like Kalydeco or VX-809.
This year’s NACFC meeting disclosed potentially emerging new technologies to treat CF 508 indications, for which CFO Ian Smith expressed his enthusiasm twice during the Vertex conference call Q&A. Ian spoke of possibilities of participation with, in-licensing of, or even buyout of, new technologies.
Then, what are those new technologies which do not involve CFTR “repair” at the protein level? It is curious because people are excited about the potential of these technologies that may compete with protein level modifications that Kalydeco, VX-809, and other correctors are engaged in. I have searched all Symposium Summary abstracts, and came up with one technology that stood out among others.
I said a technology, but it can make up a collection of many technologies. CFTR protein is made from CFTR RNA sequence called mRNA (messenger RNA). The rapidity of CFTR mRNA production is controlled by other RNAs called miRNA(micro-RNA). MRNAs are the codes for proteins, but miRNAs do not code proteins; they are instead controllers of mRNAs. A team based in U. of Iowa (incl. MJ Welsh) found a miRNA called miRNA-138 which increased the production rate of CFTR mRNA. They also found that this miRNA-138 increased the amount of 508del CFTR protein in human airway lining cells of 508 person. They also found that chloride transport across the cell membrane was increased. They also found other miRNAs which produced the opposite effects. Keep in mind that all are bench-top cellular findings, but they are interesting and exciting enough to attract the attention of CFO and Fred Van Goor. It may take 10 or more years before these findings can be translated to clinically meaningful drugs, but Vertex should look into such technologies. There can be a more direct RNA patch work to repair 508del CFTR using antisense technology, Sarepta uses. I am sure that Vertex executives are keenly aware of these potentials, [Contn']
Lobl, you have to register(free) and sign in to see the posts. Click on the most recent message. IV board allows posting figures unlike Yahoo board.
Appreciate your analysis, but I looked at Investor Village site, message boards, and did not see anything... Is it a group or something?
Last May after Ph II 809+770 data were released, some of analysts were critical about what they see in the data citing lack of dose dependence, and FEV1 signals sinking in the monotherapy phase mysteriously.
I have looked at the FEV1 data many times, and see unmistakable dose effects supported by the Cohort 3 data. The improvements was higher for the 600 mg group than for the 400 mg or for the 200 mg group, but the 400 mg dosing did not produce as much effect as the 200 mg dosing if the Day one was considered as the baseline. If the baseline was taken at Day 28 the 400 mg data is slightly better than the 200 mg. Moreover, the Cohort 3 dosed at 400 mg Q12h produced effects comparable to that of the 600 mg group, indicating the validity of positive dose effects. It is very possible that much respiratory symptoms occur during 809 monotherapy phase because mucus was not fully hydrated to be expelled. This is probably why during the 809 monotherapy phase the FEV1 decreased. I posted the slides from the ECFS presentation at the InvestorVillage Vertex site.
Third, in addition to more than doubling mono-therapy revenue from the expanded label for using 770 in qualifying groups of non 551 CF patients in the first six months of 2014, we can anticipate the six month data from TRAFFIC and TRANSPORT trials will be available in May next year based on completion of enrollment of these Phase 3 trials last month. The third quarter conference call predicted NDA filing for 809 in mid 2014, and with breakthrough drug designation for 809 and 770, the FDA will rapidly approve their use for 508d homozygous CF patients before the end of the third quarter in 2014. Count on rapid growth of 809 sales to make the 2nd half of 2014 pivotal in terms of positive cash flow at Vertex, and with EU approval to follow, the growth in CF revenue will continue through 2015 and beyond, with the potential for additional revenues from 661, second gen CF correctors, 509 in autoimmune disease, and even 135 in treatment of hep C possible following NDA submissions for these drugs
I'm not sure what turned Geoff Porges, the Bernstein analyst, negatively toward Vertex since he had been a fervent bull in the past. He admits the restructuring of the company's Incivek franchise was expected. So why would he now have such a cautious opinion towards 809, when every analyst raised their estimation of success of 809 after the 661 data last spring validated the earlier phase 2 data with 809/770 treating 508d homozygotes? Is he, like the Goldman analyst, not seeing the validation demonstrated repeatedly using a CFTR corrector and potentiator in 508d homozygotes?
1) Daclatasvir and VX 135 SVR 4= 100% and improvement in liver enzymes after a transient rise, which happened with PSI 7977 in the electron study with 400 mg dose. ( ALT was 280 in some cases, look at electron study slides)
2) Intrim analysis Transport and Traffic strongly positive and no adverse events
3) II B study cohort 4 positive for Delta 508 F heterozygous group at VX 809 400 mg PO bid doses
4) VRTX starts VX 509 phase II B joint radiology study to document stability or improvement in joint destruction
5) PFE or GILD buys out VRTX.
Shorting VRTX is suicidal. Any big news and this stock will leap above $90.
There was another misunderstanding about VX-135. If you recall the 7-day viral kinetics data in patients(Phase I), the 135+Riba effect was less than that of 135 monotherapy. In vitro study also showed that viral reduction was less with 135+Riba than 135 alone. What does this mean? The action of Riba on viral polymerase must be interfering with the action of 135. That is why Bob Kauffman said in the last cc that the trials were run to find the safety. From what the team said about the New Zealand study (135+Daclatasvir) I can be optimistic about the chance of success for this combination. Porges was pessimistic about the chance also. Bob is a soft-spoken person and never exaggerates future potential. He said that 135 is as good as Sofosbuvir in viral kinetics.
Porges also fogot about the important clinical data and FDA approval coming in several weeks. The data from R117H mutation trial will be coming very soon and approval of gating mutation other-than-G551D should be granted very soon. These two classes of mutations alone double the number of people who benefit from Kalydeco. These events are coming very soon, not in 2015 or 2016 !
I completely agree. The timing of this downgrade makes no sense relative to the information released and his supporting thesis. The 135 data is a little underwhelming, but there is no way anyone can draw a definitive conclusion that it has no value.
Remember Porges was completely wrong on the definition of relative %FEV1(he circulated in mid-2012). He is wrong again about the potential of 809. He thinks that there are risks associated with its trials, and 661 will have a better chance. I would give 95% probability for the success of TRAFFIC and TRANSPORT, phase III trials, 809 is as good as 661 and it may be better for a long-term dosing. I base my reasoning on the safety of the drug over 56 days of dosing and the kinetics of FEV1 change over 4 weeks of dosing along with Kalydeco. When the share price reaches 150 next spring, he will upgrade the stock. Most biotech analysts are like him. Tech analysts are much more informed.