Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
I haven't followed or put much stock into the HSP90 space.
Is it still a legit target or is it a bust?
at least 60ml cash Dec31,2011
degree of accumulation we've seen over the last few weeks
Financing coming IMO
I think we're at a level (around here) that Berger will likely float 10 million shares and get another $100 million in the bank.
Wouldn't be the worst thing.
I don't think Ponatinib partnership is forthcoming anytime soon.
I don't think an NDA filing is going to be a big "WOW" factor adding to the balance sheet.
Ariad needs to fund more trials in Ponatinib, and they need to fund the ALK trial.
And they need to keep the balance sheet large to continue attracting investors - a balance sheet of $75 million isn't a good look when you're burning $10-15 million a quarter.
I don't like AMRN. Chart still has a big fat gap in it.
CEO kinda put the stock down by saying there wuold be no buyout or deal
yeh, yeh, yeh, and the $5.30 gap is going to fill and the stock is going to trade at 7.50 before 9.60...blah, blah, blah. tiresome is about right.
Ariad needs new coverage from the monkeys (new sellside firms).
It's looking really tired.
I appreciate the dialog.
We will see how it plays out.
Please tell me where the fundamentals have changed in the story.
If ARRY dips below $2, I may consider adding again
Has AZN or NVS/ARRY presented some negative data that I missed
Dew, do you come away with anything substantially positive on this abstract - the fact that it now shows activity in some EGFR mutations as opposed to just being an ALK targeted drug?
I haven't really dug too deep into this; looking at some of the other molecules that they would be competing against.
Clearly, it's a positive - I just don't know how much of this is "showcasing" mouse models versus real useful clinical activity.
Macro-funds (huge asset managers) hold equity positions and index options and individual name options. When they unwind hedged positions, there (can be) massive volume prints that can cause volatility.
On options expiration days, particularly triple and quad witching Fridays, there can be large opening and closing prints in which market-makers (block desk traders) can oftentimes being a stock to a particular level (up or down) depending on how large the closing print will be. It might be a particularly interesting day tomorrow considering next Friday is the entire Russell rebalance.
If you have a good sized position in that pig, I don't think you'll be laughing too hard looking at your closing equity balance. lol.
Quadruple Witch expiration tomorrow
LOL, you're probably right.
The thing acts like real sht, you can't deny that.
This is one of these stocks I went back on a one big rule I have: don't get involved with garbage again.
It was a loser back when they failed their trial back in '09?, or '10? I got back involved because I looked at their pipeline and clearly one would think that many drugs would be worth more than $130 mill market cap considering some reallll pig trash-heaps (SNSS et al) have market caps comparable or even more than ARRY's current.
Something clearly isn't right with the company, and it probably has more to do with financing the company through Phase 3, than it does their R&D; but then again, they already failed one trial with their key drug.
Thinking now above $15 at year end, $25+ by y/e 2012.
Someone call in a Euthanasia-Expert for ARRY
She's all done.
Yes, I agree with that entire post.
Well said.
Further, I understand the company is "not for sale" but someone has to be looking at these compounds wondering what it will take for a large equity stake in the company or outright ownership of Ariad.
I'm looking to sell my holding somewhere in the mid-teens in ARIA (purely based on technicals). I think ARIA drugs are great but I just think coming from the 2's to 15's, is enough and could be due for retracement of some sorts.
I do not know what I will be doing with that capital if I will be re-investing in equities, or real estate. The biggest problem I have with re-investing the capital in equities is finding a good place for it...considering the macro-market, and problems in the global economy (I really would like to liquidate everything in the near future and take a seat back and watch what happens). If QE3 comes back on the table, I would stay long everything personally.
BTW, people hate this market right now. If some sort of new stimulus comes on the table or they clear up the EU problem, yes, the market is definitely oversold here. 7 straight down weeks...c'mon....we are due for snapback at very least
Yes.
It could be one of the reasons why they are 3rd class mTOR. What a slow process Defo/Rida has been.
Looks like we have a "sell on the news" situation going on.
Someone got wayyyyyyyy too over-anxious paying 10.18 in PM.
Thanks. It's one of the problems I have with Curis and their CUDC-101. It's showing promise in several indications however, it's IV, and they're planning on making a tablet formula later this year. It seems like a huge waste of time and money to go through trials in IV, and then switch to oral (for obvious reasons).
..as long as the Chinese bail out EU and get the markets straightened out again.
They need to crush the USD today.
It does make the drug a lot more compelling, to me anyway *(not that it wasn't compelling in the first place). It seems like it would open up a few more indications certainly ergo more revenues.
Are many companies still originating Phase 1 trials using an IV formula, or is this a thing of the past now for most companies?
It would seem like a complete waste of time to develop a drug in IV formula, go through an entire Phase 1, and then have to develop a tablet/oral pill, and do another separate trial to make sure the efficacy is the same.
I know this is off-subject from the original post, sorry.
Anyway, '113 seems a little more attractive at this point - not that it ever wasn't in the first place.
AP26113, a potent ALK inhibitor, is also active against EGFR T790M in mouse models of NSCLC
Session Info: Mini Oral Session, [MO11] Preclinical Models II
Day/Date: Tuesday, July 5, 2011
Session Time: 10:30 AM - 12:00 PM
Room: G106
[11:34 AM] MO11.12 | AP26113, a potent ALK inhibitor, is also active against EGFR T790M in mouse models of NSCLC
J.J. Miret, F. Wang, R. Anjum, S. Zhang, J. Keats, M. Cookson, Y. Ning, S. Wardwell, L. Moran, Q. Mohemmad, Y. Wang, J. Qi, R. Squillace, N. Narasimhan, D. Dalgarno, T. Clackson, W. Shakespeare, V. Rivera
ARIAD Pharmaceuticals/UNITED STATES OF AMERICA
Background:
Activating mutations in EGFR and anaplastic lymphoma kinase (ALK) are drivers in ~20% of all NSCLCs. First generation EGFR and ALK inhibitors are clinically efficacious, but are susceptible to mutation-based resistance creating a medical need for second-generation agents. For EGFR inhibitors, the T790M gatekeeper mutation accounts for ~50% of resistance. Potent irreversible T790M inhibitors are in development but can exhibit toxicity due to co-inhibition of native (endogenous) EGFR, suggesting that T790M-selective agents will be required. For the ALK inhibitor crizotinib, clinical resistance has been linked to the L1196M gatekeeper mutation. Previously, we have identified AP26113 as a potent ALK inhibitor that overcomes this and other mutations. A broad kinase screen revealed that AP26113 also reversibly inhibits EGFR harboring activating and T790M mutations.
Methods:
The activity of AP26113 against native, activated (L858R or delE746_A750 [DEL]), and T790M mutant (L858R/T790M or DEL/T790M) forms of EGFR was examined in NSCLC as well as engineered Ba/F3 and 3T3 cell lines. EGFR signaling was assessed by measuring levels of phosphorylated EGFR (Y1068), in vitro proliferation measured by MTS assay, and in vivo tumor growth measured in mouse xenografts following daily oral dosing.
Results:
AP26113 was essentially inactive against native EGFR, inhibiting signaling with IC50s >1000 nM in a NSCLC cell line (H358) and native EGFR-transduced Ba/F3 and 3T3 cells. In contrast, potent activity was demonstrated against activated forms of EGFR. EGFR signaling was inhibited with IC50s of 10-50 nM in HCC827 (DEL), DEL Ba/F3 and L858R 3T3 cells. In HCC827 cells, proliferation was inhibited with an IC50 of 105 nM. In an HCC827 xenograft model, doses of 25 mg/kg or greater induced tumor regression (>33%) and >90% and >60% inhibition of EGFR signaling 10 and 24 hours after dosing. Significantly, AP26113 also demonstrated potent activity against T790M mutant forms of EGFR. EGFR signaling was inhibited with IC50s of 10-63 nM in H1975 (L858R/T790M), and DEL/T790M and L858R/T790M Ba/F3 and 3T3 cells. In H1975 and DEL/T790M Ba/F3 cells proliferation was inhibited with IC50s of 85-350 nM. In an H1975 xenograft model, doses of 50 and 75 mg/kg led to significant tumor growth inhibition (=45%). In a DEL/T790M Ba/F3 xenograft model, doses of 50 and 75 mg/kg led to tumor stasis and 50% tumor regression. In both models, substantial prolonged inhibition of EGFR signaling was observed.
Conclusion:
AP26113 is a novel reversible inhibitor of activated and resistant mutants of EGFR, and does not inhibit the native enzyme. Importantly, oral doses that are efficacious in mice against activated and T790M mutant EGFR are similar to those active against native- and crizotinib-resistant ALK variants, suggesting that AP26113 is a dual ALK/mutant EGFR inhibitor. These data support clinical evaluation of AP26113 in patients with resistant EGFR-driven tumors.
Phase 1 trials are generally for safety and tolerability.
However, if the drug can show both safety (AND) efficacy on a broader scale and scope, it's considered a Phase 1/2 because a Phase 2 study is the one they consider the "efficacy AND tolerability" study, working upon what the P1 showed.
Essentially, they are taking the same road as they did for '534, which is to by-pass an entire and lengthy P2 because they feel they will have enough data to go straight to a Pivotal Study.
Exactly.
Session Info: Mini Oral Session, [MO11] Preclinical Models II
Day/Date: Tuesday, July 5, 2011
Session Time: 10:30 AM - 12:00 PM
Room: G106
[11:34 AM] MO11.12 | AP26113, a potent ALK inhibitor, is also active against EGFR T790M in mouse models of NSCLC
J.J. Miret, F. Wang, R. Anjum, S. Zhang, J. Keats, M. Cookson, Y. Ning, S. Wardwell, L. Moran, Q. Mohemmad, Y. Wang, J. Qi, R. Squillace, N. Narasimhan, D. Dalgarno, T. Clackson, W. Shakespeare, V. Rivera
ARIAD Pharmaceuticals/UNITED STATES OF AMERICA
Background:
Activating mutations in EGFR and anaplastic lymphoma kinase (ALK) are drivers in ~20% of all NSCLCs. First generation EGFR and ALK inhibitors are clinically efficacious, but are susceptible to mutation-based resistance creating a medical need for second-generation agents. For EGFR inhibitors, the T790M gatekeeper mutation accounts for ~50% of resistance. Potent irreversible T790M inhibitors are in development but can exhibit toxicity due to co-inhibition of native (endogenous) EGFR, suggesting that T790M-selective agents will be required. For the ALK inhibitor crizotinib, clinical resistance has been linked to the L1196M gatekeeper mutation. Previously, we have identified AP26113 as a potent ALK inhibitor that overcomes this and other mutations. A broad kinase screen revealed that AP26113 also reversibly inhibits EGFR harboring activating and T790M mutations.
Methods:
The activity of AP26113 against native, activated (L858R or delE746_A750 [DEL]), and T790M mutant (L858R/T790M or DEL/T790M) forms of EGFR was examined in NSCLC as well as engineered Ba/F3 and 3T3 cell lines. EGFR signaling was assessed by measuring levels of phosphorylated EGFR (Y1068), in vitro proliferation measured by MTS assay, and in vivo tumor growth measured in mouse xenografts following daily oral dosing.
Results:
AP26113 was essentially inactive against native EGFR, inhibiting signaling with IC50s >1000 nM in a NSCLC cell line (H358) and native EGFR-transduced Ba/F3 and 3T3 cells. In contrast, potent activity was demonstrated against activated forms of EGFR. EGFR signaling was inhibited with IC50s of 10-50 nM in HCC827 (DEL), DEL Ba/F3 and L858R 3T3 cells. In HCC827 cells, proliferation was inhibited with an IC50 of 105 nM. In an HCC827 xenograft model, doses of 25 mg/kg or greater induced tumor regression (>33%) and >90% and >60% inhibition of EGFR signaling 10 and 24 hours after dosing. Significantly, AP26113 also demonstrated potent activity against T790M mutant forms of EGFR. EGFR signaling was inhibited with IC50s of 10-63 nM in H1975 (L858R/T790M), and DEL/T790M and L858R/T790M Ba/F3 and 3T3 cells. In H1975 and DEL/T790M Ba/F3 cells proliferation was inhibited with IC50s of 85-350 nM. In an H1975 xenograft model, doses of 50 and 75 mg/kg led to significant tumor growth inhibition (=45%). In a DEL/T790M Ba/F3 xenograft model, doses of 50 and 75 mg/kg led to tumor stasis and 50% tumor regression. In both models, substantial prolonged inhibition of EGFR signaling was observed.
Conclusion:
AP26113 is a novel reversible inhibitor of activated and resistant mutants of EGFR, and does not inhibit the native enzyme. Importantly, oral doses that are efficacious in mice against activated and T790M mutant EGFR are similar to those active against native- and crizotinib-resistant ALK variants, suggesting that AP26113 is a dual ALK/mutant EGFR inhibitor. These data support clinical evaluation of AP26113 in patients with resistant EGFR-driven tumors.
...you know what they say about a falling knife.
So do the executives earn money on the spread (between strike and market price) at no risk (they put up zero capital)?
Thank you.
Huh?
What system are you on?
I hope there is a reason why there is strength beyond simply buying ahead of the analysts meeting - which is a complete joke. And the only people who would do such a thing are complete idiots and fools.
If they announce they filed at IND for their ALK-inhibitor, that's all fine and dandy, however, it would not be anything outside of what they have already stated they will be doing: which is filing an IND around mid-year, and shortly thereafter, beginning a Phase 1 trial.
What would be surprising is announcing an Asian partner for Ponatinib, and I think the likelihood of that happening is about 1%.
Very interesting stuff.
Thanks for the comment.
4th compound could explain this unprecendented strength
I own a small-cap tech stock that did this.
The scumbags (executives) bought back about 5 million shares. Most of it was CEO and Executive options that were going to expire (and the stock was well above the strike price). So, they had the company buyout the options from them (so they wouldn't have to put up their own money and flip the stock to make it look like they were sellers), instead of exercising them and diluting the stock (they just had the company do it for them on the books, and I believe, just made money on the difference between the strike and the at-market price the company bought out the options----free money, no risk to them at all). After all was said and done, the only thing they prevented was all the options that were coming due, from going into the public float. So, they effectively bought back nothing and it was all net-net.
Yet, Yahoo Message Boards loved it. They thought it was like Intel buying back $2 billion worth of stock.
This is great news for Ariad. Now they have one less competitor for their mTOR-stent business. $65 poison-pill take-over now??
LOL (must be why the stock is positive today).
Interesting.
Well beyond my area of expertise, so I ask: is creating a mutation of HIV effectively creating the possibility of another strain of a super
virus?
there seems to be a lot of interest in mek and ARRY. so, why is it a biotech dog right now with an ever decreasing market cap...? just trying to figure it out before i average dwn again in the doggy.
it definitely was not an analyst that said 40.00.
it was some imbecile from motley fool that has zero clue about the market cap and shares outstanding to come to a valuation like that.