There are none. That's why we are here.
ACTC has a smaaaaallllll chance. But its smmmaaalllllllll. And they need to get really lucky. And STEM needs to fall off the face of the earth.
See APDN as well. Different company. Different type of products.
Was that my post that you were referring to?
If so, my question was why can't management be more proactive about helping shareholders by divulging news when it comes out. Especially when an imminent 50-day 200-day cross is about to occur, and the stock went up 15% the day before on news that a different company's targeted therapy for breast cancer got positive phase III results. That was the perfect timing to release the news (which they still have not released) that showed their ONLY THERAPY may be able to treat up to 7 DIFFERENT cancers (in addition to the one it was approved for).
That news alone would have been enough to not allow the MMs to play games and would have allowed the stock to take off.
Instead, the MA cross occurred, and now we see ourselves lower than the 6.50 high that we had last Wednesday (when PBYI announced their drug got stellar phase III results). Hey, guess what. This drug is approved and being sold.
I was just saying this company's management NEEDS to be more *explicative* proactive.
Right now, if that news was released, the day the Cancer Cell paper came out (it didn't even have to be engineered or anything), we would be sitting much higher now, and all it would have taken was a NewsWire line saying "Roche scientists demonstrate that Iclusig synergizes with multiple targeted chemotherapies to destroy cancer cells, published in the top tier journal Cancer Cell."
But instead, we sit lower than we did last Wednesday.
Yjohn, so the data in the Cancer Cell paper is all in vitro. But that's how it starts. I am a dermatologist at an academic institute and I study signaling pathways that dictate inflammatory responses. One of my colleagues is working on the PD-1 trial for melanoma, and another one of my colleagues was one of the main investigators for the vemurafinib trial for melanoma. So I am in tune with the cancer signaling for melanoma. Basically B-raf is mutated in 60% of melanomas and that is what vemurafinib targets. B-raf is in the kinase signaling pathway downstream of melanocyte stimulating hormone (MSH). Mutant B-raf makes it so that melanoma cells no longer need MSH to proliferate. So they thought if you can turn off mutant B-raf, you may stop the tumor from growing and shrink it. Well guess what? They were right... Temporarily. The tumor basically gains additional mutations downstream of the B-raf so that the end product is the same. My colleague was the first person to show two mechanisms tumors get resistance to B-raf inhibitors. One of them was the MEK kinase, downstream of B-raf. Well guess what, that works too. Exelixis just had positive Phase III results with cabozantinib, their MEK inhibitor. But guess what? There is another pathway of resistance, the AKT pathway, which is completely independent of B-raf/MEK. So Exelixis just got their drug approved after my colleagues in vitro studies showed that blocking MEK can slow the growth of melanoma cells in a petri dish.
The thing about Iclusig that was shown in the Cancer Cell paper is that it can block both known pathways leading to resistance to targeted therapies in epithelial cancers (1)FGF and 2) AKT activation of STAT3, shutting down the growth of the cancer.
Now, think about this: If the cancer stops growing in a test tube, and in fact starts to die in that test tube b/c of Iclusig, what do you think will happen to the cancer inside the human body, where the immune system can find it?
It deleted my post in response to you, probably because I used her name?? But I emailed the IR person on the website on Friday, saying why not put out a PR for this paper, and I have not heard back yet. Not even a canned thank you for caring about ARIA, have a good day. It's almost like shareholders don't exist, or we're beneath them.
It seems to me that the company would rather the stock move on false buyout rumors instead of actual good things happening within the company.
How so? Remember a few months ago when Harvey favorited a tweet of an article about a buyout rumor? That's BS.
I am long since December 2013. Bought in at 6.60. Last Tuesday evening, PBYI announced positive phase III data on neratinib, a small molecule inhibitor of Her2 and skyrocketed over 200% on Tuesday after market and Wednesday during regular trading.
On Wednesday morning, someone with a fake twitter account posted a fake rumor that ARIA was going to be bought out, sparking a 5% increase in ARIA stock price.
It was found out that the account was fake, and the account was shut down. However, shorts were scared, and some started covering resulting in a +15% gain on Wednesday trading. On Thursday morning, ARIA share price gained another 11% during its intraday high, but by the end of the day, the share price was only up ~5%.
So here is my problem. On Thursday, the golden cross was imminent on the stock chart (The 50-day MA crossing over the 200-day MA), and was going to happen on Friday. This could have sparked a huge move in the stock, and trapped the 25% shorts in the stock on ANY news, seeing the moves of the two days before.
But did ARIA have any news to share with shareholders? YES!!!! An article published THAT DAY by Genetech/Roche scientists was published in a top cancer journal Cancer Cell, showing that Iclusig can be combined with many drugs targeting other pathways, including Her2, EGFR, MET, ALK, and prevent resistance to the pathway inhibitors targeting those pathways.
An announcement of this news on Thursday would have provided a way to break out of this downward trend in the stock price.
So why didn't Ariad even mention this publication? Is Harvey incompetent? Do they not care about shareholders? Do they want shorts to continue making huge amounts of money, while people like us shareholders suffer and hold the bag?
I am long for the science and the potential of Iclusig, but management needs to be more proactive to help shareholders out.
I don't think so. I think that's what they will charge for the treatment with adjuvant included (I forgot the number INO-1100 or something like that).
With the health care the way it is, insurance companies will not pay 4000 to 5000 for a treatment that is ~50% effective. People also will not pay that much out of pocket either.
The thing about VGX is that the DNA itself costs less than a buck. The disposable head of the electroporation device costs 50-60 bucks or so.
So at $500-600 its at a 10X premium. At 5000, that is 100X premium. I don't think that it will take off if that is the case. JMO
Harvey Berger likes articles propogating false rumors on twitter or Facebook. Come on... Be a real CEO
Its right there if you go to google and type in boston globe trial results give ariad a boost. There is a beautiful picture of Harvey Burger posing next to a railing next to the short blurb.
The article came out on July 24th at 6am in the online edition of Cancer Cell. The runup started on Wednesday afternoon. Even though the stock was completely oversold, it does seem odd that the false buy out rumor in the morning started the run up, but once that false twitter account was shot down, the stock price shot up even faster, as if some other news was driving it. But the article wasn't made public until Thursday morning. It could just be that daytraders got a hand in it during the buyout rumor that started that day and saw that it had breakout potential from the oversold position. It could have just been a coincidence that the article came out the next day.
Even a broken clock is right twice a day. He wants to be the one to "break the news" so to speak and claim that he was the broken clock.
But I agree, these pumper claims are garbage, almost as bad as the bashers.
My concern is insurance companies and patients aren't going to pay $600-700 for a drug that works 50% of the time, when normal people clear the virus 30% of the time. The key is that they have to look at the complete responders. Basically, if they aren't going to add the adjuvant (IL-12) to the vaccine if by adding the fourth dose of vaccine they can achieve a complete response in 60% of patients and the complete response of people getting placebo is 10-14%, then that is increasing the complete responses 4-fold, which is a 75% improvement in complete response. If that's the case, they may justify using VGX-3100 as first line for HPV CIN-2/3 for $600, and reserving the LEEP procedure for the treatment failures of the VGX-3100.
A culposcopy (part of the LEEP) generally costs about $500 and a LEEP procedure costs anywhere from 500-1000 depending on insurance. Its not a pleasant procedure, so often you have to add mild sedation or general anesthesia, which can add $300-2000 to the procedure. So at a minimum, the LEEP costs $1000, but may cost up to $3500. If you can reserve LEEP for the 40% of patients who don't get clearance with VGX3100, you can justify VGX-3100 as first line tx on a cost basis, as well as an attempt to prevent cervical scarring, miscarriages, sexual dysfunction, etc. in a larger percentage of women.
Older people don't respond well to any vaccine. Thymus has trouble putting out new naive T cells as people get older, because it involutes.
For some reason, African Americans respond poorly to some vaccines/infectious agents. It may be an HLA/antigen presentation problem.
I actually think a lot of the problem will be local and not systemic T cell immunity. I have no doubts that the vaccine will generate effector T cells in the periphery of most of the vaccine recipients. The problem is that locally, these effector T cells may be shut down by the virally infected cells or by the local antigen presenting cells. Viral infection drives type I interferon production, which is a major antiviral response activating NK cells and CD8 T cells, but at the same time causing expression of PD-1. The problem is one of the highest induced genes in antigen presenting cells or epithelial cells exposed to type I interferon is B7-H1, otherwise known as PD-L1. Chronic over-expression of type I interferon therefore drives chronic expression of PD-L1 expression on APCs or HPV-infected epithelial cells in the local tissue of the viral infection. When the effector T cell gets to the right tissue, but sees the PD-L1 signal, sends a negative signal to the T cell through PD-1, preventing them from working, and basically causing them to sleep. That's where Roche comes in, with their PD-L1 inhibitor.
This doesn't play as much of a role in the influenza vaccine, because influenza is an acute infection. No need to overcome PD-1/PD-L1 in an acute infection.
Over 260 people are now dead from this Liberian outbreak of Ebola, including 2 doctors who were treating the patients with the disease. Of note, this outbreak "only" has resulted in 60% fatality to those infected. This outbreak is somehow not as fatal as the previous Ebola outbreaks that resulted in 90%+ fatality.
Still, wow. This needs to be contained ASAP.
In your sentence "On July 24th, the peer review journal Cancer Cell published an article by Lee et al. entitled Drug Resistance via Feedback Activation of Stat3 in Ocogene-Addicted Cancer Cells"
Change it to:
On July 24th, authors from the Genetech subsidiary of Roche published an article in the peer reviewed journal Cancer Cell entitled "Drug Resistance via Feedback Activation of Stat3 in Ocogene-Addicted Cancer Cells."
The mL is the volume. Has nothing to do with dose of plasmid. The phase 1 was looking for the best volume to get the plasmid into the muscle for adequate disbursement. They found that between 0.5 ml and 2 ml worked the best, so they split the difference. I am sure they used the same dose of plasmid (milligram) in the phase 1 trial as they did in the phase 2 trial.
Your letter did not include the fact that the studies were completely performed within the Genentech group of Roche, and Ariad Pharmaceuticals had nothing to do with these studies. . Can you add that fact to the blog post, because knowing AF and Cramer, they will find some way to spin a study published in a Cell Press journal negatively
ROCHE (not Ariad) found that Iclusig can overcome resistance of tumors to targeted cancer chemotherapies. They published this finding in a top tier journal. Could adding low dose Iclusig to any of the above chemotherapies prevent drug resistance to the above chemos? Could adding Iclusig to the chemotherapy regimen of a patient whose tumor has already mutated and become resistant allow for the continued use (and therefore treatment) of the patient's cancer?
Partnership with Roche coming?
Scientific analysis: This journal is a top 3 cancer journal of the Cell press series. The authors of this article are from Genentech (Roche)... NOBODY from ARIAD is on this manuscript. So, they tested whether addition of ponatinib to tumor cell lines that have become resistant to drugs used to treat those tumors can overcome resistance to tumors.
They found an interesting phenomenon. In oncogene mediated cancers, they become addicted to the signaling pathway that is over-activated. When you give a drug like crizotinib or imatinib (CML), or vemurafinib (melanoma), the tumor starts to acquire additional mutations around the protein that is targeted by the inhibitor (like in melanoma, they acquire resistance to BRAF by acquiring Akt mutations or MEK mutations leading to continued oncogenic signaling). The theory of the paper is that activation of STAT3 in many cancer cells is the end product that the tumor needs to stay alive. This is mediated by two mechanisms, FGFs (fibroblast growth factors, there are 5 types of them) can directly activate STAT3, and PI3 Kinase/Akt signaling can also activate STAT3. They found adding ponatinib blocks both of these ways to activate STAT3.
Here are the drugs that addition of ponatinib in culture allowed killing of the resistant tumor cells the drugs to overcome cancer resistance: Lapatinib, Crizotinib, TAE684, and erlotinib.
Here are the pathways those drugs target: 1) EGFR, 2) HER2, 3) ALK, and 4) MET, as well as mutant 5) KRAS, and 6) MEK.
Here are the cancers this can be helpful in (corresponding to protein above):
1) Non small cell lung cancers (particularly squamous cell lung cancer 2) Breast and ovarian cancers 3) Some lung cancers that are ALK mutated and potentially ALK mutated lymphoid tumors such as ALCL (anaplastic large cell lymphoma). 4) Renal cell cancer, gastric cancers and non-small cell lung cancers. 5) Lung and head and neck SCCs, pancreatic carcinoma 6) Melanoma that has acquired resistance to vemurafinib