"I have bought as much as my allocation to this will allow me."
Good. Maybe you'll #$%$ for a while and let someone else share some constructive commentary.
Your persistent cheer leading is a royal PITA...
BTW- great call advising all your followers to buy in the 6.40's...
Pretty shiny credibility story you're working on...
I'm betting your own wife has you on ignore...
Ignore this, dipshizzle...
I still think you' ll find that eLDH values didn't change substantially enough to modify our target population. Are you suggesting they will further modify Galaxy2 recruiting to accommodate this update?
I think it important to monitor all the above. Tying together the evidentiary chain that enables a target CTC value that predicts the benefits later realized as decline in bone mets propagation and extended OS will prove in many indications to be the most valuable tool of all. If the concept proves out, we can opt to discontinue (or modify) existing early therapy that is not hitting our CTC target to alternate therapy that gives us the CTC response we want. I know there are too many extraneous bio forces at play to enable the concept in every indication - and with every therapy - but I think it's imperative to acknowledge where the value can be realized. The work currently being conducted at the Dan Haber lab at Mass Gen Hospital bears witness to the value of their herringbone chip CTC enumeration platform. See MGH newsletter Winter 2013. Enlightening read...
From Science Daily...interesting work-up
Sep. 25, 2013 — A team of cancer researchers at the University of California, San Diego has identified the existence of precursor cells in early prostate cancers. These cells are resistant to androgen-deprivation therapy, and may drive the subsequent emergence of recurrent or metastatic prostate cancer."
In metastatic disease, current conventional wisdom suggests CTC monitoring as a measure of therapeutic response. In addition to the Veridex platform, there are currently (at least) three others in late stage development that show great promise, and they are seeing clinical use in a variety of metastatic disease venues. I view regulatory acceptance of (any or all) of these devices as merely a matter of time and data cleansing. I would expect any oncodrug that claims to mitigate metastasis to have appropriate CTC enumeration data for peer review. The Veridex is slated for retirement as these newer devices characterize CTC's as to their genomic viability & vulnerability to treatment. These diagnostic attributes, once refined, will render the Cellsearch as useful as the abacus.
These are changing times, doc...
Notably, it's also being set up as a Phase 2 trial. Given AVEO's current financial crisis, I'd imagine positive results could make them a desirable partnering/take-out candidate...or less than desirable results might make them want to run at it again with ficlatuzumab. Dror Michaelson is highly regarded in the PC space, so I'm assuming the rationale is intact.
I guess we'll see..just figured it was worth posting FWIW...
If I understand your question correctly, you are asking "Why the skepticism?"
As a shareholder, I expect to see clinical trials designed in a much more transparent fashion than we are seeing today. Where are the bio marker assays? CTC enumeration studies? Every trial clinician on the planet is monitoring CTC's these days. Why has not Synta? Nearly every potentially successful oncodrug candidate these days is co-developing predictive bio markers, bio markers of therapeutic response, prognostic bio markers...
In trials of advanced disease involving bony mets, where are the bone scans, the MRI's, bone turnover marker assays, PET assays...??? To the best of my knowledge, Galaxy 2 is the only SNTA trial to date that specifically enjoins a bio marker assay as a secondary outcome measure.
Can anyone on this board answer the question of Ganetespib's impact on CTC counts in any trial indication to date? Please do so...
This trial began recruiting in July, and it may provide some valuable insight downstream.
Tivozanib and Enzalutamide in adv prostate cancer. Collaborators are Mass Gen Hospital and the NCCN.
PI is Dr Dror Michaelson of MGH
No one questions that Ganetespib has displayed beneficial clinical activity.
That issue is evident, but there are a lot of tumor- shrinking drugs in development. The ball that management must now carry is OS. Without statsig, approvable overall survival data Ganetespib is just another me-too in a class of compounds - only a relative few of which - ever become commercially successful. That fact that G has displayed a reasonable OS trend is in it's favor, but until the data becomes marketable, G is just another wannabe. You can bang your drum all day long, but you really need to address the issue that deserves your concern - and so does management. JMHO
I gotta tell ya... I'm a long here, but there was no news today. I listened.
In fact, a third of the way into the broadcast, someone made the statement...
"Now that everyone has left..."
Which was moderated by...
"That's not quite true for those of you joining us on the webcast.."
The analysts, the oncodocs, the clinicians ... all walked out before the broadcast was over. Why?
There was more interesting stuff to see...nothing new...no news.
There's no catalyst here till they have data...till they share IP on the HDC platform...
Till they partner...possibly till they decide to dilute.
Don't make it up as you go...
Be interesting to see the impact of ObamaCare.
Saw a two-part bumper sticker today...made me laugh...
"Screw ObamaCare..Does YoMamaCare?"
"Dasatinib Combo With SMO Inhibitor (BMS-833923)" in chronic phase CML
BMS-833923 is also known as XL-139, EXEL's hedgehog pathway inhibitor.
This P1/2 trial revised status to "completed" on June 13, 2013.
Be interesting to see the data...even if it can't compete with Ibrutinib.
"3 Randomized Discontinuation Designs in Early Clinical Drug Screening – how to Adapt if the Drug Works too well? The Cabozantinib Experience" Weitzman, et al.
Published Nov 2012 Eoropean Journal of Cancer
I laughed out loud when I saw this title...
That Dan Haber lab has built themselves quite a lab toy, and there must be skadds of data yet to process before approval becomes reality. I imagine regulatory acceptance is prerequisite to publishing much in the way of research data, and growing competition in the space precludes too much IP sharing. I've been looking for good investment potential in the space, but most advanced players seem to be either private or academic. Regardless, I persist in looking. I'll post what I can find. The nano-Velcro 3-way device at Cedars Sinai also shows remarkable promise, and the PI ( Ed Posadas) of the CS Cabo trial in visceral mets is a co-designer of that platform, so I expect we'll get some first-hand info eventually. "Painting" upregulated protein markers is quickly becoming state of the art, and I suspect the rush of data in the near future will be huge. GLTA
As titled from Reuters...two days ago.
Some interesting industry talk on shortening the drug approval process.
My best takeaway is that management appears comfortable in the clinical assumption that HSP90 up-regulation is directly linked to disease progression and diminished OS in both NSCLC & mBC. It's satisfying to see that we are maintaining a positively directed OS signal, but there still seems to be some confusion wrt which subset patient groups are most likely to benefit from Ganetespib. Compels me to believe that corroborative Galaxy 2 final results will be necessary for better understanding of the requisite targets before we see a successful NDA filing in lung adeno- pops. I just don't see that interim results will be considered acceptable for a fast track filing.
MBC is another issue. I hope they partner soon...That'd reinforce the wishful thinking and take some of the guesswork out of over-interpreting early results. JMHO
It'll be interesting to see bio-marker returns on the combo Abi/ Cabo trial. Has me thinking the early synergistic results may be due to Cabo ironing out this apparent "confusion" in AR signaling as a byproduct of managing cMET up-regulation.
Mass Gen Newsletter Winter 2013 (Still looking to see if ECC updates may apply)
"In contrast, researchers found
that men with castration-resistant prostate cancer had highly variable AR signaling responses in their CTCs, before and after treatment. Before treatment, some men had CTCs with androgen receptor signaling turned on (AR-on cells), others had AR-off cells, and still others had AR-mixed populations. That variability was present when looking at different patients, as well as when looking at different sets of cells isolated from any one patient.
Mixed signaling was also observed after treatment with abiraterone acetate. The presence of AR-mixed CTCs—revealing a confusion in the AR signaling pathway, which abiraterone acetate targets—was associated with an adverse treatment outcome. There
was also decreased overall survival in another subpopulation of castration- resistant prostate cancer patients: those whose percentage of AR-on cells increased after initiating abiraterone acetate treatment. Neither of these subpopulations responded to the drug."