I stopped buying last run thru the 4.70's..I'll buy a few more if the market pushes below $5 -
But I honestly expect us to test $4.90 before the politics ease. Be patient, powder at the ready.
Though I realize the import of the Comet trials to Cabo, EXEL, and long-term shareholder value...I also feel that these smaller, ancillary trial results are inestimably important as well. These research corroborations are preclusive of #$%$ in the armor" that could shipwreck us downstream, and they will comprise the rationale of acceptance in the near-term until Cabo attributes are better understood. Look what just happened to ARIA...
Cabo is the same drug that was being touted for "unprecedented" results two years ago.
Well, hey - guess what? - The results are still unprecedented, the science is still intact, and the news just keeps getting better. I expect some huge volumes to ensue if they push this back below $5 --
If you're not buying...you're crying...
"Jinlu Dai1, Honglai Zhang1, Andreas Karatsinides1, Jill M. Keller1, Kenneth Kozloff2, Dana T. Aftab3, Frauke Schimmoller4, and Evan T. Keller5,*
+ Author Affiliations
1Department of Urology, University of Michigan
2University of Michigan
3Translational Research, Exelixis Inc.
4Clinical Science, Exelixis
5Department of Periodontics and Oral Medicine, University of Michigan
↵* Corresponding Author:
Evan T. Keller, Department of Periodontics and Oral Medicine, University of Michigan, 5308 Cancer Center, 1500 E. Medical Center Drive, Ann Arbor, MI, 48109-0940, United States email@example.com"
This is all spinoff research from the David Smith UMCC P2 bone micro environment work up.
Very good stuff...
PubMed ePub ahead of print, 10/4//13... Yup, you read it correctly. I'll repeat it...
"Cabo prevents tumor-induced bone lesions"
"Cabozantinib inhibited progression of multiple prostate cancer cell lines (Ace-1,C4-2B, and LuCaP 35) in bone metastatic and soft tissue murine models of prostate cancer, except for PC-3 prostate cancer cells in which it inhibited only subcutaneous growth. Cabozantinib directly inhibited prostate cancer cell viability and induced apoptosis in vitro and in vivo and inhibited cell invasion in vitro. Cabozantinib had a dose-dependent biphasic effect on osteoblast activity and inhibitory effect on osteoclast production in vitro, that was reflected in vivo. It blocked MET and VEGFR2 phosphorylation in prostate cancer cells and osteoblast-like cells, respectively.
These data indicate that cabozantinib has direct anti-tumor activity; and that its ability to modulate osteoblast activity may contribute to its anti-tumor efficacy."
Interesting that this indication was in the news just last week wrt to the dilemma of Mr. Finn of Buzzards Bay, MA, govt shutdown, and lack of personnel to update and enlist new patients. I was surprised to find this MGH-sponsored P2 trial currently added and listed as recruiting...
"A Phase II Study of Cabozantinib (XL-184) Monotherapy in Patients With Advanced Cholangiocarcinoma After Progression on First or Second Line Systemic Therapy"
#$%$ Smith is an Aussie aviation hero with a large cultural following...
Medxwatcher, thx for posting. In looking for further info based on your storyline, I found this, and I think it was posted today-
"Beginning Friday, patients seeking experimental treatments in new clinical trials will no longer be delayed from joining those studies as a result of the government shutdown.
The National Institutes of Health received permission Thursday to recall a handful of furloughed workers to reopen its clinical trials registration website and start processing new applications, which had stopped during the shutdown.
Many hospitals, including Dana-Farber Cancer Institute, require patients receiving experimental drugs to be formally enrolled in a clinical trial registered on the site. Leo Finn, a Dana-Farber patient, told the Globe Wednesday that a drug he desperately needs for his metastatic bile-duct cancer would be delayed because he would not be able to join a new trial.
Finn was contacted by his Dana-Farber physician Thursday and told that he could join the new trial and get cabozantinib — a drug approved for thyroid cancer but still experimental for other cancers — next month as planned."
This is really good news for patients, and an interesting slant on Cabo in the news...
This is the important question, of course, but I would encourage you to consider the relevance of the biomarker survey before we begin to discuss the drug combo. We know that Cabo displays a clinically reliable reduction in 12-week CTC counts that meets the bioassay criteria. We also know that Cabo moderates elevated LDH in this same 12-week timeline. These markers have been associated with improved survival...as have been Cabo's notable pain reduction, bone scan response, and diminished narcotic intervention for pain relief. Responsibly tying all these markers together into a predictive mechanism that satisfies regulatory acknowledgement may not happen soon enough to help get Cabo approved in the prostate space, but the medical community is quickly gaining momentum in it's acceptance of the emerging pattern of concurring markers that certainly appears to suggest improved OS, if only in mCRPC. Going forward, I will encourage the opinion that each indication will be different, as may each stage of disease progression.
All this certainly lends an air of intrigue to the Cabo/Abi combo...but the fact is - we haven't been dealt enough info to make much informed discussion except to say early results are encouraging. This could hold up thru P1 results, or that early synergy could fizzle or be bested by the changing landscape of PC treatment. There is simply a lot that we won't know till results are in...
But the results to date are very striking, and I am more optimistic with each new clinical reassurance.
Doc Scher wouldn't waste his time developing such a biosurvey in mCRPC unless he saw promise in it, and it is very encouraging that many of the same markers that were noted in the Abi trial apply to Cabo as well. Blast or bust - this is going to be great fun to watch...
Hopefully, we'll all make a buck or two...
Once again I am thunderstruck by the vicissitudinous undulations of abject buffoonery which surround me.
Jonesy, you don't by any chance work for big gubmint, do you?
Interesting early release editorial posted in the JCO 10/2/13...the inference being that OR per RECIST may not present best predictive criteria for OS in every targeted therapy. I encourage this read...The Krajewski, et al findings are compelling in VEGF-inhibitor treated RCC ...
"Although objective response per RECIST (defined as a 30% or greater decrease in summed tumor diameters) does have some value as a prognostic marker,5 some investigators have recently studied whether alternate definitions of response can be derived on the basis of biology rather than historical precedent. These studies aim to identify a specific response phenotype, rather than a tumor genotype, that offers insight into disease biology. Studying patients with advanced colorectal cancer treated with cetuximab, Belgian investigators have shown that a 10% diameter decrease optimally predicts for improved survival in patients with KRAS wild-type cancers.6,7 Investigating pa- tients with advanced renal cell carcinoma treated with first-line vascu- lar endothelial growth factor inhibitors, Krajewski et al found that a 10% diameter decrease optimally differentiated patients with a poor prognosis from those with a good prognosis"
"I use to think that if I made a lot of money in the stock market I would feel at peace. However, I found out that all the bad things I did to people and all the bad things people did to me came back to haunt me in the end..."
You are messing with the hook, Dos Ecces...
"Treating other people with respect is better than being haunted with regrets after."
Learn it...Live it.
(CNN) --- 4hrs agon- Michelle Langbehn, 30, has endured nine months of chemotherapy, two cycles of radiation, a spinal fusion and several tumor removal surgeries. But the cancer that's attacking her body continues to spread, and her future treatment options are limited.
There was hope for the Auburn, California, mom -- a clinical trial that's testing a new drug called Cabozantinib that's been approved to fight other cancers. Researchers at the National Institutes of Health had gathered Langbehn's medical records; they were set to evaluate her status on Monday to make an official enrollment decision, she says.
Then the government shut down."
This nonsense can't be helping anyone...
You just don't get it.
These folks aren't bashing the company..nor the drug.
They are bashing your #$%$, incessant posturing.
Cut it out, poser.
"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."