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R/S now or later?
I'm proposing that Peregrine do the inevitable and split 1/5 now, as opposed to later.
Any thoughts on this subject?
At the current dilute pace we will be back to 240MM shares and $.43 price.. And, so why not be ahead of the curve and R/S now?
All the best,
John
Way to "seize the day" with that post Horatius!!
Is Dr. Jefferies still associated with TPIV? Isn't he the mastermind behind TAP?
All the best,
John
IFU,
And the biggest of all, Myocardial Infraction. EOM..
All the best,
John
you're not being positive..EOM
That's positive, and thanks..EOM.
Can you link that please.. And if so, I apologize for missing it..
All the best,
John
It's a possibility that no patients have been treated. Unless I've missed the PR stating that the "first patient has received bavituximab" in Sunrise?
What if they just scrap the whole trial, and dump clumsy Bavituximab, and focus on Bavi2.0? I'd be all for it, and have been saying it all along..
All the best,
John
I'd like to hear anyone's opinion on the difference between exposed PS in a necrotic environment, and exposed PS through an apoptotic event?.
Freaking don't eat soy sauce?? Really!! After all the teachings were still at "soy sauce"?
Unbelievable, and I'm dumbfounded by the lack of understanding here..
All the best,
John
It's a methodical, hint of "been there done that", experienced vision with a tinge of guidance, IMO..
It's to early to divvy up the pie, but there is pie..
All the best,
John
Similar to cholesterol, there is both good and bad phosphatidylserine. The possibility to block the bad, and induce or elicit the uptake of good PS exist.
It's possible to block PS' immunosuppressive effect, and at the same time stimulate the uptake of PS via macrophages. These cells would then secrete high levels of anti-inflammatory cytokines, growth factors, interleukin 10 etc..
Why not just inject loaded PS liposomes at necrotic site, and let the uptake happen simultaneously with Bavituximab's immunostimulatory effect?
Let me guess, JazzBM already thought of this too :)
All the best,
John
What part of "there is no partner" do you not understand?
Either there is no partner or they don't want a partner at this point. Peregrine is fully funded to an early lookin, and bavituximab either works or it doesn't at that point.
Cards will be on the table within 2 years, IMO.
Stop with the partner debate, it ain't happening, IMO.
All the best,
John
Maybe they're starting a phase 3 Cotara trail, for the third time? :/
Bio, let's be specific.
If it becomes SOC no BP is going to be denied use. So why not just wait and pay a licensing fee?
BP will need us and we will need them, and it will be part of the PTP (physician treatment plan), IMO..
All the best,
John
Unfortunately they turned a deaf ear, and had second thoughts?
All the best,
John
I don't believe Peregrine is any closer to a partnership than they were 10 years ago. Peregrine will either make it alone or not at all, IMO. If by chance P3 NSCLC is successful then maybe we have offers, maybe?
Wouldn't it be cheaper to just pay a licensing fee to use Bavi?
It would be different if Bavituximab were a mono-therapeutic, but it's not, IMO..
All the best,
John
Provenance, Authoring and Versioning
Wouldn't expect many to know that...
All the best,
John
Another example of being ahead of the curve. I've asked a question more upstream than TIM, TAM, RAGE or any other PS receptors.
There's more than one way to skin a cat (not politically correct:))
Bio,
As you might know, a cellular membrane contains a lipid bilayer. In recognition of this, wouldn't all released microvesicles contain cargo such as lipid particles? Wouldn't a percentage of this cargo be PS?. In my opinion, and understanding yes they would..
Signaling an immune response to inflammation involves host-pathogen interface, better known as cell to cell communication. This type of interface would be necessary in order to (A). Facilitate an immune response, (B) Delineate cell phenotype, (C) Initiate gene transcription. etc...
A pathway in which a cell facilitates these communications is done by releasing microvesicles into an extracellular environment. These vesicles would then be up-regulated by immune facilitators, such as phagocytes, macrophages, dendritic cells, etc.. These microvesicles carry with them predisposed receptors, dependent upon which type of response is necessary, such as an inflammatory response.
Once these microvesicles are meet with their target facilitators, in this case dentritic cells, they are ingested. dentritic cells would then release signaling chemicles, such as cytokines to coordinate an appropriate immune response. In this case it would be an inflammatory response.
Let me tie this all together now, and answer your question;
CP,
CP,
"Knee jerk" is a slang term meaning; a quick, off the cuff, less thought-out decision, or response.
Thanks for the dialogue, and likewise regarding your thought provoking post.
FYI, I do realize it's my delivery and approach that seem to be more problematic here. I'm working on that :)
However, intellectual humility can be misconstrued as unassertive in my line of work. My confidence tends to come across as egotistical at times.
All the best,
John
CP,
Hi Wook,
Acknowledgement and board apologies.
I wanted to admit a significant over-site on my behalf and give credit where credit is due. Although, I must say that my philosophies are independently thought provked, and beyond just copy and paste discovery. My theory that exosomes and microvesiculation are intertwined with Bavituxima's MOA, went beyond just targeted outcomes, but also ramifications or obsticles in Bavi's therapies.
The truth and acknowledgement.
It's my understanding that Dr Thorpe first made reference to signalling chemicles in abstracts presented at AACR-2011:
Question for the board.
Can anyone explain to me how manipulating microvesiculation may affect progression, angiogenesis and possible treatment of solid tumors?
Please use your own words and no copy/paste literature answers.
I would like to create a dialogue of discussion regarding Peregrines recent acknowledgement, that part of Bavituximab's MOA includes targeted micro vesicles such as exosomes..
All the best,
John
The difference being that JBM was a copy and paste machine, with inside access. I'm more hands on with real experience and functional understanding of how things work.
I never did read JBM much, and scoffed at his lack of scientific understanding. If I wanted to read a peer review paper on specific topics I could do that myself.
However, I prefer to push the envelope scientifically speaking, for the purpose of understanding, and amusement, not financial motivation.
Why don't you look in JBM's archives and search for the "fountain of youth theory"?, or "micro dose escalation"?, or "signalling pathway manipulation via microvesicle tagging"? or the numerous other possibilities of Anti-PS that I've proposed?
It's not going to be there, but don't be surprised if you hear about sooner rather than later :)
Hi JBM!
All the best,
John
Ironic ASCO subject and conversation before it was released Cloak!. It's also ironic that Bavi's MOA now includes exosomes as a target.
Remember this post?
I've provided a testament to my theory below.
Trafficking of biological material across membranes is an evolutionary conserved mechanism and is part of any normal cell homeostasis. Such transport is composed of active, passive, export through microparticles, and vesicular transport (exosomes) that collectively maintain proper compartmentalization of important micro- and macromolecules. In pathological states, such as cancer, aberrant activity of the export machinery results in expulsion of a number of key proteins and microRNAs resulting in their misexpression. Exosome-mediated expulsion of intracellular drugs could be another barrier in the proper action of most of the commonly used therapeutics, targeted agents, and their intracellular metabolites. Over the last decade, a number of studies have revealed that exosomes cross-talk and/or influence major tumor-related pathways, such as hypoxia-driven epithelial-to-mesenchymal transition, cancer stemness, angiogenesis, and metastasis involving many cell types within the tumor microenvironment. Emerging evidence suggests that exosome-secreted proteins can also propel fibroblast growth, resulting in desmoplastic reaction, a major barrier in effective cancer drug delivery. This comprehensive review highlights the advancements in the understanding of the biology of exosomes secretions and the consequence on cancer drug resistance. We propose that the successful combination of cancer treatments to tackle exosome-mediated drug resistance requires an interdisciplinary understanding of these cellular exclusion mechanisms, and how secreted biomolecules are involved in cellular cross-talk within the tumor microenvironment.
http://www.ncbi.nlm.nih.gov/pubmed/23709120
Crutch,
You've got a link to the PPHM Credit Suisse coverage?
Thanks,