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cheynew

10/01/16 6:57 AM

#274078 RE: geocappy1 #274077

They could sell the remaining 200 million shares left on the shelf and accomplish the same thing. Then, ask for an increase in authorized shares when they need it. Let the new partner buy some on the open market if they want more than that. No way am I in favor of a reverse split under any circumstances.

biopharm

10/01/16 7:13 AM

#274079 RE: geocappy1 #274077

I think it can be simple to negate problem party controlling pphm. Even if stock goes to $2.. Pphm does RS at 1/2 lowering OS to say 125M and pps of $4. It immediately sells new partner controlling interest of 126M shares at $___ a share. Pphm uses money to do R&D and new partner protects from old group who no longer can control pps.



Thinking outside the box and hoping Peregrine makes it before we all start losing our minds (since it will help that also!) : )

Would it be good for Peregrine to hand over the control of so many shares to just one other Big Pharma such as Merck ( just using Merck since they come in after AZ and must have been for some big $$ reason ??) and MAYBE Peregrine just says who cares about someone holding 50% or so of the stock currently and use that as leverage for later down the road, and try and make 3 even deals with other Big Pharmas say for 15% each so a total of about 45%

This way.... you have more competition with your PS Targeting, UNLESS of course the money is OVER THE TOP offered by someone like a Merck

I still say there is a way to play this to "p o s s i b l y" keep that already big BP who may own around 50% in the loop and that already big BP may not have such an incentive or find it useless to keep the stock low because Peregrine the longer Peregrine sticks around in the $10-30 range the more stock options Management picks up... the more stock other partners pick up.... because all know, eventually... this will pop up out of control.

Damn, the amyloids are spinning out of control in my brain and amyloids must be tied into these biomarkers for Oct 10 and if not... soon will be: (just pointing out TBI for now...)

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Amyloid PET imaging: applications beyond Alzheimer’s disease

Ana M. Catafau corresponding author and Santiago Bullich
Clinical R&D Neurosciences, Piramal Imaging GmbH, Tegeler Straße 6-7, 13353 Berlin, Germany

As a biomarker of beta-amyloid, positron emission tomography (PET) amyloid imaging offers a unique opportunity to detect the presence of this protein in the human body during life. Besides Alzheimer’s disease (AD), deposits of beta-amyloid in the brain are also present in other neurodegenerative diseases associated to dementia, such as Parkinson’s disease and dementia with Lewy bodies, as well as in other processes affecting brain function, such as cerebral amyloid angiopathy, brain trauma, Down’s syndrome and meningiomas, as shown by post-mortem pathology studies. Furthermore, in systemic amyloidosis other organs besides the brain are affected, and amyloid PET imaging may be suitable for the identification of these extra-cerebral amyloid depositions. Finally, the potential use of amyloid PET tracer accumulation in cerebral white matter (WM) as a marker of myelin is being investigated, leading to some promising results in patients with WM lesions and multiple sclerosis. In this article, a review of the ongoing research pointing to a broader application of amyloid PET imaging in clinical practice beyond AD is provided.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4339781/



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Public Workshop - Advancing the Development of Biomarkers in Traumatic Brain Injury, March 3, 2016

8:05am-8:15am Keynote Address: History and Lessons Learned from Clinical Trials in TBI Col. Todd E. Rasmussen, MD, FACS
Director of DoD Combat Casualty Care Research Program, US Air Force Medical Corps

http://www.fda.gov/MedicalDevices/NewsEvents/WorkshopsConferences/ucm483551.htm



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CSF biomarkers linked to mild brain injuries

Sept 29, 2016


Sept. 29, 2016—A new study published online included 16 professional Swedish hockey players and examined whether persistent symptoms after mild traumatic brain injury were associated with brain injury as evaluated by cerebrospinal fluid biomarkers for axonal damage and other aspects of central nervous system injury.

The hockey players had prolonged postconcussion symptoms for more than three months, according to the article by Kaj Blennow, MD, PhD, of the Sahlgrenska University Hospital, Sweden, and co-authors. The study also included 15 neurologically healthy control patients (JAMA Neurol. Published online ahead of print Sept. 19, 2016. doi:10.1001/jamaneurol.2016.2038). The authors reported increased cerebrospinal fluid neurofilament light protein and reduced amyloid ß levels in hockey players with repeated mild traumatic brain injury and postconcussion syndrome, findings that suggest evidence of white matter injury and amyloid deposition.

“Measurement of these biomarkers may be an objective tool to assess the degree of central nervous system injury in individuals with PCS and to distinguish individuals who are at risk of developing chronic traumatic encephalopathy,” the report concludes.

http://www.captodayonline.com/csf-biomarkers-linked-mild-brain-injuries/




Anyhow, Amyloids will certainly be part of the discussion sooner or later and all tied into PS Targeting... I bet there is quite the matrix going on charting out all the biomarkers associated with once PS Targeting begins. I remember a hockey player tweeting about all this....

and maybe Joe Shan mentions "hockey stick" enrollment subconsciously as he was thinking about brain injury within hockey... for some reason ... hmmmmm