ond, James Bond, the character is often portrayed as the...

ond, James Bond, the character is often portrayed as the ultimate and best agent to have on your team. He often must lay low...before bursting out and showing his true colours, his capabilities and skills in an action packed scene much to the satisfaction of world wide audiences....


Hmmmmmmmm In probably the same way, iPPS will one day be viewed by many many more as being the best, well...agent to have on your side.An agent that will, in my opinion, work wonders defeating the enemy and evil forces of what we know as the last untreated disease left globally, OA.Yes sorry for the weird subject...what I mean is I'm Bond fan....hence the 007...but the trial and subsequent data in this post that I'm referring to is actually 008 ... Bond 007 plus 1.

Another two part'er tonight...references are at the end of Part 2. Some pretty cool quotes to come and action intense scenes in this one, as always, please enjoy.






_{Not unlike Bond, we are going to shoot through to the hall of fame..}


Remember Bond's arch nemesis, the evil network of...


_{Defeating SPECTRE is not only Bond's aim..it should be ours...}



What are you on about Mozz, I get the connection of Bond...the agent...and how invaluable he is to MI6...and how invaluable iPPS is to PAR shareholders...But SPECTRE? How do we fit in - in terms of addressing them?

Easy, iPPS will address and duly tackle the evil force of SPECTRE ...


Synovitis

Plundering precious cartilage

Endema Lesions proliferation

Cascading cytokines
TKA (Total Knee Arthroscopy)

Runaway Inflammation

Enduring pain







Meet agent COMP and ADAMTS5 (Are you guys groaning as much as I am in these analogies? @Absentfriend is gonna have a field day)...These are just two bio markers that were reported on, back in our Phase 2B. The reduction of these tells us that iPPS has some efficacy in the reduction of these, this implies that iPPS is reducing OA...and it's doing this safely. But Par-folk, this data was extracted from the serum....remember this point, we'll refer to it later in this post.




_{On the 29th of Aug 2019 we got the above breakthrough news on the effect of iPPS on two key biomarkers...this was in the serum....}






Ok so far we have some great evidence from the serum, we understand that getting a course of iPPS can lead to a reduction of these biomarkers, we also understand that it can reduce pain and increase functionality and we have evidence of some 900 plus SAS patients so far. What we must now do is start on a new directive ...a new mission...

WHEN do we go on our very own British agent mission Mozz?

Well IND for EMA (Europe) is imminent...as I have posted about in the past I have never held a bio tech through a P3....we have two of these about to commence (OA and MPS VI)...what an exciting journey this is going to be.One of our first sub-missions within this P3 is of course 007 plus 1 = 008. Quarter 3, no not 2023...not even 2022...it's primary end point readout is Q3 THIS year...2021...sure there could be delays...but it might occur around this time...

Let me tell you, if it's positive, the chance of that deal occurring and being bigger than what it could be as of the time of this post will be HIGHER. We will NO longer be dealing with JUST a safe pain solution that LASTS (Durability of some 9 months [subject to verification in P3]...) WE will be dealing with a real chance of some degree of DMOAD.

Paradigmers, there is no such thing currently in the world.NO drug has been shown to comprehensive halt or slow down the disease of OA to date. There has been some evidence that our drug can do this at least to some extent in some patients. This body of evidence will be tested THIS year in a P3 setting. I'm reiterating again, if there is some degree of this, we will be in a different ball game altogether...we will be promoted from little league to major OVERNIGHT. Yes it will be Diamonds are forever once our SP starts moving...

YES of course the granting of TGA provisional is big...yes of course the starting of an official IND is large...but I tell you, it's the raw data of 008 that will cause waves in the scientific and investment community.Yes @poolboy I am doing this research on his Majesty's Not-so-secret service, I might have my Gin and Tonic shaken and not stirred if you will.






Now Paradigmers, in other posts from me recently I have come up with a hypothesis For your eyes only.... Namely that I suspect that our results from 008 are going to be even better than the serum results from our 2B....I'm hoping it will surprise The living daylights out of us?

Now Mozz, my friend and buddy, you cannot simply traverse through the halls of HC and tell the folks that you have a suspicion and leave it at that...you need a Licence to kill OA. Paradigers, tonight I give you the link...WHY do I have this suspicion, what is my theory, how is it formed, what is it based on...give me the analysis. Ok here is my theory...We know for a fact that iPPS acts in multiple ways to reduce inflammation and one of the benefits is to reduce Bio Markers...this is a test of how well our drug works on the addressing of OA. Now putting a few details together...for example the Heat map as presented by Dr William Robinson, see this post --------> HEAT MAP

From this and other evidence, we also know that the biomarkers are higher in the synovial joint compared to just the serum, ie in the blood. At least in theory there is more 'heat' in the synovial joint, more cytokine action, more inflammation...I'm guessing, and it is only in my opinion, that the reduction here will be at least a little more prolific than the results we obtained from the serum. At the end of the day if the results are only as similar as what we got in P2B, it will still be compelling and form the link between the wondrous action of iPPS in the serum AND what happens also in the joint.





Whats a Bond film without the many tools and tricks of the trade? Mate, in the same way The Scientific Q's and clues are out there for us in the form of what tricks and mechanisms iPPS employs...like a gun to an agent...this will be one of the main sophisticated weapons we will one day use to treat the masses, my views.




_{A number of Q's have appeared throughout the history of Bond, here is a sample, there have been a few older ones too...}



Well and good Mozz - Let's do some more research into the link between iPPS and possible results from 008 later this year.

I have also determined through research that iPPS is marvellous at getting INTO the joint, at the recent Doc forum we heard Dr Robinson specifically state that one reason for failure of a lot of OA related drugs is their inability to penetrate into the joint. Don't forget OA is not a peripheral problem of some part of the joint...it involves the ENTIRE joint.

Let's turn to some evidence, this next quote backs up the suggestion that the levels of COMP are higher in RA compared to OA as well as higher in people that have OA compared to someone that doesn't have OA.

"COMP levels were higher in synovial fluid compared to serum levels in both groups (P <0.01)."¹

The researchers went on to say,

"COMP levels were higher in synovial fluid compared to serum levels in both groups (P <0.01). Amongst RA patients, synovial COMP levels showed a significant positive correlation with synovial membrane thickness on ultrasonography (P <0.001), and significant negative correlation with the cartilage thickness (P <0.001). "


Look at that P level...lower the better, it means raw proof at significance confidence levels for these statements. What does the above quote mean Mozz?

1) In healthy joints, we want the synovial membrane thickness to be only a few cells thick...why? As it allows for the production of fluid to lubricate and nourish the joint.....if it's too thick (when it is inflammed for instance) then it gets swollen with excess fluid and then it can start to hamper the joint and cartilage destruction is the next step.²

2) The second part of the quote above states that there is a negative correlation with cartilage thickness...obviously we want this bit to be thick and rich...Indeed COMP levels are important..it's a real indicator of the underling OA. What a breakthrough that was observing iPPS leading to reduced levels of COMP in the blood, now we just need to see this occurring within the joint/synovium as trial 008 progresses....


This concludes PART 1 of this Spy thriller...In part 2 we will tackle some more amazing research and quotes on our mission with Bond...We'll add more weight to the theory of how I suspect iPPS is not just a passive molecule...we will discover the whole relevance between BOND and iPPS...we'll talk about Rose and you'll find out who is she, a Bond girl or something else?