Hi Doc
First things first, I never said anything was a sure thing... so seems you may be the one that is delusional because it seems the only person purporting that anything is 100% certain is you? Of all things, you've come out and said an anonymous posters 'conjecture / borrowed guesswork' on what a company was intending to do when running a clinical trial which spans over a decade, is 100% correct... all this from your comfy chair at home. I'm still waiting for your side kick
@whytee to respond to the question I've asked for a third time, he only needs to chose between a) or b).. and the FDA's already given him the answer, so it really can't be that hard.
On the mechanism of action of Revascor
@DocMcstuffins , I think you are looking at it from your understanding of heart failure, which is a reasonable thing to do. I don't doubt your line of thought, as it is mainstream. But I think you either intentionally or unintentionally missed the point. Mesoblast's primary objective with Revascor is to treat the local inflammation in the heart. The by-product of the cells has benefits to the heart and vasculature through secretions of beneficial factors such as IL-10,
PDGF and FGF2.
Inflammation was always the primary target and core to the mechanism of action of Revascor as well as Mesoblast's other product Ryoncil. Benefits to ejection fraction would have been a mainstream acceptable explanation of why patients were experiecing less stroke, heart attacks and cardiac death .. but through conducting the phase 3 trial, it demonstrates that the reduction in storke, heart attacks and cardiac death in heart failure patients is more likely to be due to the targeting and reduction/removal of inflammation.
So I find it highly amusing that it appears your lack of understanding of what Mesoblsat are trying to do has lead you not make much sense of the results they have generated, and instead you go off and suggest that the company running the trial is the one that doesn't know whats going on. Hmmm... so I don't have an issue at all that you are skeptical of the results, and I agree it is reasonable to be skeptical. But at the same time, I think it is also reasonable to be optimistic, which is what most of us here are trying to express (bar a handful of posters with more extreme views).
But suggesting that IV would be better than a direct injection into the inflammated heart muscle, which is what they are intending to treat, still doesn't make much sense.. and actually suggests you may have misunderstood the proposed mechansim of action. But for treatments where MEsoblast are trying to target systemic inflammation, like SR-aGVHD using Ryoncil... where a number of organs are at risk due to cytokine release syndrome, than an IV makes sense.. and guess what, that is how Ryoncil is administered.. intravenous infusions. So with all due respect, I think Mesoblast know what they are doing here, and if you are skeptical about the trial results generated by the phase 3 trial, then I must say I'm highly skeptical of your suggestion of IV administration would yield better results... I might be wrong, and you've gone and worked with these cells before and conducted your own clinical studies, which I'd be happy to take a look at.. but if not, then I think I'll just ignore your IV suggestion as unsubstantiated for now.
You might be scratching your head a bit.. what is this guy going on about.. inflammation.. heart failure... don't take Mesoblast or my word for it... have a read of the following journal, which was published in 2019 so it doesn't include our trial results (which will be published after peer review), and I've taken a few screen grabs to highlight a few points... and its chronic inflammation in the heart that Mesoblast are targeting. And while nothing is certain, it shows that people in the field believe that inflammation has a key role to play in heart failure, which is not yet fully understood.. and Mesoblast are trying to figure it out through conducting clinical trials, with very promising results that if you don't mind make me optimistic about the treatment, without ever suggesting that it is a sure thing.role of infllammation in CHF
you can see other trials using synthetics trying to inihibit TNFa and IL-6 either have no effect on death or an increased rate of death.
Here is the conclusion, which suggests that inflammation has a role to play and there is more to chronic heart failure than you suggest.
So I hope you see the hypocrisy in what you just said about someone not really knowing what they don't know, Doc.
Hope you do come around though, because I believe any good doctor would want to see Mesoblast succeed.
(20min delay)