You said: "If systemic inflammation was such a risk to stroke,...

You said: "If systemic inflammation was such a risk to stroke, anti-inflammatories would be theorised to have an effect on it (steroids, NSAIDS, TBFa inhibitors, etc). Aspirin does, but not because of the inflammatory effects." I would like to address a couple of points regarding the above statement.

1. Systemic inflammation is a risk factor for some types of strokes including ischemic stroke (the most common type of stroke). It is however not a risk factor for other types of stroke including intracerebral hemorrhage (the second most common type of stroke). Remember we are presenting new data to the FDA from the DREAM trial data that Rex-L shows greatest treatment benefit on Major Adverse Cardiovascular Events in high-risk heart failure patients with Diabeties and/or Myocardial Ischemia. It would not be an unreasonable hypothesis IMO that this new data set strongly supports the brain-to-heart interaction understanding (i.e. link between ischemic cerebral events and disturbances in heart function); thus why diabetic and/or ischemic patients with high CRP (inflammation biomarker) showed the greatest treatment benefit in terms of MACE, which as you are aware includes strokes, and is an endpoint the FDA has previously accepted for approval of multiple drugs to reduce CV risk in diabetic patients. ((Now does it make sense why we are pivoting towards diabetic patients))...

2. It is not best practice to argue that because traditional anti-inflammatory medications (both steroidal and non-steroidal) have shown minimal/no effect on stroke risk then future treatments possessing anti-inflammatory properties such as Rex-L (which have shown to reduce stroke risk in a relatively large multi-centre double blind placebo controlled phase III trial) do not reduce stroke via acting on the inflammation pathway. We as public shareholders (or non-holders) do not have access to the new information MSB will be presenting to the FDA but I would think the inflammation story goes a long way to explaining the decreased incidence of MACE events (including stroke) -- as seen by the greatest benefits of diabetic an/or ischaemic patients with higher CRP levels (versus minimally inflamed subjects). In other words not all medications are created equal, and maybe, just maybe, Rem (or Rex) - L is the stronger (and safer) anti-inflammatory therapy for more serious conditions. This is plausible because the addition of MSC to SOC therapy for COVID-ARDS, DDD seems to be more powerful than the traditional anti-inflammatories alone (and more safe and likely durable).

You said: "But I'm skeptical. Because as you've pointed out, previous studies have shown a significant effect on LVESV as well with these treatments, and this failed to replicate that." Let me respond:

What we are talking about here is positioning Rex-L as a complimentary therapy to the current regiment of medications prescribed to primarily address the pump overload/dilatation problems. Yes these medication may reduce hospital visits due to said mechanisms/mechanic, but Rex-L has blown these other therapies out of the park in terms of reductions in Major Adverse Cardiac Events. So having not shown a significant effect on LVESV is of no concern to me as a MSB shareholder -- as now we will not be expecting to compete with Big Pharma on this MOA an potentially ruffle feathers, but instead we can add value in reducing MACE and complementing Big Pharma).

In short, Rex-L it is a much needed therapy for a large number of patients, it's MOA fits with current thinking regarding reducing inflammation leading to a reduction in atherosclerotic plaque formation and subsequent infarction risk (we were able to stabilise disease progression from Class II to Class III). The patients that respond best were high CRP and are diabetic and/or ischemic (and earlier on in the disease process before the heart is too fibrotic) support the current medical thinking/theory of why reductions in MACE occurred in the landmark DREAM trial.

I agree with @ImaScientist great post this morning that there is a strong rationale for local injection versus systemic injection (likewise with treating CLBP a localised injection was of course chosen). Regarding Rex-L reducing significantly Heart Attacks and Cardiac Death in inflamed patients (I acknowledge that we are largely on the same page regarding accepting the proposed mechanisms with current medical theory). However, unlike yourself, I trust that the reduction of stroke in ischemic patients is not a scientific anomaly and therefore it is wise to stick with a local injection into the inflamed heart. Also I have trust in SI and Dr Perin's expertise (I mean a systemic infusion would be relatively easier as you have highlighted before, so there must have been a good reason to go with a local injection - and at least in my mind and others, local delivery seems quite plausible). I agree that your view is largely fixed, but just giving my 2 cents worth.

Have a good day off