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Posted On: 09/11/2024 10:29:16 PM
Post# of 148844
Very odd outcomes in that trial.
At p = .41 it was nowhere near statistically significant in primary or secondary endpoints (stat sig is .05 or better). Primary endpoint was Time to recurrent non-fatal decompensated heart failure major adverse cardiac events (HF-MACE) that occur prior to the first terminal cardiac event (TCE). There is a long list of secondary endpoints the first being Time-to-first terminal cardiac event (TCE).
So no difference between placebo and their drug in initial heart failure or death. But the results from the pre-specified posthoc analysis would indicate there should be improvement in the primary and secondary endpoints.
Mesoblast had a p = .043 in their Covid trial so the results for their heart failure trial isn't a surprise.
Mesoblast targets some of the same cytokines as leronlimab but goes about it an entirely different way. Their MPCs switch the macrophage type from Type 1 (inflammatory) to type 2 (anti-inflammatory). Which in sufficient numbers could cause immunosuppression. But I don't think immunosuppression would be a problem because it obviously doesn't lower cytokine production or activation enough.
Leronlimab on the other hand switches macrophages from type 2 to type 1 but then controls production and activation of inflammatory cytokines through blockade of CCL binding. The results from our NASH trial show significant reductions.
Quote:
The primary endpoint was similar between treatment groups (HR: 1.17; 95% CI: 0.81-1.69; P = 0.41) as were terminal cardiac events and secondary endpoints.
The primary and secondary endpoints of the trial were negative. Positive signals in prespecified, and post hoc exploratory analyses suggest MPCs may improve outcomes, especially in patients with inflammation.
https://www.sciencedirect.com/science/article...9723000244
At p = .41 it was nowhere near statistically significant in primary or secondary endpoints (stat sig is .05 or better). Primary endpoint was Time to recurrent non-fatal decompensated heart failure major adverse cardiac events (HF-MACE) that occur prior to the first terminal cardiac event (TCE). There is a long list of secondary endpoints the first being Time-to-first terminal cardiac event (TCE).
So no difference between placebo and their drug in initial heart failure or death. But the results from the pre-specified posthoc analysis would indicate there should be improvement in the primary and secondary endpoints.
Mesoblast had a p = .043 in their Covid trial so the results for their heart failure trial isn't a surprise.
Mesoblast targets some of the same cytokines as leronlimab but goes about it an entirely different way. Their MPCs switch the macrophage type from Type 1 (inflammatory) to type 2 (anti-inflammatory). Which in sufficient numbers could cause immunosuppression. But I don't think immunosuppression would be a problem because it obviously doesn't lower cytokine production or activation enough.
Leronlimab on the other hand switches macrophages from type 2 to type 1 but then controls production and activation of inflammatory cytokines through blockade of CCL binding. The results from our NASH trial show significant reductions.
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