"there was no systemic absorption of brilacidin"
I doubt that's true - it would make brilacidin unique among small molecules, and I doubt IPIX has the expertise or wherewithal to have developed and validated an assay that would confirm that categorical statement. Happy to see the data if it exists, though.
"Whenever I look at SAEs in a clinical trial, I always compare increase compared to placebo. When its 2 or 3 subjects increase in SAEs (only 1 in each subcategory), it simply isn't a reliable increase in SAEs."
When there is a considerable and consistent increase in Serious Adverse Events, then that has to be considered a significant signal. It's seems to be more than the kind of random variation you seem to be talking about, not least because it's an increase. In the world of post-marketing surveillance, even one SAE against a denominator of maybe millions is regarded as a signal that needs to be explored, reported and if necessary results in labelling changes up to and including new contraindications or even withdrawal.
In early clinical stage work such signals in a relatively small population need to be taken even more seriously, not brushed under the carpet.
In aggregate, in the OM study brilacidin had 13 serious AEs, against placebo's 8. That's a fairly striking number that should not be brushed under the carpet. (The number of SAEs differs from the number of patients affected because some unfortunate patients suffered more than one serious adverse event from brilacidin.)
"As someone who claims to have insight into how big pharma and drug trials work, surely this would be common knowledge, right?"
I would work on trying to construct a valid factual argument and forget the ad hominem stuff for now. The latter only really ever works, if at all, if you can do the former properly.
