Standard methodology at this stage of per-clinical work is to compare with freely growing virus culture. Comparison to active antiviral substances are usually introduced later, some times as late as in phase II/III clinical trials.
I know at least two ways of calculating viral load reduction. The common ones:
1.
Control is baseline viral load in cell culture or in patient's blood. This one you encounter when docs are demonstrating treatment progress (HIV, for instance)
viral load at treatment start, baseline: A
viral load after X days in treatment: B
reduction in percent: 100*(A-B)/A
reduction in log10: log10(B/A), B< A gives negative number, B>A positive
2.
Comparison between two near identical groups of patients or cell cultures (obtained by splitting initial cell culture in two, in case you will ask). One left untreated or treated only with delivery vehicle (liquid into which study drug is dissolved for delivery a.k.a. placebo) another gets the drug in delivery vehicle.
Viral load with delivery vehicle only at evaluation time is now A.
Viral load with treatment at evaluation time is now B.
In IPIX press release for VERO (kidney) cell results there is this :
"... compared to vehicle control".
No reason to assume that methodology would have changed between kidney and lung cell tests. So, it seems that they used method 2 to calculate load reduction. Good, I prefer it because it negates effects from delivery vehicle.
So, how good are Brilacidin results? One usually compares results to similar tests done previously with other antivirals. At this point I don't know any that would approach Brilacidin score. That may change.
Last: I love to have you around, LR. You make me think hard. That's good, very good.
Market Data 
Markets 
AI
