AHA ASSERT Trial Results Reaction
This post is part of 7 a 16 part series of posts taken from the transcript of an interview I (JL) conducted with Resverlogix (RVX.TO) co-founders Dr. Norman Wong (NW) and Donald McCaffrey (DM).
What follows is a lengthy and candid interview about the history of Resverlogix, recent events at the American Heart Association meetings, and future plans for the company.
I’ll be publishing two interview segments a day so not all of the links may be active if you are viewing this near the end of March 28-April 5, 2011.
Part 7
Read more: /#ixzz1ICn4u9sI
NW: We were given an unfair shake in the AHA panels analysis of our ASSERT data. If you
look at the ASSERT data, when we design a clinical trial, before you come in, we look at
what we think we will see. There are two things that we designed the trial to look at. One
was ApoA-1 increases, and the second one was HDL increases. Those were the two things
that we designed. So if you look at the graph that Don's showing up there, this tells us that
there's asignificant dose dependent increase in ApoA-1, that as you give more of the drug, which
tells us that it's dependent on the drug, we get higher levels of the ApoA-1. If you look
at the trend, meaning that overall three groups, the p-value is statistically significant. We
missed that primary endpoint and that yellow bar by the smallest margin possible. .06 versus
.05.
DM: Some of the reasoning behind that is because ApoA-1 is very hard to measure and
analyze. HDL is easy. ApoA-1 is very hard. So even one fluctuation and that makes a
difference. But unfortunately in the placebo group, we had three guys in there that all went
over 30% increases in their ApoA-1. So clearly they started exercising and new diets or
something. It's too bad they weren't taking the pill, too. If the placebo increase wasn't at
1%, even if it was .8%, we would have been significant all the way through. So the placebo
guys changed it somewhat as well. It was just an unfortunate scenario.
JL: You want a lethargic placebo group.
NW: If you look at it, just the smallest margin possible, that's how we missed. If we had
missed it by .2 that would be different.
DM: But also, this was a trial that took in everybody, 299 patients. And if they were already
really healthy, it didn't matter. So that's what the trial was designed to do. We wanted at
least half of them to be the sick patient population that eventually will get this drug, and half
of them not. We need to understand what's going to happen with this drug in humans, so you
give it to everybody. The Merck trial, they had already done their screening, and they did a
lot of screening to . . .
JL: To optimize.
NW: Oh yeah. They knew what they were going after.
DM: So now if you take the population that's actually going to get this drug, this is the result
we presented. These are the guys who are actually going to get this drug. A patient who's got
low HDL, then you see a 13% increase in ApoA-1. Not 5.6, 13 in our true patient population.
Here in the HDL, over 20% versus 5% or 6% in the overall trial. So we'll do some publications
on this important information over the next couple months and put this stuff out in a full
scientific data set. So here, even though we did have a really good HDL at 21%, this is the
large particles. This is the one that if you have one milligram per deciliter more than me, you
have 26% less chance of cardiovascular disease. Well, that's where we were the most
successful. And in our patient population, we're at 32% increase, not 21. So are we working?
You bet we're working.
What follows is a lengthy and candid interview about the history of Resverlogix, recent events at the American Heart Association meetings, and future plans for the company.
I’ll be publishing two interview segments a day so not all of the links may be active if you are viewing this near the end of March 28-April 5, 2011.
- Background of Dr. Norman Wong
- Early History of Resverlogix
- HDL Biology
- American Heart Association Meeting – 2010
- CETP History
- Importance of HDL Type
- AHA ASSERT Trial Response
- ALTs
- Investor Reaction
- The Next 2 Years
- David vs. Goliath
- Alzheimer’s Therapy Potential
- Upcoming Assure Trial
- Volatility of Resverlogix
- Resverlogix is Expanding
- More on the sell-off
Part 7
Read more: /#ixzz1ICn4u9sI
NW: We were given an unfair shake in the AHA panels analysis of our ASSERT data. If you
look at the ASSERT data, when we design a clinical trial, before you come in, we look at
what we think we will see. There are two things that we designed the trial to look at. One
was ApoA-1 increases, and the second one was HDL increases. Those were the two things
that we designed. So if you look at the graph that Don's showing up there, this tells us that
there's asignificant dose dependent increase in ApoA-1, that as you give more of the drug, which
tells us that it's dependent on the drug, we get higher levels of the ApoA-1. If you look
at the trend, meaning that overall three groups, the p-value is statistically significant. We
missed that primary endpoint and that yellow bar by the smallest margin possible. .06 versus
.05.
DM: Some of the reasoning behind that is because ApoA-1 is very hard to measure and
analyze. HDL is easy. ApoA-1 is very hard. So even one fluctuation and that makes a
difference. But unfortunately in the placebo group, we had three guys in there that all went
over 30% increases in their ApoA-1. So clearly they started exercising and new diets or
something. It's too bad they weren't taking the pill, too. If the placebo increase wasn't at
1%, even if it was .8%, we would have been significant all the way through. So the placebo
guys changed it somewhat as well. It was just an unfortunate scenario.
JL: You want a lethargic placebo group.
NW: If you look at it, just the smallest margin possible, that's how we missed. If we had
missed it by .2 that would be different.
DM: But also, this was a trial that took in everybody, 299 patients. And if they were already
really healthy, it didn't matter. So that's what the trial was designed to do. We wanted at
least half of them to be the sick patient population that eventually will get this drug, and half
of them not. We need to understand what's going to happen with this drug in humans, so you
give it to everybody. The Merck trial, they had already done their screening, and they did a
lot of screening to . . .
JL: To optimize.
NW: Oh yeah. They knew what they were going after.
DM: So now if you take the population that's actually going to get this drug, this is the result
we presented. These are the guys who are actually going to get this drug. A patient who's got
low HDL, then you see a 13% increase in ApoA-1. Not 5.6, 13 in our true patient population.
Here in the HDL, over 20% versus 5% or 6% in the overall trial. So we'll do some publications
on this important information over the next couple months and put this stuff out in a full
scientific data set. So here, even though we did have a really good HDL at 21%, this is the
large particles. This is the one that if you have one milligram per deciliter more than me, you
have 26% less chance of cardiovascular disease. Well, that's where we were the most
successful. And in our patient population, we're at 32% increase, not 21. So are we working?
You bet we're working.