I would appreciate a little help in understanding IL28B. To my understanding when IL28B is identified it represents a sub type of Genotype 1 patients that are more responsive to treatment. What I'm confused with is the different IL28B types, such as cc, and tt, and if there are others. Is the cc type the only one that represents being more responsive, or is it all IL28B types? I only have a weak grasp of this and would greatly appreciate if somebody could enlighten me. I'm just trying to understand the relationship of SVR results between Vertex and VRUS drugs. I saw info on Vertex reducing treatment time to 12 or 24 weeks, and increasing SVR into the 90% range when using IL28B as a predictor. I also see VRUS using IL28B in selecting subjects for their posted results that include interferon, also with SVR in the 90% range. I just dont understand the difference between IL28B cc, and IL28B tt. Thanks in advance for anybody willing to enlighten me on this.
Without delving too deeply into the differences in variants there's one thing I would like to point out. Stratification between variants being done in VRUS' studies is to prove that this metric is no longer needed with PSI-7977 because the drug works equally well for all patients regardless of whether the patient is IL28B, CC, or TT. The metric is highly relevant in studies with Incivek to determine which patients will respond well to treatment as you well know.
I did see in the VRUS trial info the statement "Stratified by IL28B and baseline HCV RNA", but I didnt quite understand how that was applied. I didnt see another reference to just how that was applied in the trial patient selection. I didn't see info comparing the various common predictors, just the statement that it basically didn't matter. I'm questioning this because I've come to realize that in reading trial results sometimes what is NOT said can mean quite a bit. As far as I can tell the trials could have selectively been with the easier to treat patients with low viral loads, European decent and with other high predictors of SVR. I've seen drug companies do much worse that just leave out significant data. I try to work under the theme of "Trust your fellow man, but cut the cards"
"Does that answer your question? "
NO. The fact is that VRUS dropped the 7977 monotherapy after all their hype because the SVR was only 60%.
The fact that the 7 day monotherapy for genotype 1 was better than genotype 2 and 3 does not mean anything especially when they acknowledged that mono was a failure.
Be my guest to conclude whatever you want from that data. However the real results are when VRUS shows SVR trial results for all oral for genotype 1 -- years away-- maybe good maybe not so good. No one knows until head to head trials are run.
Meanwhile my advice to you is if you have some paper profit in VRUS, I would not spend it yet. Good luck.
Your statement sums up all the recent stock price action in VRTX, VRUS, and IHBX. It represents the most ignorant, irresponsible way of investing. Do not let data and facts get in the way of a great story. Shoot now and ask questions later. A bird in the hand is not worth anything if there might be a better bird in the bush. Obviously, you have been "...getting in (to VRUS) before events fully develop". For me, I will "watch from the sidelines" when it comes to investing in VRUS. I cannot believe the endless stream of BS out of this company with very little to back it up. They sure have convinced you. I am going to take the other side of this bet and stick with Vertex.
"There is a possibility that the patient selection in VRUS trials is skewed toward the easy-to-treat population. I remember a conference call in which the CEO said they didn't have many Black Americans among trial patients, and that might be why the numbers look better than others. You see patients with African ancestry have predominantly a T containing allele while a majority of patients of European ancestry have a C-allele."
Highlighting race is highlighting IL28B status which I explained is becoming as irrelevant as interferon-based treatment. If the CEO made such a statement I guess he's not trying to pull a fast one. Right?
"How in the world can you trust any of their data when they run trials without a control? Look at their trial design for Nutrino it is a joke"
What would you suggest they use as a control group for NUTRINO?
"What would you suggest they use as a control group for NUTRINO?"
I understand where you are coming from - an all oral therapy compared to a control that contains an injection is hard to blind.
However, is the following a possibility, and if not, why?
- Interferon injection
- Placebo pill
- Placebo injection
It's important to understand what third, gladpick, or VRTX for that matter care about isn't what the FDA cares about. What the FDA cares about is public health and meeting unmet need. GT1 data will be coming out from ELECTRON study showing the efficacy of PSI-7977/Riba just as it did in GT2/GT3. NEUTRINO is studying how the drug works in patients that can't take a P.I. when combined with interferon.
Ah, yes. Not thinking on all cylinders tonight :) I think I'm getting my physics terms confused.
I looked at the PR again. It was Fission I was confusing myself with. Fission is open label, but why not run it as I proposed in my last post? That would allow it to be blinded.
Positron is blinded, and I assume Neutrino will be blinded in the same way.
Couple more questions.
Assuming Electron and Quantum data is good for GT1, why wouldn't Neutrino look only at GT1? The reason I ask is because if Positron is specific to GT2/3 who are interferon intolerant, then why would VRUS need a second phase 3 trial aimed at the same patient population (GT2/3 who are interferon intolerant) but with the addition of GT1 who are interferon intolerant (and other rarer genotypes)? What advantage is there in having GT2/3 at all in Neutrino?
Also, why look at interferon intolerant patients only in GT1? Why not just go as broad as possible in Neutrino and have the criteria simply be "patients with HCV"?
Lastly, what is defined as interferon intolerant in the studies - any idea? Is this someone who was previously treated with old SOC and dropped out early? Is this someone who has never had interferon but just doesn't want to take it ever? Just seems a bit nebulous to me.
In one of their recent conference presentations, Pharmasset was asked to define interferon intolerant and was unable to come up with a consistent answer when asked 3 separate times by different analysts.