Genocea Biosciences' (GNCA) CEO Chip Clark on Clinical Trial Data of Genital Herpes Immunotherapy GEN-003 (Transcript)

| About: Genocea Biosciences, (GNCA)

Genocea Biosciences, Inc. (NASDAQ:GNCA)

Clinical Trial Data of Genital Herpes Immunotherapy GEN-003 Conference Call

March 31, 2015 9:00 AM ET


Maren Killackey - Stern Investor Relations

Chip Clark - President and Chief Executive Officer

Seth Hetherington - Chief Medical Officer


Marc Frahm - Cowen and Company

Stephen Willey - Stifel

Alan Carr - Needham & Co.

Andrew Peters - UBS Investment Bank

Christopher James - FBR & Co


Good morning and welcome to the Genocea Conference Call. At this time, all participants are in a listen-only mode. Following the formal remarks, we will open the call up for your questions. Please be advised that this call is being recorded at the company’s request.

At this time, I like to turn the call over to Maren Killackey of Stern Investor Relations. Please proceed.

Maren Killackey

Thank you, operator. Good morning. This is Maren Killackey with Stern Investor Relations and welcome to Genocea’s conference call to discuss positive 12 months durability data from its Phase 2 dose optimization trial evaluating GEN-003 for the treatment of genital herpes.

This morning we issued a press release covering this data. We have also prepared a slide presentation to accompany today’s webcast. And that presentation along with the release is available at under the Investor Relations tab.

Today on our call we have Chip Clark, President and Chief Executive Officer; Seth Hetherington, Chief Medical Officer; and Jonathan Poole, Chief Financial Officer.

Turning now to Slide 2, before we begin, I would like to remind everyone that statements made during this conference call relating to Genocea’s expected future performance, future business prospects, or future events or plans, may include forward-looking statements as defined under the Private Securities Litigation Reform Act of 1995. All such forward-looking statements are intended to be subject to the Safe Harbor protection provided by the Reform Act. Actual outcomes and results could differ materially from those forecasts due to the impact of many factors beyond the control of Genocea.

Genocea expressly disclaims any duty to provide updates to its forward-looking statements, whether as a result of new information, future events or otherwise. Participants are directed to the risk factors set forth in Genocea’s 2015 Annual Report on Form 10-K and other periodic reports filed with the Securities and Exchange Commission.

With that, let me pass the call over to Chip.

Chip Clark

Thanks, Maren, and good morning, everyone. I’m so pleased to be reporting further positive data for GEN-003 today, this time at 12 months after dosing the final measurement time-point of the Phase 2 dose optimization trial.

Let’s look at Slide 3 in our slide-deck. At 12 months and with no boosters given, GEN-003 has demonstrated a sustained and statistically significant reduction in viral activity. GEN-003 has also demonstrated sustained efficacy across multiple potential Phase 3 endpoints at levels similar to a year of taking antiviral therapy daily.

We believe that these data underscore the potential of GEN-003 to be a once-year or potentially even less frequently dosed treatment for genital herpes. We believe an annual regimen would provide multiple benefits to patients and enhance GEN-003’s already attractive commercial profile. And in addition, we are already evaluating the two best performing doses from this dose optimization study in a recently initiated Phase 2b efficacy trial.

Let’s move to Slide 4 and let me briefly review the agenda for today’s call. First, I will remind you of our clinical strategy to this point. Then Seth will provide an overview of the Phase 2 dose optimization trial including the study goals and an overview of the positive 12 months data. After that, I’ll discuss the potential of GEN-003 to significantly benefit patients, review our ongoing Phase 2b trial and outline our anticipated upcoming milestones. Finally, we will open up the call to questions.

Moving now to Slide 5, you may recall that in our Phase 1/2a trial, we tested a tenfold difference in dose and not only demonstrated clinical proof-of-concept, but also that the efficacy of GEN-003 was durable out to at least six months post dosing. From that trial, we determined that the 30 µg per protein, 50 µg of adjuvant was the best-performing dose, but that there was potentially an even better dose between 30 and 100 µg per protein.

So we then designed our Phase 2 dose optimization trial to evaluate six combinations of protein and adjuvant with this in mind. The results of this trial have demonstrated overall that the 60 µg per protein dose groups are more effective at reducing viral shedding than the 30 µg per protein, and that we have a clear adjuvant dose-response.

We continue to see the 60 µg per protein, and 50 and 75 µg of adjuvant doses as the most promising, which is why we have advanced them into our Phase 2b efficacy study. And we only have increased confidence in that decision from today’s 12-month data, which Seth will now discuss.

Seth Hetherington

Thanks very much, Chip. Let’s turn to Slide #6 and I’ll just take a moment to remind you of the trial design for the dose optimization study. We enrolled 310 patients with a history of recurrent genital herpes into one of seven dose groups: six active arms, as Chip outlined, plus a placebo group.

I just want to remind you that the placebo patients were only followed for the first 28 days after completion of dosing as a comparator for safety and tolerability. The primary endpoint of this trial was to evaluate the impact of each of the active doses on viral shedding as measured by the change from baseline. Viral shedding is the most objective and is a very efficient approach to demonstrate the antiviral activity of GEN-003, particularly in a small trial and is therefore a perfect endpoint study for the purposes of efficiently identifying the best dose for late-stage clinical trials.

As you probably remember, viral shedding rates were measured over four 28-day observation periods before dosing to establish each subject’s baseline shedding rate, then immediately after the third dose and again at 6 and 12 months after that last dose. The clinical trial also included a number of secondary endpoints in order to explore the potential effect of GEN-003 on clinical disease. And these included the proportion of patients who were recurrence free at 6 and 12 months after the last dose, and the time from the last dose of GEN-003 to the next lesion outbreak.

Reporting for these endpoints, we had the subjects come into the clinic, get examined and a swab sample was taken for a PCR test to look for HSV-2 DNA. We have also collected data on the percentage of days that patients reported the presence of herpes genital lesions during these same 28-day observation periods that we use for viral shedding. And finally, we follow the patients for safety, tolerability and immunogenicity.

In Slide 7, we show graphically the rates of viral shedding compared to baseline across the different dose groups. There are two key findings here. First, as expected for the period during which we followed the placebo patients, there was no change in viral shedding for those subjects. Secondly, the doses with the greatest and most consistent reductions in viral shedding over time are the 60 µg of protein combined with either 50 or 75 µg of the Matrix-M2TM adjuvant.

These are shown as the blue lines on the chart and both doses reduce viral shedding at 12 months versus baseline by a statistically significant amount of 64% and 52% respectively. It’s clear from this data that we expect any maintenance dose of GEN-003 to be given no more frequently than every 12 months and we can’t rule out the potential that this antiviral effect will persist for even longer.

Let’s move to Slide 8. This shows the percentage of subjects who are recurrence free at 12 months after the last dose of GEN-003. Just to remind you, this was the primary endpoint in pivotal trials for oral antivirals that are currently approved for the treatment of genital herpes, including Valtrex and Famvir, and it’s likely a Phase 3 endpoint for the GEN-003 program as well.

You can see that by this measure at 12 months, 20% or 30% of subjects receive GEN-003 at our most promising doses remain recurrence free. It should be noted that the study was not powered to distinguish between these doses on this measure and there are no statistical differences across any of the doses.

For reference, we have included in our chart the results against this measure for Famvir and Valtrex from their Phase 3 trials for active and placebo arms. Note that these were much bigger trials, running approximately 200 patients per arm.

With the caveat that there are differences in patient populations across studies, we’re very encouraged with how GEN-003 has performed against these historic measures and that the results are not too dissimilar from those that were achieved with daily antiviral medication.

Now, let’s move to Slide 9. Here you see the Kaplan-Meier plot of the time to first recurrence. This is an endpoint which typically needs a much larger group to be robust. But we think we’re at least seeing reasonably encouraging trends here. Without the placebo arm in the trial, we cannot draw any firm conclusions, but based on the historic data from antiviral trials which I referenced in the prior study, you would expect this steep decline in placebo to continue in contrast to the extended time to first recurrence for the active arms.

You may also notice that the curves differ from those we presented at the six month data point earlier, that’s because we identified a programming error in that dataset, which we have now corrected. The error was isolated and doesn’t affect any of the other endpoints for this current trial. This 12-month time to first recurrence data is consistent with rest of the data we presented today and supports confidence in GEN-003’s efficacy profile as we advance our current Phase 2b trial.

In Slide 10, we are showing the reductions for patient reported lesion rates during each of the four observation periods. We again observed sustained and statistically significant reductions through the 12 months across multiple dose groups supporting our overall confidence in the efficacy of GEN-003.

Looking back at our clinical program to-date, give us a full picture of the truly exciting potential of GEN-003. We have now demonstrated the antiviral effect of GEN-003 in two separate trials and with this current trial have actually improved both the magnitude and the durability of the efficacy compared to the previous Phase 1/2a trial.

In secondary endpoints we’re also seeing evidence of the clinical effect. The success to-date of our Phase 2 program positions us very well to enter into Phase 3 with a well-defined optimal dose.

Now I’ll turn the call back to Chip, to further discuss the implications of the data for the commercial opportunity for GEN-003.

Chip Clark

Thanks, Seth. Let’s move to Slide 11. These data strengthen GEN-003’s already compelling value proposition. We’ve once again demonstrated GEN-003’s efficacy. And furthermore, we believe we have at least doubled the expected time between maintenance doses, which we anticipate will be given at most once-yearly. Regardless of the current treatment paradigm, the GEN-003 value proposition looks even more compelling than we previously thought.

In contrast to episodic therapy, GEN-003 has the potential to reduce the frequency of outbreaks and lead to sustained reductions in viral shedding rates, which is thought to be the cause of the epidemic spread of genital herpes. And for those patients who take daily suppressive therapy, we think the GEN-003 value proposition is clear.

We offer durable efficacy via novel mechanism of action. And with GEN-003 potentially as a first-line therapy, orals could now be used as a rescue medication if outbreaks occur. GEN-003 also offers greatly improved convenience over the oral antivirals, which may drive significantly better real-world efficacy than oral antivirals, which rely on high and sustained levels of treatment compliance for optimal benefit.

So let’s turn now out to Slide 12. We are excited to progress the GEN-003 program, which most immediately involves advancing our recently initiated Phase 2b trial, the details of which are outlined on this slide. The goal of this trial, as you know is to confirm the activity of GEN-003 manufactured with Phase 3 processes that increased scale.

We’ll be using the same endpoints measured in the Phase 2 dose optimization study and we enrolled about 135 subjects across the U.S. with the same enrollment criteria as in previous studies.

These subjects are randomized to one of three dose groups, placebo, 60 µg per protein, 50 µg of adjuvant, or 60/75. And we will be monitored, all patients we will be monitored for 12 months. Dosing commenced in late January and remains underway.

Let’s turn now to our upcoming milestones outlined on Slide 13. We’re firming up our guidance here now that we have greater visibility into the dosing schedule from the ongoing Phase 2B study. We expect rather to report efficacy data as measured by viral shedding rate reductions from the study at the immediate post-dosing observation period in the third quarter of 2016.

Then around the end of this year, we expect to announce six months clinical efficacy from the study. This placebo-controlled data represents the first opportunity to measure GEN-003 manufactured with Phase 3 processes against the potential Phase 3 endpoint of percent lesion free at six months post-dosing. And we’ll of course be following these patients out for 12 months and we’ll report the 12-months data later.

Additionally, following the Phase 2b viral shedding data, we expect to commence another Phase 2b study to explore the potential additive effect of GEN-003 in combination with chronic suppressive antivirals. And if it is additive, which is reasonable to expect, its value proposition to patients and physicians would be further enhanced given the potential for maximum disease control through combination therapy. We expect the efficacy data from this trial to be available in the first-half of 2017.

Finally, we look forward to our end-of-Phase 2 meeting with the FDA, which we now expect to occur in the first quarter of 2017. We continue to anticipate starting Phase 3 trials in the second half of 2017.

Moving to Slide 14, in conclusion, we’re hugely encouraged by what we are seeing in the program. We’ve demonstrated an even greater impact on viral activity than in our first trial. And that suggest the potential of GEN-003 to have a durable effect at least out of 12 months beyond the initial dosing.

We have shown clinical efficacies through 12 months post-dosing across potential approval endpoints and we believe that this stronger profile really forces the potential for GEN-003 to serve as a new cornerstone treatment for genital herpes.

And finally, the Phase 2b trial is going well. And with the confidence of the strength of GEN-003 efficacy now demonstrated in two trials, we’ve shifted much of our focus to preparing for our FDA end-of-Phase 2 meeting early next year and for the start of Phase 3 in the second half of 2017.

With that, I would like to open the line for questions, operator.

Question-and-Answer Session


Thank you. [Operator Instructions] Our first question comes from the line of Marc Frahm of Cowen and Company. Your line is now open.

Marc Frahm

Hi, thanks for taking my question and congratulations on today’s data. Given what you’ve seen in kind of the durability of the response at 12 months, is there plans to either extend follow-up of these patients or maybe the Phase 2b that’s going on to 18, 24 months?

Chip Clark

Thanks, Marc. You’re ultimately getting at how is it we’re going to explore the questions of the optimal booster dosing schedule if, I am understanding your question correctly?

Marc Frahm

Yes, exactly.

Chip Clark

Yes. So, Seth, could you take that, please?

Seth Hetherington

Sure. We are in new territory here. This is really groundbreaking information and data that we’ve generated. As we’ve said all along, we adapt to the data as it comes out. So you’re exactly right, we are currently thinking about how we can follow these current patients out further in a rollover protocol to collect more information to understand how the durability goes.

And this will also impact what we do for long-term follow-up in the current trial and future trials as well. So stay tuned for details. We obviously know that it’s no sooner than 12 months for booster dose and maybe beyond that. And we will be thinking of ways that we can explore that in the near future.

Marc Frahm

Okay. And then, when we think about there isn’t really much deterioration of the recurrences from 6 months to 12 months, and these have this kind of stable 30% something population. I understand you probably haven’t been able to look at the 12 month data. But when you go back to the six month data and with those people, is there any kind of correlation back to baseline either maybe their baseline shedding rate or lesion rate or something in their immune response to the vaccine, that kind of separates those 30% from the other 60% - [50%, 60%] [ph].

Seth Hetherington

Yes, it’s a good question. Currently we just have this top line data. And the final dataset after going through the QC procedures will be available to us. And that kind of analysis would be very helpful for us to figure out how we design our follow-ups and potential booster doses in patients. So thanks very much for that question.

Chip Clark

Yes, Marc, and has been our custom, Marc, we’ll be presenting data at the scientific meeting and so I expect that the time at which we would be able to share such data.

Marc Frahm

Okay. And then, one last question on the potential combine with the oral antivirals, I mean what do you guys view as a meaningful - clinically meaningful increase in control from the kind of what looks like comparable between GEN-003 and oral antivirals?

Chip Clark

Seth, would you take that?

Seth Hetherington

Yes. That’s a very good question. We’ve given this a lot of thought. We think that the most - that’s probably the best analysis for that type of trial is something along the lines of proportion of patients that are recurrence free at 6 and 12 months, which for antivirals at six months currently stands at about 50% and it’s about 30% at 12 months. So we think that there is room for improvement. And you can guess what a reasonable increase in that number might be, let’s say, 50% increase to 70%, or 12 months 30% increase to 50%, something in that order of magnitude.

But we’ve not really finalized the trial design nor have we finalized the statistical analysis to use to come up with difference, but you could kind of see where we’re thinking.

Marc Frahm

Yes, okay, thanks a lot.

Chip Clark

Thank you, Marc.


Okay. Thank you. Our next question comes from Stephen Willey of Stifel. Your line is now open.

Stephen Willey

Yes, hi, thanks for taking the questions and congratulations on the data. I guess, I have a question about the - about the lower dose data actually, and then - and just as it pertains maybe to the 30/50 dose which is a dose for which we have prior 12 month data as well. And I guess, if you look at the 12 month data in this study, looks like there’s a decent sustaining of the viral shedding response at the 30/50 dose, I guess, which was not observed in the prior Phase 2 study at 12 months.

So I was just wondering, if the durability at 30 here was surprising, and I guess, how do you rationalize, I guess, what are the two conflicting data points when you think about Phase 3 trial design?

Chip Clark

So, Steve, I guess, you’re just really trying to understand if we should think of the results from this trial at 12 months as consistent with what we saw at 12 months in the first study for the 30/50 dose.

Stephen Willey


Chip Clark

Yes. So, Seth, could you take that, please.

Seth Hetherington

Yes, actually they are consistent, Steve. You’ll remember that in the first study we had to run a protocol amendment that allowed us to collect the samples at 12 months, because we had no idea of what we’ll be seeing. And as the trial evolved and we got more data, we extended the observation period and the collection of data at 12 months.

By doing so, we missed a lot of data from subjects at the 12 month period. And there is no statistical testing that was done at 12 months because when we had the - when we missed that data from those patients, the statistical model that we used falls apart and you can’t really do the analysis the way we had planned it.

So consequently, what we may have called a rebound in the shedding rates among those patients really had a wide range of confidence intervals. And I think that what we’re seeing now with the 30/50 dose, you could look at that curve and say, well, maybe it’s rebounding, maybe it’s not, it’s still a little bit undetermined, whereas clearly the 60/50 and 60/75 are rock-solid. So I think that results really are very consistent within the boundaries of what we can conclude from the statistical analysis, and given the numbers of patients that we have available now at 12 months versus what we had back with the first study.

Stephen Willey

Understood, that’s helpful. And then, just with respect to when we might see the immunogenicity data from this, I guess, that would accompany the full presentation of results. Is that - is it too early to think of something like ASM, which is now I guess the new ICAAC as being an option or should we be thinking about this as kind of being the second-half event?

Seth Hetherington

We will probably have a presentation at ICAAC. I can’t tell you for certain whether the immunogenicity will be included in that. If not, it would show up in a fall meeting most likely.

Stephen Willey

All right, I appreciate the color. Thanks, guys.

Seth Hetherington


Chip Clark

Thanks, Steve.


Thank you. And our next question comes from Alan Carr of Needham. Your line is now open.

Alan Carr

Hi, thanks for taking my questions. I wondered if we could continue along Steve’s questions a little bit, going back to that Slide 7. There isn’t awful lot of volatility with some of those doses and maybe we expect to see something like that with the symptomatic data. But maybe you could give us your thoughts on why there might be so much volatility in viral shedding with a few of those doses going from post dose three. For example, the - looks like the 30/75 dose was around quite a bit. I’m wondering what you all think might be going on there.

Chip Clark

So, Seth, you…

Seth Hetherington

Yes, that’s a very good question. We’ve learned an awful lot about viral shedding measurements over time in patients being treated with GEN-003 and I think it applies broadly to the field. Viral shedding is an episodic event. It’s sporadic. It’s not sustained, yet many of the episodes one misses, because they are of short duration. So sampling is important.

And you have to strike the balance between frequency and duration of sampling with obviously the logistics of collecting all the samples from patients et cetera. I think we found a good balance. We know that three patients per arm is sort of minimal to get at least an idea of the overall trends, and 45 is clearly better. And as we go up in our sample size we’ll get even smoother curves, because the jumping around of an individual patient will get balanced out by the others in the - in each of the dose groups.

I think the key point, Alan, is that when you look at these curves you have to look not at any given specific data-point, but you have to look at all the data together. It’s the totality of the picture that the curves are giving you that’s important. So what we see here is first of all, consistency with the ranking of doses showing that the 60/50 and the 60/75 are our best doses. And the consistency from the prior trial to this trial showing that in fact GEN-003 overall has shown a terrific amount of the efficacy in reducing viral shedding, consequently demonstrating its antiviral effect.

But I think we just have to understand the biology of this disease. It’s that it is very episodic. It’s unpredictable. And you have to take that into account when you look through data. That’s why we do what we do. We look at multiple endpoints. We look at it in multiple ways, multiple analysis plans. And we look at the overall picture of the data rather than getting focused on any one aberrant data-point at any one time.

Alan Carr

Thanks. Another question, you mentioned, I think maybe you mentioned earlier about going out farther than 12 months. Is that - how far out are you farther following these patients or is this the last assessment?

Seth Hetherington

Yes. Currently in the current protocol, this is the last assessment for these subjects. And we are thinking about ways to reenroll them into a follow-on program to get longer-term data and that’s what we are just starting to think about now. Again, we are reacting to the data. It’s an empiric finding and we will follow the data to come to a final conclusion.

Alan Carr

How far out are you following the patients in the Phase 2b trial? Did that go past 12?

Seth Hetherington

It only goes to 12 months currently. But you can imagine that we might think about amending that.

Alan Carr

Okay. And then the last one, timing of the end-of-Phase 2. You moved it to early 2017. I guess, can you talk a bit more about that?

Seth Hetherington

Sure. As we’ve gotten closer and progressed through our trials, we’ve just gotten better clarity on when data would be available, the kind of data that we want to bring to the end-of-Phase 2 meeting. And I think that we’ve just got a little bit more precise now. And now it looks like the first quarter of 2017 is more reasonable time point. Importantly, this probably does not affect, we do not believe it affects the timing of the start of our Phase 3 trial.

Again it’s a confluence of the number of different factors that have to come together to be prepared for Phase 3. And we think that’s still somewhere around the middle of 2017.

Alan Carr

Okay, great. Thanks very much.

Chip Clark

Thank you very much.


Thank you. And our next question comes from Andrew Peters of UBS. Your line is now open.

Andrew Peters

Hey, guys. Thanks for taking my question and congrats on the data. Just wanted to ask a couple of related questions to some of that were asked earlier, specifically just on the viral shedding and its relationship to kind of more of the clinical endpoints.

When I look at the 50/50 arm in particular, looks like the viral shedding actually improves to be meaningfully between 6 and 12 months. Whereas the lesion free rate doesn’t kind of track along the same line. So just want to understand the relationship or the correlation between viral shedding and the clinical endpoints.

And how do you think about or how you think FDA thinks about that relationship and what they’re likely going to view as kind of the most important endpoints heading into the end-of-Phase 2 discussion? Thanks.

Chip Clark

Thanks, Andrew. Seth, that’s for you.

Seth Hetherington

Yes. There are number of points in there. So tell me - just remind me if I missed any, because there are several questions in there.

First of all, your question is about the relationship between shedding and a clinical expression of the disease as such as clinical lesion rates. There is no question that viral shedding really underlies any expression of this disease. If there is no active viral shedding, if there is no active viral replication, you just are not going to have outbreaks. You’re not going to have transmission.

The relationship between lesion rates and viral shedding is not lockstep. And the reason is that the majority of shedding is subclinical. So when we measure shedding, we’re measuring the totality of shedding that’s occurring when lesions are present and shedding that’s occurring when the patients are having no outbreaks.

So the actual direct relationship measuring one versus another is not going to be absolutely lockstep. It’s going to be approximate. It’s clearly going to be related. But you can’t take the lesion rate curves and superimpose them on the shedding rate curves, because, again, lesion rates are when there are lesions present and there is symptomatic shedding. What you’re not seeing in that curve is all the asymptomatic shedding that’s going on, which is the bulk of the shedding.

And I’ll remind you that asymptomatic shedding is very important, because that’s the time period during which most of the transmission of this disease occurs. So hope that explains the first question. You had another question about how does the FDA view this.

This is what we expect. We certainly know that in our Phase 3 programs we’re going to need a clinical endpoint. Shedding will not be the endpoint for that clinical trial, because what matters is, in any Phase 3 program is what benefit do you bring to the patient. But the FDA certainly understands the public health implications of reducing viral shedding.

And what I would expect they would not want to see is a product that improves the patient’s clinical status, but has no impact on viral shedding, because that may actually increase the likelihood of transmission and the continuation of the epidemic of genital herpes. So to be able to say that we have a product that does both reduces shedding and reduces clinical symptoms for the patient is what the FDA wants to see, and we would agree with them. We think that’s the most compelling profile for a product like this to have.

Andrew Peters

Okay. Great, thank you. And then, I guess, just want to understand again in the 60/50 arm, the viral shedding, the 64% I think jumped out, and a lot of people just wondering how impressive it was.

Is there anything that you guys saw pre-clinically to suggest that maybe an improvement at 12 months over six months would be possible? Or how do you think about that data-point in particular, given kind of the pretty significant improvement over the last six months?

Seth Hetherington

I don’t think it was preclinical data that really made us confident even at the six month time-point that we would see durability at 12 months. The preclinical studies only go out so far. They’re animal models. And they’re not - you can’t temporarily directly correlate what you see in an animal model with what happens in people.

What I think has impressed us throughout is that the immunogenicity data that we had from our first trial showed durability of antibody levels, neutralizing antibody levels and T cell responses, which nobody has shown before out to 12 months and very stably so. So I think we had a pretty good reason, particularly once we saw the six month data from our current trial and show how flat those curves were in viral shedding. I think we had pretty good confidence even at that point that we’d see something good at 12 months.

And now the question is how far out does that go. And as I mentioned before, that’s something that we will be following in future trials and probably in modifications of current trials.

Andrew Peters

Great. Thank you. And congrats again on the data.

Chip Clark

Thanks, Andrew.


Thank you. [Operator Instructions] Our next question comes from Christopher James of FBR & Company. Your line is now open.

Christopher James

Hi, good morning. And let me add my congratulations on a really strong dataset. Just a follow-up to, I guess, the - just a small tweak to the previous question on Slide 8, where we’re comparing GEN-003 versus orals at percent recurrence. Have you looked at or have you compared viral shedding rates with GEN-003 to orals at 12 months? I’m just interested in understanding how those two correlate across the different paradigms of treatment. Thanks.

Seth Hetherington

Sure, I’ll answer that, Chip. There is no data that I’m aware of on viral shedding using antivirals after 12 months. All the data is short-term as in four to six weeks kind of data. So I don’t have anything to go by. I think that this graph, number eight that you - as you referred to is really helpful. And that again it shows that we’re in the right ballpark for providing clinical benefit to patients. Caveats being that there are differences across clinical studies that - when you make such a comparison.

But at least I think at first blush, this is pretty good. And I think we have confidence in the Phase 3 program. And I think we just have a lot of optimism.

Christopher James

Great, that’s helpful. And then, Chip, you talked about the real-world efficacy of orals. Do you have any data on sort of what that looks like for Valtrex in particular?

Chip Clark

There is no good data to point that, Chris. We’re simply noting that in a Phase 3 clinical trial conditions are optimal for encouraging patients to take their medicines. But we would expect simply that given the convenience of the GEN-003 dosing regimen that there wouldn’t be, we would say, less risk that patients would be - would not be compliant and therefore greater likelihood that the patients would enjoy the full benefit of the medicine.

Christopher James

Right. Yes, would expect the real-world of the orals to be significantly less than what you are showing on the graph. And then, I guess, how do the KOLs think about a booster dose at 6 months, 12 months and beyond? I mean, is that obviously better compliance at 12 months, but how do the KOLs feel about sort of the 12 months, 6 months or even potentially 18 months?

Chip Clark

Yes. It’s an interesting question, Chris. I mean, we as - as I think this audience knows, all of the market research we’ve conducted today with patients and physicians and payors tells us that every six months dosing is quite attractive. And so we haven’t done substantial testing on the value of 12 months versus 6. But the anecdotal evidence we’ve collected suggested it would be valued highly. I think it’s just a matter of our doing more research to be able to quantify the benefit. We certainly see it as upside.

Christopher James

Great. And then, one final one if I may, will the Phase 2b be powered to detect differences across different - the two dosing groups?

Chip Clark

That’s for Seth.

Seth Hetherington

Yes. In our current study, probably not powered, it’s going to be mostly just showing differences in tolerance, and overall safety - overall efficacy for antivirals, as you can see.

Christopher James

Thanks, Seth. I appreciate it.


Thank you. And at this time, I am showing there are no further participants in the queue. I would like to turn the call back to management for any closing remarks.

Chip Clark

I would simply echo what I said at the outset, which is that we are incredibly happy with the data that we are sharing with you today, and look forward to continuing to keep you abreast of further developments in GEN-003. Thank you very much for your time today.


Ladies and gentlemen, thank you for your participation on today’s conference. This concludes your program. You may now disconnect. Everyone have a great day.

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