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ASCO 2018 Presentation for DCVax-L - Sunday, June

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ASCO 2018 Presentation for DCVax-L - Sunday, June 3, 2018 - transcribed

Linda Powers

Welcome everybody. Thank you very much for coming. Is it too loud or too soft? Too soft? Can you hear me now? Ok.

Thank you very much for coming this afternoon. We really appreciate it. It’s been an exciting week. This week, our publication came out about interim data from our Phase 3 clinical trial of DCVax-L for glioblastoma brain cancer. That was eleven years in the making… the data in that trial. That trial’s been underway for eleven years. Also this week, the federal Right to Try legislation was signed into law in the U.S. to enable patients with life-threatening diseases to gain access to treatments while they’re still in clinical trials. So an exciting week on both fronts.

Today, in our presentation, we’re going to focus on the science and the medical aspects of DCVax-L and the DCVax-L Phase 3 trial. We do also have some business activities underway, that we will be, hope to be able to talk about in the coming weeks. But today’s focus is the science and the medical aspects. So our line up today that are going to be speaking… first will be Dr. Bosch, our Chief Technical Officer of Northwest Bio. He’s going to review and expand upon the data that were in the publication, particularly the highlights and some insights into those data.

Next will be some of our patients. We have a total of five patients or family members here to give us their experiences today. These are not patients from the Phase 3 trial. They're from our early stage Phase 1 trial or compassionate use cases. Four of the five have glioblastoma brain cancer. One of them has very different cancer called merkel cell carcinoma. Northwest has treated diverse cancers in compassionate use patients, and this is one of our patients. Merkel cell carcinoma is a cancer of the skin and tissue, which is more aggressive than melanoma. It’s a bad cancer, just as glioblastoma brain cancer is a bad cancer. And just to give you a little advance glimpse, two of our patients are nearly four years out, that you’ll hear from today. Two of our patients are six years out, and one of our patients is fifteen years out… from diagnosis. Let me say these patients are only going to relate their personal experiences with DCVax. These experiences may or may not be typical of other patients. Also, DCVax is experimental. It is not approved by FDA or other regulators. And we and the patients are not going to make any conclusionary statements about whether it’s effective or safe. Only the FDA or a regulator can do that. But they’re going to tell you about their experiences.

Then we’re going to hear finally the clinician’s viewpoint. Unfortunately, our principal investigator of the trial, Dr. Linda Liau of UCLA, is not at ASCO at present. She had a patient emergency. But we’re very very fortunate to have Dr. Keyoumars Ashkan, who has been the lead investigator for the Phase 3 trial in Europe, and has worked with DCVax and ourselves for seven years. He has seven years of personal experience with his own patients receiving DCVax.

So, one last point before we start our line up is a correct-the-record point - there’ve been a lot of claims flying around since our publication came out. And one of the claims that some folks have put out, including a group in the UK, is that this treatment will never be viable because the cost will be impossible because it costs 250,000 pounds sterling per year. That is factually wrong. It is just wrong. That information was not checked with us. It has never been the case. It is not the case. So… suffice it to say we’ve worked for years to make DCVax a practical product with the goal that it will be widely available and viable.

So with that out of the way, let’s turn to our line up. Dr. Bosch…

Dr. Marnix Bosch - minute 4:43

It truly has been an exciting week. And it’s really capped off by this conference here where a lot of progress is being reported on these cancers. And we are very happy that we are in the position to share some of our progress in the treatment of newly diagnosed glioblastoma with DCVax-L.

And I’m going to walk you through the data that was published last week, and I’ll give you some of my interpretations, and some interpretations of the company as to the status of the data and what they might mean. Of course, the final deliberations will only be made once the data are unblinded. So far we’re talking about just a blended group of patients, many of which have been treated with the drug, about 90%, and the rest have not received DCVax-L. So for now we’re treating this as a single population, and the data I’m talking about are about that single population.

This is the obligatory disclaimer.

But let me just jump in right to the product, what we believe it can do, and how we believe it actually works.

I don’t have really time to tell you about the manufacturing process, which is relatively straight forward and simple, or the extended biology of it… this is just not the forum for that. Two key take home points for that. One, it is fully personalized. We’re using the patient’s immune cells, and we’re using the patient’s tumor antigens. Now remember, glioblastoma is a very heterogenous disease. Your glioblastoma differs from your glioblastoma; and even within a certain patient, their glioblastoma is vastly heterogenous. And there have been many immunotherapy attempts to try and treat glioblastoma. Typically they use one antigen or two antigens. And if you think about the heterogeneity of the disease in a population of cells, no body should be surprised that those therapies don’t have much of a chance to be successful because not all cells carry that one antigen. And even if they do, they are likely to down regulate that antigen population that don’t have that antigen will grow out. What we do instead is we use all the antigens that are present in the tumor. The mechanism as to how we do that is not really relevant at this point in time. If we do use surgical tissue, we make a preparation from the surgical tissue, we load that to charge the immune system against all the antigens present in the tumor.

Here’s how it works. The [??dentil??] that you can see here is loaded with the antigens that are coming out of the tumor lysate. And then they interact with what are called T cells. And the T cells are really the cells that travel through the body and can go to the brain tumor. They can indeed go across the blood brain barrier, they can start their battle with the tumor at that point in time. Multiple immunizations will continue to load up and arm that army of T cells. And what you get after awhile is these T cells are present in the tumor, not before vaccination, but after vaccination. These little brown dots that you are looking at are actual T cells that are present in the tumor as a consequence of vaccination. Now there’s helper cells, sorry, let me go back one… there’s what are called helper cells marked by their CD4 antigen, there are killer T cells, the ones that actually eradicate the tumors cells present in the tumor, and then there are the right [??] effecter [??] A factor [??] memory phenotype which are the ones that you need to combat the tumor. So this is just to demonstrate that to postulate a mechanism of action actually works in the patient in vivo because these are real patient samples.

So what did we find? What are the results from the trial? I need to give you a little bit of introduction into how the trial is put together, and for you to understand how we identify patients for the trial. Because there’s always for every trial, there’s a screening process. The screening process gives you a balance. The balance is that you want a well-defined patient population, but you also want sufficient patients in your trial. If you make your population too narrow, you’re not going to get enough patient population. If you make it too wide, the data become hard to interpret. So we have inclusion criteria like every trial does. The first screening is based on patient symptoms and an image, an MRI image of the brain, where the tumor becomes visible. Those patients at that point in time are entered into the screening process. Some of them fall out during the screening process, they don’t make it for various criteria that they don’t meet, and in the end, we end up with the population of patients we want. The patient in the process undergo a process called leukapheres where we collect the white cells from the patient. Those become the dendritic cells that we use to activate the immune system. And then they undergo radiation with temozolomide like every GBM patient in the world does these days. And then we enroll the patient, and we randomize them - two-thirds get the treatment, one-third gets the placebo. So that at the end of the trial, we can compare the results of the treatment to the results obtained in the placebo.

So, what are the results of that screening process? I actually need my glasses for this… I’m getting older than I thought I was… oh that’s much better. So here are the parameters that we screen patients on, and you can see that because we screen patients based on symptoms and MRI, it turns out that not everybody has GBM. So those patients don’t make it to the trial. Those are patients with lower grade glioma… patients that will have a much better prognosis than GBM patients. We can’t have those in the trial because they would contaminate the pool. Same for patients who have a really small tumor for whom we can’t get enough tumor lysate to make the product. Small tumor patients would do typically really well. They don’t fall into this group. So we can’t go through this criteria one by one. In the end, we have a population of 331 patients randomized into the study to product and to placebo. And when we reflect on this, it turns out that we eliminated a few patients who would have a bad prognosis. We also have eliminated a lot of patients who would have a good prognosis. And we end up with a balanced population. And if we review that population for known prognostic factors, factors that determine how well you’re going to do, we find that our population reflects the general GBM population very, very well.

So those points are highlighted here (Patient Demographics slide). The demographics that we have in our trial are comparable to other GBM trials, especially with regard to what we call known prognostic factors, one of those is age. If you’re younger, you’re likely to do better. Another one is the status of the MGMT gene promotor. The MGMT gene determines how well your response to temozolomide, the chemotherapy that everybody gets. If the promotor is methylated, you’ll do better, because your can’t get rid of the temodar (another name for temozolomide) as quickly. And we’ll come back to that point later in this presentation.

Now you don’t need to read all of these but if you were to go to literature and say, okay, how does a trial for GBM look like for patients? You’ll find something that looks like something like we have up here.

This is a rather complicated slide and I’m not going to walk you through it all. What is important here is that in the survival analysis, all these groups that we have here, because we randomized to drug and to placebo, we get different populations in the trial. Right now, I’m just lumping then all together. I’m giving you survival results from that population lumped together. And one of the reasons why that’s actually relevant, is become almost 90 percent of the patients actually have received DCVax at some point in the trial. How does that work if you randomize two to one (2:1)? Originally we have this two to one distribution. Then patients come to the clinic. They go through their scans, and at some point in time, they may have shown what’s called disease progression on their scan. The tumor is getting bigger a certain amount. We call that progression. At that point in time, we tell the patients no matter what you had before, you can now have the active treatment. That’s a very important recruitment tool because if patients come to us they say well I want to be in the trial but I don’t want to be a placebo patient, which a lot of them actually don’t want. And I wouldn’t want it either. Then what we can do is we can provide the drug at the time of tumor progression. So that’s why we ended up with 90 percent of the patients being treated with the drug.

I’ll give you a glimpse of the safety data. It’s what everybody else asks about first.
“Oh, it’s a cancer treatment. It must have terrible side effects.”

This treatment actually has very, very limited side effects. Patients get a little bit of redness and in duration, swelling at the injection site. They may get a low fever for a couple of days. But it’s really, really minimal compared to other treatments. This is a breakdown of serious adverse events. (Safety Overview in ITT Population slide)

If you do a trial, you monitor safety in part by tracking adverse events and serious adverse events. And then you ask the question of those serious adverse events… stroke, paralysis, etc., how many could be possibly attributed to the treatment? That’s an important safety assessment. Because if you’re making patients sicker while you’re pretending to treat them, you don’t have a good safety profile. It turns out that only seven of the 331 patients had any serious adverse event that was deemed at least possibly related to the treatment. Of course, they have other serious adverse events because these are patients with brain cancer. And we have not from day zero treated or cured everybody. And we have patients on placebo. We have patients irrespective of what we do, that weren’t going to do well anyway. But this is the important take home point. Seven patients with serious adverse events that are at least possibly related to the treatment.

Some background data (Background Survival data slide), because I’m going to talk about survival data. You need to place those into context. I’m gong to give you some background data. I’m not going to do direct comparisons. It’s a bit too early to do that.

The historical data tell you that average overall survival, median overall survival, have the patients live shorter, half live longer, is approximately 15 months. Patients with a good prognosis, good methylation status of the MGMT gene, do better, live on average 17 months. That’s historical data. Recent clinical trials roughly mimic those data in their control populations. So in other words, patients that get treated with radiation and temodar, like every other patient. And you see that these data are a little bit better. In the clinical trials, people do a little bit better. So you can expect that. But it’s not dramatic. Again, mind you this is in the control populations from those trials.

And then again, the methylated MGMT patients do better. And the ones who are un-methylated do relatively worse. Keep that number in mind, by the way, 14.7 months from randomization. It becomes relevant later on.

Minute 16:14
(Survival from Surgery slide)
Here’s our overall survival data. This is the first time that we’re able to present this to any audience other than the publication that we put out. You saw some numbers about median overall survival… that’s the easiest one to look at… we have in the patient population, which remember, is a blended population, where some patients got placebo, most patients got the drug at some point in time, but all of those are lumped together in this population. We’re not, we haven’t unblinded yet, some don’t know yet who got the treatment and who got the placebo. The blended median, is 23.1 months.

Now this slide is a little bit hard to see. You can see that this graph isn’t smooth. There are little sticks sticking up from the graph. Those sticks are patients that are alive and going through the process. Now just to give you an idea, the steeper the curve, the worse the treatment is. The worse the survival of the population is. This is a relatively flat curve, and there are all these patients that are still moving through the process. They’re still being treated, they’re still on the trial. Part of the reason while we’re not yet unblinding the trial, because we’d be losing a lot of data of those patients that are marching along, and are continuing to do very well.

Just to give you a summary of some key points that I’m going to go over in the next ten minutes (Survival findings: Key Points slide).

For one, when we look at the literature, we conclude that your overall survival in the Intent to Treat population - the 331 patients - is longer than is observed in historical and contemporary controls. I gave you those controls, you can make that comparison for yourself.

Even more importantly, this extended survival is not seen in one selected sub-set. Because we know what factors contribute to overall survival. And that is for instance age. Patients who are older in the trial and who are younger all seem to do well. Patients who have a performance status that is either very good or not so good seem to do well. The same, whether your tumor got completely removed - you can never completely remove GBM - it’s called a complete resection - patients who had the tumor completely or not, do well. Same for lymphocyte count, same for MGMT methylation status.

And this is just to give you a glimpse of what it looks like. (Survival from Surgery: Prognostic factors slide) Here we’re comparing, for age, we’re comparing younger patients versus older patients. Younger patients do a little bit better, you see the median, where half the patients have died, half are still alive has shifted a little bit. That’s validation of the data. It shows that our population is behaving the same as other GBM populations. We do see that difference.

We see also for performance status. We see it for lymphocyte count. We see it for surgery. That one’s actually statistically significant, so it may have some further meaning. That is also often seen in GBM populations.

So the only thing that’s out of the ordinary here is how far these lines go out. There’s nothing else outside the ordinary. In other words, it re-emphasizes the points that all populations, in general, appear to do better.

Now here’s the story about MGMT methylation status. (Survival from surgery by MGMT methylation status slide) I told you that MGMT methylation status determines how well you respond to temodar. So, if you’re MGMT methylated, you’re gonna do better. You can tell, the difference here is quite significant. It goes from 19.8 months to 34.7 months.

I was pointing at the screen there, it doesn’t work.

But look at this 19.8. I showed you previously that unmethylated MGMT patients had 14.7 months. So already, even in the bad population - unmethylated MGMT gene - we’re seeing the shift. How large the shift will be in the end we don’t know because we’re not at final analysis.

But then there is this rather remarkable shift to the right in the MGMT methylated patients. I’ll spend two minutes on that. Because typically in the literature those curves are apart, but they’re not as far apart as what we’re seeing. They’re typically apart by about seven months.

So we have about eight months that we need to explain, because seven months to fifteen months is about eight months.

So we asked the question, who are these patients? Are they younger? Did they have complete resection? Do they have better lymphocytes? Whatever… And we could not determine, we could not find a factor why these patients are living longer. They’re not younger, in fact, they’re older. Etc., etc.

So, what one can hypothesize at this point in time, and no further than a hypothesis, is that we’re actually looking at a treatment effect that explains the shift from 17 to 15 months difference between those two curves.

That treatment effect needs to be validated once we look at the unblinded data. But it is a completely tenable hypothesis at this point.

Let me shift then to the long term survivors (Long-Term Survivors slide). We have a population of patients, and these are the ones that have survived the longest since they got into the trial. And we want to explain their survival as well. Just like when I explained the difference between MGMT methylated and unmethylated.

Minute 21:23
So, the top one hundred patients, 100 out of 331, is about 30%. What that means is that the average eligible patient who would go into the trial, would have a 30% chance to fall in that population. Those are odds that I think most patients would be quite pleased with.

They’re predicted kaplan meier-derived… that’s kind of a complicated word… but their kaplan meier-derived overall survival prediction is 40.5 months. So if you make it to that group, suddenly your survival expectation has gone up quite a bit, from 23 months to 40 months.

Now what does that group look like?

They are a little bit younger then the overall population. More of them have the MGMT methylated promotor so you should expect that they all would do a little bit better.

But not this much better.

In fact, we did a statistical prediction and we found that if you were to predict their survival, they would not come close to that forty months that we observe here. There has to be something else. And by the way, only three percent of these patients had all three positive factors. So it’s unlikely that those factors explain what we’re seeing. There must be something else. What else could it be? It could be other factors that have not been identified yet. It could be that DCVax-L treatment pushes them to that point. Again, a tenable hypothesis. Unproven. Needs to be validated from the full unblinded data. And of course, it could be a combination of those two factors.

One last point before I get to my final conclusions. This is a question. If you are in the trial for a period of time, does your survival expectations change? And we’re seeing a pattern here. And the pattern is that yes, it changes, and at some point in time, it changes, quite what I would call, dramatically.

So for instance, if you were in the trial and survived for that 24 months or more, your life expectancy is about 38 months. In fact, it’s 38.6 months. If you were operated on 30 months before we did the analysis and you are alive, 67 patients at the point of analysis (MARCH 2017), your life expectancy has increased. But look, you have greater potential here. But if you’re six months longer in that trial, suddenly your survival time, your expected survival time, the [??] term is kaplan meier-derived survival estimate, my translation is expected survival time, or survival expectancy, goes from 46.5 months to 88.2 months. I’ll give you an interpretation of that in my take home message that comes next.

Of course, we can at this point in time not conclude but at least state DCVax-L is very well tolerated in newly-diagnosed GBM. The blinded data from this population, in which most receive the vaccine, suggest a possible survival benefit. And this benefit is observed in patients with both favorable and unfavorable status.

I talked about the extended survival of patients with methylated MGMT that sets up the notion that these treatments may be cooperative. They may help each other. It may be that if temozolomide can control the tumor for a little bit, DCVax-L can help you a little bit more. Again, it’s a hypothesis that’s tenable based on the data.

I described a possible treatment effect which may be responsible for some of the observed survival outcomes, and we find that long-term survivor outcomes in the longest populations can’t be fully explained by known prognostic factors. So there’s something else going on which may or may not be DCVax treatment.

We found that life expectancy increases substantially past a certain threshold. And the overall data, and that’s sort of my logical (biological) interpretation based on the slide I showed you with the T cells going to the brain combined with these survival data, suggests that DCVax-L immunization sets up a battle between the immune system and the tumor. And the immune system may actually win that battle in some or many cases. The Phase 3 final data will tell us how many and by how much.

The timing to unblind the trial… you saw all those patients that are still alive… we have to wait to see how they do before we unblind. So that’s my final conclusion here. That the timing to unblind the trial will be dependent upon the rate of accumulation of events. If patients continue to live, the temptation to unblind is great, and the pressure to do it is huge. But it could be a terrible mistake. So we’re going to be very, very careful and deliberate in making that decision.

Now I need to thank a lot of people, and I’m not go through the whole list. For one, the patients and their families, THANK YOU.

Linda Powers - 26:12 minutes

So I hope you found the overview and the data interesting and encouraging as we do. Now, we think that it’s important to hear a little bit from a personal perspective, the personal experience of the patients who have actually been taking the DCVax, and who are the data points. So let’s hear from the patients.

Kristyn Power - minute 27:00

Hello. My name’s Kristen Power and I’m from Canada. In July 2014, we received the terrifying news that my dad was diagnosed with GBM. At that time, he started radiation and he was able to complete radiation, but he wasn’t able to tolerate chemo. So because of that, he had another recurrence in the Spring of 2015. In 2015, there weren’t a lot of treatment options because of his inability to take chemo. In October, following his complete resection in June [2015], he had another recurrence. At that time, we fought for a third surgery, and they were able to resect 70% of the tumor. 30% of the tumor remained, and it was a fast growing tumor. We were told that he likely had about two weeks to live. We contacted Northwest and we were able to obtain the vaccine compassionately because we preserved the tumor tissue, and he started treatment. Today, my dad is almost four years out from diagnosis. He continues to be stable. He’s improving. If we look at his cognitive function, his conversations are improving, his physical mobility is improving, and everything is looking really good. We’re really, really grateful for how Northwest has treated us. They treat as almost part of the family. They answer the phone, they answer all of our questions, they’ve been amazing. I think that’s it. Oh, when dad was diagnosed, he was in his sixties. So, that’s one of those negative prognostic factors.
So he was over sixty, he didn’t have a complete resection, he wasn’t able to take chemo, he had a fast growing tumor, and he’s still doing good.

That’s our experience.

Jason Charles - Kat’s [Cure] husband - minute 29:13

Hello. Can you all hear me? Good. My name’s Jason. I’m from the UK. I’ve come over with my beautiful wife. It’s her fault that I’m up here today. So in 2013, me and my wife celebrated the birth of our son, Jacob. Three months after that, my wife was diagnosed with glioblastoma. What followed then was obviously quite an intense journey. She went under radiotherapy, three different types of chemotherapy, she’s had three major brain surgeries, one of which was an eight-hour awake craniotomy. She's amazing. In 2015, we were advised by the NHS, or our doctors at the time, that there wasn’t anything else that they could do, understandably. She’d gone through everything that they could throw at her and there was ninety days, three months, six months left to live. Being stubborn, like we are, we refused to accept this diagnosis. So we did our research, googling, and we discovered DCVax. Almost three years later, Kat’s right there [points to her] - three years after that ninety day prognosis. She’s still working part-time as an analyst for a bank. And she’s still the mother to our now five year-old son. I asked Kat to describe what DCVax is and she just said, “Wonderful. DCVax is a wonderful drug.” She says she’s now got her life back. She can be my wife, and she can be a mother. She simply jumps on a train every six months now, she has a quick jab in the arm, she has a coffee, she hops back. I’m a terrible husband, I don’t even go with her any more. So one thing that we want to make clear is there are no side effects. We’ve seen the side effects from the various different chemotherapies, and therapies that are out there, and there are no side effects with my wife. There’s no battling, as a result, but what’s even more important, is that there’s now no more tumor. It’s completely gone, which is what they said wouldn’t happen. So yeah, she’s been cancer-free for a little while now, which we’re very, very thankful for DCVax, and that’s the reason we’ve flown all the way from the UK is we really want everybody who has glioblastoma to have the same opportunity that we’ve had. Thank you.

Sarah Rigby - minute 31:55
Hello. My name is Sarah Rigby, and I live in Hong Kong, and I’m six and a half years now past diagnosis.

So a part of history of my story is I was forty-six when I was first diagnosed. It was devastating, actually, and as a mother of two boys who were twelve and thirteen, it… I found myself worrying more about them than I was worrying about myself, per say. Because I was thinking, you know, I’m not done, yet, you know. I don’t have time for this diagnosis. I’ve got to keep going. And yet the doctors were saying to me, well, six to, and the most optimistic ones were saying eighteen months. But it didn’t sound much to me, and it didn’t sound long enough. And I think, similar to Jason, I had a group of friends and family who were prepared to get busy and look for options. The doctors didn’t, at my hospital didn’t seem to have any other options other than the standard treatment. But we came across DCVax and that was the beginning of my relationship with the company. And in that time, I’ve had an MRI every six months.

I am symptom-less. I have no sign of active disease in my brain.

But really, I guess from my perspective, and something I’d really just want to say to you is what it feels like to go from thinking that it’s all over, and it’s all over quickly, before you have a chance to finish bringing up your children. What it feels like to suddenly have that extra bit of time to know that you can carry on being a mother to your children. And these days, my boys… they’ve both left home. They both finished school. They both did well into their exams. And funnily enough, they’re both studying to be doctors. So they’re in the UK, and I say to them sometimes, you know, boys, I hope you’re not being doctors to cure me. I’m, you know, doing fine. I hope you’re not curing cancer. And they say, no, no, no, mom. But you know, they’ve done extraordinarily well. And you know, maybe I’m sort of over egging it if I think maybe that’s due to the fact that I was there to finish off them growing up. But I not only survived that time that I never thought I would have, I survived in a way where I was healthy. I felt good. I looked good. Life was good. I could go back to living the life that I was living before I was diagnosed. And that’s powerful. That’s really powerful. That’s quite something. I never had to think about I was a cancer patient. I was a wife. I was their mother. I went back to work. And I’m very aware that I’m in nice contact with a bit of wood here, so I’ll stroke it a lot, and say long may it continue for me. I still take the vaccine every six months. And I would just like to echo as well what Jason says is that I talk passionately about this smart technology that allowed me and my family to carry on since my diagnosis. And I just want other patients to have had the positive experience that I have had. Thank you.

Alice - 36:25

Hi! My name’s Alice, and I live in Florida. I had the benefit of being a breast cancer survivor. So I got to do the whole eight months of torture, prior to becoming a metastatic merkel cell [patient]. As I was getting ready to celebrate the eight months, or eight years, nine years actually, almost ten free of cancer, the metastatic merkel cell showed up. So as my doctor was getting ready to fire me, I told him, I said, no, no, not yet. Because the multiple choice pathology came back on my arm and it turned out to be merkel cell. So two years after that - at that time he had shared with me that there was no chemo that would work on merkel cell. And two years later, it became metastatic. And during that two years, I had been making up my mind on how I would tell my husband and my son that I refused to go back and do chemo again. And that I would make the choice to leave the planet before I would go back through that. And that was a decision that was not going to be an easy one. My son was in college, and my husband and I had a wonderful life planned. We were getting ready for retirement. Luckily my friend who was a doctor. His wife demanded that he find a cure for me, and he had knowledge of this process, and he contacted the company, and in turn, gave me the information, and I contacted them. And in no time at all, they accepted me as a compassionate case. And, not many people can say that they got to go to Israel to be cured, and I was blessed with that experience. Today, he is a wonderful doctor who actually gives me my injections here in the United States. It’s quite interesting. I get the phone call, Alice, your bomb has arrived in the office. When will you come in for your shot? And, the best part is, you know, it was a week long process, sometimes two weeks, every time I got my chemo shot. And now, I go in, and then I’m out. I’m running around, enjoying my friends, going to dinner after I get my shot from my vaccine. And I’m six years out. Actually six and a half, ‘cause Sarah [Rigby- another compassionate care patient] and I were very close to each other, the time frames, when we both enjoyed our blessing. You know, and my husband (someone says something) - yeah, they gave me nine months to live. Nine months to live. And no fix. No fix.

It was, you know, and now people are going to have the right to try. You know, it’s like I feel so blessed to be able to share and speak about this product to people. I just, you know, I just don’t have words. I … don’t make me leak!… you know, but, you know, life is good. All of us should have an opportunity to not to have to choose to leave the planet. Thanks.

Brad Silver - minute 40:35

Hi there everyone. My name’s Brad Silver. I was an aquatic athlete. I come from Huntington Beach, California. I was an all-American swimmer, all-American water polo player. I was on an athletic scholarship for college. I played all over Europe, and also played in the Maccabiah Games in 1993, and again in 2001. And, in 2003, I was in my lifeguard unit, driving on the beach, and I had a major headache. First time in fifteen years that I actually went home sick ‘cause I had to. And got home, ran and saw my doctor. He said, “You have a migraine headache. Here’s your migraine meds.” I took those, felt better, but had that same headache two days later. Went to go see another doctor and he also said, “I think you have a migraine, but I’m not a neurologist.” He sent me to a neurologist. That doctor decided for me to go get an EEG, have lab work, and an MRI. All of my lab work was clean, the EEG showed that the left side of my brain was no longer working, and the MRI showed a golf-ball-sized tumor in my left frontal lobe. That was fifteen years ago. Not bad.

I’m really lucky because when I went to my first doctor, who did my biopsy, he told me surgery couldn’t be done. At that point, I had a two-year-old daughter, my wife was eight months pregnant with our second child, and I decided to ask a new doctor … A) can you do surgery? and B) what do you have for a clinical trial? And luckily, I had Dr. Linda Liau at UCLA, and had a great surgery. Started radiation. Finished that. Took my break, and got my first opportunity to get my shot of the DCVax. When I was forced to be on all of the other things, my side-effects from the chemo, radiation, I had a really hard time being the old me. When I had my shots, ‘cause I’d always have a one month break from chemo to get my booster shots and my initial shot, those were the times that it felt like I didn’t have cancer. I had all my energy back. I didn’t have concerns. I didn’t have to change myself. And that continued to go on, and on.

After two years, they said, “Let’s go for a little longer. Keep doing your MRI every three months.” And then at five years, they said, “Alright, now let’s start to do it every six months.” And I got to ten years, and they said, “How ‘bout every year or so?”

And the beauty of it is, it has allowed me to, one - I got to see my son be born. He was born nine days after my surgery. We walked into the hospital with my wife. She was having a C-Section so we could make sure I would get to see my son. And I had forty stitches on my head. And the nurse in the front looks at me and says, “Sir, I think you’re in the wrong area.” And I said, “No I’m here to see my son be born.” Great part, yeah, I was tired nine days after surgery. I’d laid in a bed next to my wife, but I got to be there. And [two] -I got to continue to be me.

When I did get through that first two years, and I was done with anything except for booster shots, I sat with a great friend, and he said, “You know what? It’s time for you to go back to living your life as you. Stop thinking you need to live your life around your cancer.” And that’s what it did for me. It opened my mind, opened my heart to make sure I could go back to being the silly old me. But the silly old me is a dad, a teacher, a coach. I’m a very happy person. And for fifteen years, you’re seeing one up here, but it ten or more years, I really hope you see a lot more people who have gone through this DCVax-L. I’m blessed. I feel that it keeps me here. And I want to share it with so many people to have you share it with others too. Please, let them know, even as strange as I am. I’m here. And I really hope more are. Thank you.

Dr. Keyoumars Ashkan - minute 45:44

Good afternoon everybody. Can you all hear me? I’d just really like to start out by saying how humbling it is to sit there and listen to our patients talking. Because as a clinician, everything I do, and I’m sure that this is true for the other clinicians as well, is for, and only for… the patients. Also this crystalizes what medicine is all about. Medicine is a science, but it’s equally an art, and patient experiences, patients and what they go through, really, really matters. So that’s a very, very hard act for me to follow for the next five minutes, but I shall try.

So I wear two hats. I’m a neurosurgeon, a clinician working in Kings College Hospital in South London, I deal with patients with glioblastoma day in, day out. I’m also a scientist, and a neuroscientist that obviously does research and understands research. So I fully recognize the limitation of the data that we published earlier this week - and the nice presentation that Marnix showed. What we have at the moment are interim data. And of course, we have to wait for the mature data to come out, for the data to be unblinded until we can make the final conclusions. But the clinician in me cannot help being excited about what we have here. Day in, day out, I sit in the clinic and I see patients with glioblastoma, and I go through the same things over and over again. Limited treatment options: surgery, radiotherapy, chemotherapy, and then ending the conversation with a poor prognosis. So anything that gives us hope, and if it is cautious optimism at this stage, is very, very welcome.

On a personal level, I’ve been involved with DCVax for the past seven years or so, and it’s been very interesting times. Because as I say, I work in London, so UK time and US time are very different. So my days are spent doing my clinical work, operating, seeing patients, etcetera. At nights, I’m on conference calls to the states for research. So again, it’s very nice to see that after seven years of sleepless nights, it hasn’t been wasted either. And you know, the data that Marnix presented also really very much is in harmony with my own personal experience, both in the trial and also outside the trial. So I don’t think it is a one-off. I think it is what we are actually seeing. And I really look forward to the eventual final data when it comes out.

Let’s face it. We work in a field in which advancements are very slow. Really, the last very major development in the field of brain tumor management was over a decade ago when Temodor, as you call it, Temozolimide, as we call it, [??] pathway. And we haven’t really had anything that fantastic to get really excited about. So I think, just about, I think, I think, I hope, we are there with this… DCVax.

So why is GBM difficult to treat, and why do I think DCVax is special? The answer is very complex but actually very simple. It is… GBMs are difficult to treat because of the genetic heterogeneity. And Marnix has already alluded to that. So we now know in a patient, any patient and any given one time, the same tumor, different locations within the same tumor have different genetic characteristics; and therefore, they can behave differently. Now imagine that amongst different patients, and also imagine that from across time, when the tumors recur. So really, in order to be able to cope with that genetic heterogeneity, we need two things, and that’s, I think, what DCVax brings into the equation. So when we produce DCVax, we need as much of the tumor as possible. So that’s what we do. We go in there and take as much of the tumor as possible and that gives us access to the fullest spectrum of the antigens, proteins, all those things which are related to the genetic diversity of the tumor. And therefore, when we make the vaccine apheresis and that gets rid of that all sampling errors. We have the whole lot of the tumor. And I think that’s one of the key aspects of DCVax. The other important aspect is that stimulates the immune system… it works with the immune system. And to my mind, the immune system is the most intelligent system we have available in the twenty first century. Why? Because over millions of years, it has evolved to be able to cope with all those diverse insults that nature throws our way. Different bacteria, different viruses… our own immune system can adapt to cope with that variability. And what better to stimulate the immune system against the genetic diversity of glioblastomas? So I think the science makes sense.

So DCVax is personalized, but also has got other advantages. From my point of view, as a clinician, the first thing we learn in medical school is first, do no harm. And you’ve seen the risk profile based the available data that Marnix presented looked good. And also, it’s very easy to deliver. It’s an intradermal injection so actually it’s quite easy to access and to do for the patients.

So I think what we have at the moment… it is interim data. We’ve got to be very cautious. We have to interpret it within those boundaries. But I think it is something to be hopeful. But there is still a lot to do. We have to work towards unblinding this study. I know Marnix explained the reasons that it’s been delayed, but as a clinician, I’m still going to push for it, because I think that’s very important. That’s what we need to be able to understand the impact of this. So I shall continue asking day in, day out.

We also have to work with the regulatory bodies, and we probably ought to do that now, right, not even waiting, because we want this to be available to all the patients. Again, while it’s very nice about these studies… yes, those patients who are in better prognostic groups are going to benefit more… but there is a benefit to all patients. We want this available to absolutely everybody. And absolutely everybody cannot afford everything. So the cost needs to be brought right down, and again, I’m going to be fighting for that, because I want this available to all my patients. We need to get the prices down, work with the regulatory bodies, approve it at a price which patients can afford. And I think that’s incredibly important. And you know what? I think you have to do all that… why? Because we owe it to these guys [points to the patients on the stage]. Thanks very much.

Linda Powers - minute 52:00

Well that concludes our program for today. I wanted to say, on behalf of the whole Northwest Bio team that we’re really, really grateful to all our patients. Our patients are our best ambassadors, our best advocates. They tend to be really passionate, and very helpful in telling fellow patients about the treatment and we’re really grateful that they were all able to share their stories with us. We’re also grateful the investigators in the trial, a number of who are here with us, including the principal investigator Linda Liau who could not be with us today. Keymour is the lead investigator in Europe. We were really blessed to have 69 co-authors on that publication last week. That’s pretty unheard of. And we even had a couple who said afterwards, Hey I wanted to be on it” so 69 co-authors among our investigators, meaning, just as Keymour said, their own personal experience with their own patients - it’s the picture that Marnix described for you.

I want to just reiterate what I said at the beginning. As a company, we fully endorse, and it is our goal, for this technology to be widely available to patients. We don’t want this to be a treatment of last resort. We want this to be a frontline treatment. We’ve worked long and hard to make it practical. There’s only one manufacturing process per patient. We manufacture the whole set of doses for multi-year treatment in one batch. Then we freeze those doses, and we’ve validated the frozen shelf-life for years. So then it’s just an off-the-shelf product out of the freezer, although it’s fully personalized for that patient. So we’ve worked for years and years to try and make this a very practical product to be widely available.

Right now, it’s made by hand. That is a very obviously, expensive process. It’s the same thing that the T cell people are dealing with. And there will be steps in the future, whether it’s economies of scale, whether it’s closing the system and having to have clean rooms with people in space suits making this by hand, which is what it is today, or full end-to-end automation. So there’s a lot of steps to be done in the future. I would say to anyone who can help us, help us provide funding, provide technical support, help spread the word, help us. We want to get this to everyone. Thank you.







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