Q3 Geron Earnings Conference Call - 2
Turning to GRN163L, our telomerase inhibitor drug. In July we published in the Tetrahedron Letters a new patented method for synthesizing the monomers that are used to build the 13 mer oligo which is GRN163L. This is new chemistry invented at Geron and is significant both because it decreases significantly the cost of generating the monomers and it also reduces the chemical complexity of the synthesis of the monomers yielding both higher quality monomers, which in turn produces a less expensive drug with greater purity. As in any drug development program, as we progress in Phase Is to Phase II studies, the agency appropriately wants evidence that we are increasing the purity of the compound in question. And this chemistry goes a long way to doing that, as well as reducing the cost of the compound.
An important paper was published in July in the Journal of Regenerative Medicine by our collaborator Hans Keirstead at UC Irvine which speaks to the safety of the OPC1 cells. In this study, Hans gave a mild contusion injury to the rats which over three to four weeks spontaneously heals and the animals fully recover. What he then did was inject the full dose of OPC1 cells into that mild contusion and demonstrated no impact on allowing those animals to recover normally. That says to us that even in a mild contusion state, these cells have no negative impact on the normal healing process and that's a really important study that the FDA had actually asked us to do. We've also in that study repeated the survival, full distribution throughout the lesion and exuberant myelination that we have published on before, and as I mentioned earlier now, our IND enabling studies are out to 12 months with full survival, engraftment and continued myelination.
Turning to our TAT triple zero 2 drug, our small molecule telomerase activator. In August Cal Harley presented new data on the mechanism of action of this compound. You will recall that through the–an analysis of traditional Chinese medicine extracts done in Hong Kong we identified a true small molecule that is a specific and potent upregulator of telomerase in telomerase competent cells and we've published a number of studies years ago demonstrating a potential breadth of utility in particular chronic diseases in which cellular senescence plays a major role for the concept of telomerase upregulation. This compound in this presentation was shown to stimulate a wide variety of cytokines from HIV subject CD8 cells which are critical to enhancing those cells' anti HIV effects, so this includes rantes, myp1 alpha and myp1 beta. The observation now is that this drug in vitro will re-awaken or – through telomerase activation mechanisms – the declining function of the patient's CD8 lymphocytes which, during the period of infectivity but asymptomatic status, are responsible for containing the virus in terms of the number of cells that are infected and in terms of viral load because the virus replicates indefinitely the telomerase upregulation mechanisms in the immune response are overwhelmed and there is progressive clonal senescence of the specific anti HIV CD8 clones. As those cell lines decline in function and number, you see viral load increased and patients progress with the polyclonal immune dysfunction that we recognize as full blown AIDS the disease. So we demonstrate that incubating those cells with our TAT double O, double–triple 0 2 drug, we upregulate telomerase and actually regain the ability of those cells to suppress HIV. We've also in this study demonstrated that that mechanism is clearly secondary to telomerase activation because all of those antiviral activities induced by the drug can be blocked if we pre-incubate with GRN163L, our telomerase inhibitor. So this compound is going beautifully in terms of pre IND studies and scale up manufacturing. We have preliminary animal PK and bioavailability and we know that this drug is orally active and that therapeutic doses can be easily achieved through oral administration.
Turning to the patent world. In September we announced the dismissal of appeals of two patent interference decisions that were relating to our nuclear transfer technology. You'll recall that the Board of Patent Appeals and Interferences had previously ruled in favor of Geron on all counts of two separate patent interference proceedings dealing with our nuclear transfer estate. University of Massachusetts and Advanced Cell Technology had appealed those decisions and have now dismissed them completely. These patents relate to our animal cloning technology that we acquired from the Roslin Institute in 1999, the so-called Dolly the Sheep Estate. In 2005 Geron and Exeter Life Sciences established a joint venture company called stART Licensing, Inc., to manage and license IP rights for animal cloning and as you recall, just recently the FDA has indicated its plans to allow milk and meat from cloned animals into the food supply which hopefully will create some demand from the industry for licenses to this IP estate and, again, we have retained to Geron all rights to the nuclear transfer technology for human cells.
In August we announced a major collaboration with the University of Edinburgh to conduct preclinical safety and efficacy studies on the three cell types that we're working on in our wholly owned subsidiary, Geron Bio-Med, and those are hepatocytes for adne drug testing and liver failure, osteoblasts for bone-forming cells and chondrocytes, the latter to – for musculoskeletal disorders including osteoarthritis, osteoporosis and bone fractures. So this work is really an extension of the contract that we had previously held with the Roslin Institute. Now this work will take place at the University's Center for Regenerative Medicine which is based at the University's Center for Biomedical Research which combines an 870 bed teaching hospital with the University of Edinburgh's medical school and research institute which is located on a 100 acre science park development and the Center for Regenerative Medicine is now headed by Professor Ian Wilmut who led the team that cloned Dolly the sheep. So the progress on those three cell types in our UK operation we can expect to accelerate. So that's the conclusion of my formal comments. We'll be happy now to open to Q&A.
COORDINATOR: Ladies and gentlemen this begins the question and answer portion of today's conference. For questions at this time, please press star followed by 1. Again, that is star followed by 1 for questions at this time. Our first question will come from the line of Mark Monane of Needham & Company. Please proceed.
Q ... actually it's Mona ... Hi David. Hi Tom. A couple of questions. One actually relates to some recent news that the US Patent Office has agreed to reexamine the validity of three of the fundamental patents that were issued to WARF and I wonder if you could maybe expand a bit more on this and what the implications might be for Geron and outline maybe if there's any sort of set timelines with the reexamination process. And then the second question I have actually relates to any plans that Geron might have for data presentation this quarter, particularly at ASH or the EORTC. Thanks.
DR. OKARMA: Sure. Hi, Mona. Thanks for those questions. You're correct. The, the Patent Office has decided to grant the requests to reexamine the fundamental WARF patents that Geron, to our knowledge, has the only, world's only, commercial license to. The impetus for the reexamination is a lot of academic frustration and some taxpayer organizations' distaste for broad enabling patents. To our view, the basis for the challenge is not material. We do expect the patents to be confirmed and their validity and frankly, if that's in fact the outcome, the strength of that patent and our licenses would thereby be increased. These processes can take awhile and obviously they are, they all have appeals attached to them, so I expect that this will be an issue that will carry on for well over a year before its final resolution. I would say that – you also asked what the significance is to Geron. We think generally this is a good, strong patent and we like having an organization the size and power of WARF policing it for us. On the other hand, we've obviously surrounded each one of our therapeutic cell types with Geron's own owned patent estate which would survive intact regardless of the outcome of the WARF validity challenge.
Your second question is upcoming presentations on 163L. We will have two presentations at the EORTC meetings next week in Prague – one on the pharmacokinetic data on the low dose cohorts of 163L in both the CLL subjects and the solid tumor subjects and a second one from Geron describing some preclinical combination synergy studies with 163L and other agents in lung cancer and ovarian cancer. The data on our drug will be early and it will not include any pharmacodynamic data because of mandatory batching rules from the protocol. Those data are not yet back. We hope to have them in time for the ASH presentation which is in December so that that second presentation on the drug ought to have a bit more PK/PD correlation. The object of all of this data obviously is to teach us how to use this drug in multiple clinical settings as a single agent. So the reason for studying CLL and solid tumors in the separate trials is to give us a feel for how various co-morbidities affect the metabolism and PK of the drug. So some of the solid tumor patients, for example, would be carrying co-morbidity in liver function and renal function which would not be the case for patients in CLL and there is a precedent for there being different PK/PD relationships for a variety of targeted agents between liquid and solid tumors, so to rule that out we're simultaneously looking at those two kinds of cancers. We will be filing another protocol later in this year and I'll announce that when we've gotten a green light from the agency – it will be on a liquid tumor that we think actually might be a registration pathway, either as a single agent or in combination.
Q Great. Just one follow up actually on the, on your ongoing GRN163 trials. Can you share at all what dose level you're at?
DR. OKARMA: Well, by the end of the year - although we won't be able to report it because the data will still be pending - we will be in the lowest therapeutic cohort. So I think that the take home message is that the really full story of how, how high we can dose, demonstrating the safety of the compound and hopefully impact on tumor burden and telomerase targeting CLL cells will be a story for the spring.
Q Thanks a lot.
DR. OKARMA: You're welcome, Mona.
COORDINATOR: Our next question comes from the line of Joel Sendek of Lazard Capital Markets. Please proceed.
Q Hi, thanks. Just following up on that question. If I recall correctly, there are eight dose cohorts for your studies of 163 so I'm wondering how long it will take to get through all of them and when we might have some clinical response rate data available.
DR. OKARMA: Yes. It's the same answer as I just gave to Mona. I think we will have real significant data at the AACR and ASCO meetings which would include multiple cohorts in the therapeutic dose range. You're right, there are six or seven dose cohorts in each trial, starting with very low doses and, frankly, going to doses that exceed what we think we would ever need to give in order to achieve telomerase inhibition, but we obviously wanted to study a broad range of doses to again, to learn how to optimally use this compound. I should also mention that we have modified the solid tumor protocol to reduce the infusion period from 6 hours to 2 hours, with obvious impact on enrollment and we've had no problems with any DLTs in moving from 6 hours to 2 hours. So the simple take home thus far we've seen no problem in administering this drug, even over a 2 hour infusion.
Q Okay. And then a question on the stem cell program. I'm wondering when the preclinical studies will be kind of wrapped up and you'll be able to start the clinical portion.
DR. OKARMA: Right. Well as we mentioned in the summer at the analyst day, we had our pre IND meeting on this topic with the agency in May and to our surprise they really wanted a lot more animals followed for a lot longer than frankly we thought was necessary, but we're going to give them what they want understanding that this is the world's first, you know, human clinical will cells derived from embryonic stem cells. So, for example, there will be nearly 2500 immune compromised, spinal cord injured rats who will receive various doses of these human cells in various portions of the IND enabling package studying all elements of potential tox and tumorogenesis. We have added hundreds more animals in response to the agency's demand and this will incur a delay in filing from December of this year which was our original target to probably mid year next year because it will simply take 6 more months to generate these animals, but the IND package – now that the content has been completely agreed upon – we've really dramatically lowered our risk of a failed IND submission because, assuming the data continue to go the way they have been – we will absolutely provide the agency with the comfort that they need to allow this clinical trial to move forward.
Q Okay. That's helpful. Thank you.
DR. OKARMA: You're welcome.
COORDINATOR: Our next question comes from the line of Ren Benjamin of Rodman. Please proceed.
Q Hi. Good morning and thanks for taking the question. This has, this question has more of a mechanism of action point of view to it. As far as the embryonic stem cells in particular, the OPC1 cells are concerned, you mentioned earlier on in your prepared talk - and maybe I heard it wrong - that the cells survive for approximately 12 months and so I was curious, you know, a) how you, how you determine that, and then how, if you can, could you extrapolate that to a, sort of a real world scenario. You know, would these cells cease to function at, after 12 months and, and then somehow affect the integration of the spinal tract neurons or are you thinking of it more of kind of like a supportive, a supportive niche where they come in, they call up the sprouting of axons, and, and, and then can, you know, kind of die off on their own, but now these axons are already sprouted and, and sort of doing their job.
DR. OKARMA: Thanks for that, Ren. That question let me know I wasn't clear in my prepared comments. So, first, the survival data are up to 12 months and that's derived by injecting the cells into spinal cord injured rats and keeping them alive for 3, 6, 9, 12 months and then sacrificing the animals and doing intensive histology throughout their spinal cord. And we obviously have stains that allow us to distinguish between rat myelin and rat glial cells versus human myelin and human glial cells. So the point I'm trying to make is that there's no evidence of any loss of the cells for up to 12 months after injection. Now that's interpreted by our neurology people as evidence that this is a permanent restoration of the glial population in the spinal cord injured area, and that's the object of the exercise. So we expect these cells to live indefinitely and not have to, do not expect to have to reinject them at all, that's obviously subject to continued, you know, survival work in both the animals, and once the human clinical trials start. But this is, like the rest of the cell types, purported to be a permanent and complete restoration of the tissue architecture and function – in this case of the spinal cord injured human. So the impact of myelination and of the neurotrophic factors is indefinite, until the actual neurons have healed to the best of their ability. So this is really good news that these cells appear to survive indefinitely. We will continue to follow some of these animals, but you have to understand that these are genetically immune compromised, spinal cord injured rats who were also given cyclosporine, because remember this is xenogeneic thing, it's a human cell in an animal, and these cells–these animals require reverse isolation and manual expression of their bladders three times a day – an extraordinarily expensive and difficult animal model to maintain for 3 months, let alone 12 months. So these are data that, you know, we think it's important to generate not only for the FDA and for our patients and investigators, but for ourselves, to prove the principle. And we're doing the same kind of long term survival experiments with cardiomyocytes in heart failure and islets in the diabetic rat. So this is a really good news story that, that OPC1s manufactured according to our GMP protocol, frozen, thawed and injected at full human doses in the spinal cord injured rat appear to survive indefinitely.
Q Terrific. Thanks for the clarification. Kind of expanding on, on that then, but more on broader terms, can you take us through, you know, from, from everything that you've learned from the, from interacting with the FDA, this being one of the first embryonic stem cell products to, to come close to clinical testing now, what, what all have you learned from the FDA. So, so I guess what I'm trying to get at is what are the steps necessary in, in this pre IND package. I mean you mentioned the 2,500 immunocompromised rats, you mentioned that there are primate testing going on. Can you give us a little bit more detail. How long does the FDA want you to follow these animals. I imagine that the toxicity studies in primates would be quite long. Would you be able to start a clinical trial before the final results are, are completed. Maybe just some details regarding your interaction.
DR. OKARMA: Sure. First of all, I did not say we're doing any primate studies. In fact, we are doing none, no primate studies whatsoever.
Q Okay.
DR. OKARMA: The agency was not at all interested in our doing that for the simple reason that the efficacy which has been overwhelmingly documented, to their satisfaction and to ours, took place in the only validated model of spinal cord injury which is the rat model; there is nothing validated in the monkey. And because we can, for every data point in any of these tox studies analyze hundreds of animals at a data point in rodents, compared to one or two animals in primates because of the expense of the monkey model, the agency is very happy to accept all of our tox data in this spinal cord injured rat model. So what we've learned is that – first we had quite a turnout at the agency, I mean the room was standing room only, everybody, you know, showed up. I think they were extremely surprised - pleasantly - at the details of our CMC section, I mean we've done many, many GMP production runs demonstrating the uniformity of production, the narrowness of the product specs – this process really works. And that of course is a fundamental improvement over any other cell therapy where, you know, you don't have a self-renewing source or a scalable manufacturing process that resembles a biological. So that part of the meeting was terrific, you know, they had no suggestions or issues with the whole CMC program. Where we were a little surprised is the number of animals and the duration of followup that they wanted for biodistribution, standard tox, and tumorogenicity. I would say that their biggest concern is the formation of tumors and part of that comes from, you know, the, what I would call contaminated academic literature where people are publishing animal experiments with cells that have not been grown to, in a way to exclude the possibility of there being contaminating, rogue, undifferentiated ES cells in them. We do it that way. We have not yet seen a single tumor in any of our IND enabling studies. Nevertheless, they want full 12 months in several different settings with increasing doses of OPCs, and in a separate 12 month study they want us to be spiking the OPCs with increasing doses of live, undifferentiated ES cells so they can get a feel for how pure the OPC prep needs to be to eliminate the possibility of tumor formation. So with the statistical package that's in front of them now, if we see no tumors in both of these 12 month studies, then at the 95 percent confidence level we can predict less than a 1 percent chance of any tumor formation in any human receiving the full dose of cells. So, it's a very powerful package. The problem of course is that they could care less about how difficult it is to - and expensive it is - to run these studies. I mean this is not a simple give an animal a tumor and give him the drug and see what happens - this is a spinal cord injured model, it is difficult to start with. These are nude rats so they have no immune systems and we put on top of that a couple of immune suppressive regimens to insure that the cells survive for a long period of time so we can make valid observations about tox, tumor formation and biodistribution and we've had some loss of animals due to infection, because these are all handled under reverse isolation for out, for up to 12 months. So it's, it's a big deal, you know, in the sense of the extreme nature of the animal model that is the only one around capable of being scaled to provide us and the agency with a sufficient number of animals at each data point. But you know, coming back to the helicopter view, there's really nothing different qualitatively about the regulatory path to an IND for embryonic stem cell-based therapies versus oligonucleotides or small molecules. It's the same bucket of information that they want, it's just that they are holding us to an extremely high standard because this is such a new technology and, you know, we're willing to give them what they want.
Q Thanks. Finally, I may have missed this in the beginning from your prepared remarks but can you give us an update on, on the vaccine program and what's happening there.
DR. OKARMA: Yeah. Sure. And, and I – thank you. I didn't mention that. Imminently our IND will be submitted to the agency for a hematologic malignancy and at your conference, Ren, I'll unveil what that plan is, and just to say here that we've put a lot of thought into the next clinical program. And the parameters that we think are most important are two. One–first and foremost, create a clinical protocol in a disease setting where we can generate very hard evidence that the exuberant immune responses our dendritic cells generate does in fact have impact on disease progression. That's very hard to do in prostate cancer as you know, so we've picked a malignancy in a particular therapeutic setting where we think that demonstration can be optimized. The second is that this is a indication that we think is a registration pathway if we do in fact show robust immune responses, a great safety profile as we've shown before and impact on disease progression. So although it's, it will be a Phase I/II and not a Phase II had we gone straight forward into the prostate cancer, the size and the definitive signal that we will get from this protocol is really worth that small step backward.
Q Okay. Sorry, one, since I have you on the phone, one, one last question with the, with the embryonic stem cell program. You mentioned that the studies in, what, was it, the question is have the studies in rats started with the, with the 12 month follow up already, or, or are they –
DR. OKARMA: – oh, yeah, we'll have our first 12 month study done this December.
Q Okay.
DR. OKARMA: So, yeah, I mean we are very far along. By first quarter of next year we will actually have most of the data that they have asked for, but we're having backup animals and we're having parallel studies which won't come out until the June-July timeframe to really, you know, hammer this down, so there's no wobble in the IND submission.
Q Right.
DR. OKARMA: We're very far along and that's why I can be pretty confident that we expect to be able to deliver to the agency exactly what they want and perhaps more.
Q Perfect. Thank you very much.
DR. OKARMA: You're welcome, Ren.
COORDINATOR: Our next question comes from the line of Steven Brozak of WBB Securities. Please proceed.
Q Hey, good morning, gentlemen. I'm looking at this and, and, you know, you've, you've belabored the point about the rodent studies that you're talking about to the point where when you do achieve that proof of concept it is going to be unique. How are you guys preparing for, you know, what I would think would be the potential collaboration specifically in the, amongst academia. They're going to come there and say ‘you've got something that's unique,' now there's going to be a whole different set of eyes that are going to be going to say ‘okay, even though there are some potential restrictions, this, this is so totally different we want to go out there and exploit this.' How are you – and, and, frankly, in the past you guys have been also unique in terms of your willingness to collaborate – what are you planning on doing and what kind of a model are you going to use?
DR. OKARMA: Well, I'm not quite sure I understand your question. If you're referring to the other elements of the program, namely, our activities with clinical trial sites and protocol generation, I can summarize that really quickly. We have now had initial and followup and qualification visits to over 20 neurotrauma centers in North America, every one of whom wants desperately to be part of this protocol. Their reasons are we have shared with them what we've demonstrated, what is being generated in the IND enabling studies, they are highly confident that this is a cell type that they want to put into their patients. The clinical protocol is nearly completely done and has taken into account the variety of different mechanical approaches that are taken in the neurosurgical repair of the contusion injury – remember we're starting with complete thoracic lesion patients who have a chest lesion and have complete loss of bowel, bladder and lower extremity function, and that's for safety, so the protocol will be dose ascending, starting with a low dose moving up to the therapeutic dose, just as in our 163L trial. So, we are, we formed an escrow committee, we are beginning now to write the IND in December, we have chosen our CRO, we have on staff people for the clinical protocol development – physicians and CRO type people – and we are beginning the process of IRB contacts because it is true that there'll be lots of people who will have their toe in the water here, not just the FDA and the investigators, but the IRBs, and we will have those addressed in parallel with filing of the, of the IND.
Q So you oper–you know, obviously everyone's hoping for good news which you guys are monitoring very carefully, but the idea is that this, this will be something that will be seminal and that a lot of people will be looking to participate with you in – that's, that's as simply as you can put it.
DR. OKARMA: Yeah. And, you know, the opportunity to fund some of this with Prop. 71 is obviously not lost upon us. They have published their, their tome of philosophic tenets which does include the reservation of considerable amounts of money for translational research – read: clinical trials. I, I am not sure whether money will be available in the ‘07 timeframe because of these lawsuits and their possible appeal, but, you know, it's a, it's a pretty good bet that if money becomes available, this would be I think a, a program that would receive high attention from the Prop. 71 people, given its uniqueness and it's first, you know, in line. And I, what I would also say that, you know, this is not a do or die exercise here, the, the success of the platform clearly would be aided and abetted by a successful, early, spinal cord injury trial. But we are marching forward with cardiomyocytes and islets, and we will take those into the clinic irrespective of how we do with the OPC1 product. Again, because the data in animals strongly reinforces the same principle – that cardiomyocytes and islets are going to do the same thing with respect to permanent restoration of tissue function that we've now elegantly documented with OPC1 in the spinal cord injury.
Q Great. All right. Look forward to hearing about it. Thank you.
COORDINATOR: Our next question comes from the line of Mark Gross of California State University. Please proceed.
Q Thank you for taking my question. To date have you seen any drug related adverse events in the 163L trial.
DR. OKARMA: No.
Q Okay. Excellent. I wonder if you could clarify the settlement between stART and ACT; did ACT pay stART's legal expenses and what is the $750,000 in mile–milestone payments all about.
MR. GREENWOOD: You're correct. There's a, there's a settlement in place to conclude the litigation if you will of the, at the patent office which is not uncommon. ACT lost the initial decisions but filed appeals and the appeals can be lengthy and expensive. The settlement to ACT and – which is shared with the University of Massachusetts – is a small fraction of what we estimate our appeal costs, legal expenses related to the appeals, would be. The milestone payments reflect commercial events and are modest in size against the, the significance of the events. So if we achieve those events, we will be delighted to pay those small milestones.
Q And did ACT pay stART's legal expenses or just their own?
MR. GREENWOOD: Just their own.
Q Okay. Well, the last question. As I understand –
MR. GREENWOOD: I, I'll, I'll, I'll, I'll be more explicit. ACT paid a portion of stART legal expenses. So from the point of handshake to the point of signing the final agreements, ACT paid stART's legal expenses–
Q –oh, okay–
MR. GREENWOOD: --and that amounted to, you know, some, something just over $100,000.
Q Okay. Last question. As I understand the tentative protocol for the spinal cord injury trial, it's going to be randomized but not blinded, and I'm just wondering about that. It seems like all the patients are going to be operated on anyway, that it wouldn't be that much harder to blind it and avoid any, any possible placebo effect.
DR. OKARMA: Well, you, you can't really do that in a Phase I/II trial, that's sort of a standard no-no.
Q Okay.
DR. OKARMA: The randomization is simply to try and increase the precision of our being able to say, attribute, positive outcomes to cells. These subjects, you know, come in right after the accident and then there are several days of intensive evaluation and as you could well imagine, an extraordinary amount of information flow to these patients basically in terms of their outcome and, you know, it's a pretty heavy message to receive that, you know, the MRI shows a complete thoracic lesion and based on, you know, analysis of hundreds and thousands of patients like you, the odds of any recovery are zero. I mean that's a big thing to swallow and it's in that wait that we need to achieve informed consent to enter these subjects into our trial. And based on the feedback we've gotten from the neurosurgeons, they think some subjects will simply be afraid to add that cell burden to their recovery, and they will decline. And we would ask those subjects to be in the control group which simply receive standard neurosurgical reconstruction. Now, you know, that whole design will evaporate if even early on we see inklings of responses in the subjects who receive cells. I mean, obviously the patient care environment here – the patient advocacy groups – are all over this possibility, because there's no alternative, you know, as they should be. So everyone's going to have their eye on this trial. And another thing to point out is because these are complete lesion subjects, even minor responses of improved bowel or bladder control or physical mobility or even skin sensation is probably approvable because any of those improvements have a huge impact on the cost and quality of life. So, for example, Christopher Reeve died because of an infected decubitus ulcer that he could not feel, and because of the loss of neurotrophic activity at the skin, these ulcers can literally form within an hour and break down and get infected, which is why these patients have to be rolled on an egg crate every hour. Well, if you recon--if you have even 20 percent return of sensation, you will feel the breakdown of the skin and possibly even have more resistance against that occurring. That's a huge functional improvement and would be the basis of, of an, of an approval. So in some senses, you know, the, the spinal cord injury program seems spectacular, you know, and that in an intervention that if works would be a miracle and in some ways that's perhaps true, but in a more objective way, you know, embedded in the, the, the neurosurgical medicine of treating spinal cord injuries and the science of rehabilitation, small improvements in these complete lesion patients have dramatic impact, so that in some ways the bar for approval in spinal cord injury is lower than you might think.
Q Okay. Very exciting. Thanks very much.
COORDINATOR: Our final question will come from the line of Dennis Williams of []. Please proceed.
Q What would be the worst case scenario for the company if the patent office rejected the WARF patents.
DR. OKARMA: I don't think there would be a worst case scenario. I think clearly we have protection for all of the programs and all of the base technology we use on our program. I think it might make it somewhat easier for competitors to enter the field perhaps if there was, if there were no requirements to achieve a commercial license from Wisconsin, but, you know, we're so far ahead of the game, we've staked out our territory on the cell types that we're committed to and they are protected. So, again, I, I, I certainly don't predict or hope that the WARF patents become invalid for both specific and general purposes about, you know, patent prosecution rules in this country, but if the worst case were to occur, there would be virtually no impact on us.
Q Thank you.
COORDINATOR: Ladies and gentlemen, that concludes the question and answer portion of today's conference. I will turn the call back to Tom for any closing remarks.
DR. OKARMA: So, I just appreciate the folks that tuned in and I appreciate your questions. They were all good, and it also enabled me to clarify some points that I may not have made quite as clear in my prepared remarks. So thank you very much and we look forward to chatting with you in the next quarter.
COORDINATOR: Thank you for your participation ladies and gentlemen. Have a great day.
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