August Confernece Call Transceipt including Q&A
Benitec Biopharma's (BNIKF) CEO Greg West on Q4 2017 Results - Earnings Call Transcript
Aug. 30, 2017 12:22 AM•BNIKF
Benitec Biopharma Ltd. (OTCPK:BNIKF) Q4 2017 Earnings Conference Call August 29, 2017 6:00 PM ET
Executives
Greg West - Chief Executive Officer
David Suhy - Chief Scientific Officer
Georgina Kilfoil - Chief Clinical and Development Operations Officer
Cliff Holloway - Chief Business and Operations Officer
Analysts
Jason McCarthy - Maxim Group
David Blake - Bioshares
Marc Sinatra - Lodge Partners
Operator
Thank you for standing by, and welcome to the Benitec Biopharma Quarterly Corporate Update Conference Call.
If we make any forward-looking statements, we note that such statements involve risks and uncertainties relating to the difficulties in our plans to develop and commercialize our product candidates, the timing of the initiation and completion of preclinical and clinical trials, the timing of patient enrollments and dosing in clinical trials, the timing of expected regulatory filings, the clinical utility and potential attributes and benefits of the ddRNAi and our product candidates; potential future out-licenses and collaborations, our intellectual property position and the ability to procure additional sources of financing.
All participants are in a listen-only mode. There will be a presentation followed by a question-and-answer session. [Operator Instructions].
I would now like to hand the conference over to your first speaker today, Mr. Greg West, CEO. Please go ahead.
Greg West
Thank you, and good morning, everyone, and welcome. We have on this call our executive team; Bryan Dulhunty, Cliff Holloway, David Suhy and Georgina Kilfoil. And David Suhy and I will give the briefing, which will take about 15 minutes and then we’ll take questions. As a reminder, these calls are in line with our commitment to provide quarterly reporting following our U.S. listing on the NASDAQ in 2015.
Today I will talk about our clinical progress and our orphan and oncology programs being in the clinic next year, as well as a brief overview of the financial results for the fiscal year 2017. David Suhy will brief you on our manufacturing capabilities.
We are now at an inflection point as we transition to becoming a clinical stage company once again. We are translating our science into measurable clinical outcomes, which we are hopeful will result in significant patient benefit and commercial value for Benitec.
Over the past two years, we have used this forum to describe the building of a broad scientific pipeline by harnessing the power of DNA-directed RNA Interference or ddRNAi, of which Benitec is the primary stakeholder of this proprietary platform and has the potential to apply a unique approach to treating human diseases, including the opportunity to silence disease causing genes for extended times with a single treatment.
For example, in hepatitis B, we have shown a sustained and significant reduction in viral load, greater than a 4 log reduction, and a further 2 log reduction in s antigen, when a single treatment of our ddRNAi therapeutic, BB-103, was combined with the standard of care therapy in a preclinical chimeric mouse model. Viral load and s antigen levels are two important biomarkers in determining clinical efficacy.
We are also working with collaborators to identify novel adeno-associated virus capsids that may have the potential to transduce tissues like the retina in a way that is both acceptable for patients and commercially valuable.
In relation to transitioning to the clinic, we are focused on two programs. The first of these is BB-401, our oncology program. BB-401 is an antisense EGFR asset for the treatment of head and neck squamous cell carcinoma and is scheduled to enter the clinic in a Phase 2 human study in quarter one 2018. EGFR is overexpressed in up to 90% of these types of lesions. This compound has performed well in previous early-stage clinical studies in patients with refractory forms of the disease to existing therapies.
Manufacturing of the clinical supplies to support the Phase 2 trial is well underway. From the clinical perspective, we have assembled a team of oncology key opinion leaders from the U.S., UK and Australia to review the prior clinical and trial data and assist in designing a robust Phase 2 clinical study to determine the clinical efficacy of BB-401 as a monotherapy.
When the final protocol design is in hand - with the final protocol design in hand, we are now turning our attention to the clinical site and vendor selection. It should be noted that the epidermal growth factor target for BB-401 and follow-on program, BB-501, is a key factor in many epithelial malignancies and its activity enhances tumor growth, invasion and metastasis. Hence, we intend to explore other potential indications, including rare cancers in future EGFR development programs.
OPMD is the second program that I’d like to focus on, given that entry into the clinic is planned for the second-half of 2018. Oculopharyngeal muscular dystrophy is a rare progressive, muscle-wasting disease caused by mutation in the poly(NYSE:A) binding protein nuclear 1 PABPN1 gene. This is characterized by eyelid drooping, swallowing difficulties and proximal limb weakness.
There are currently no approved drugs for OPMD. The only treatments offered are palliative in nature designed to help alleviate the symptoms of the disease. These are a surgical - there’s a surgical procedure called a myotomy, in which the throat muscles are physically cut to relieve the tension or by injection of botox into the muscles.
We know the sole genetic basis for this autosomal dominant disease is the expression of a mutant protein. Several months ago, Benitec and its collaborators published preclinical data in the journal Nature Communications, which demonstrated the utility of the silence and replace-based approach, and clearly demonstrating that the treatment was able to correct several phenotypes of the disease including significantly reducing the levels of fibrosis and intranuclear inclusions, the latter of which is the hallmark of the disease, as well as restoring muscle strength back to normal levels in an animal model of the disease.
In recent weeks, we have released news of a significantly improved construct for OPMD, through the development of our innovative single vector system to both silence and replace the OPMD disease-causing gene. We have demonstrated that this single silence and replace vector system can restore muscular function in the preclinical mouse model.
OPMD is a rare orphan indication. This classification provides us with the opportunity to take advantage of regulatory strategies, which could accelerate the commercialization pathway. OPMD is an attractive commercial target for Benitec. Not only are we able to service a high unmet medical need, we are also able to show the benefits of our technology in this type of orphan disease.
Earlier this year, BB-301 was granted orphan designation in the EMA and we anticipate applying for orphan designation in the U.S. at the appropriate time. Orphan designation, both in the U.S. and Europe confers several significant benefits, such as market exclusivity, protocol assistance, scientific advice and waivers or reductions in registration and other fees.
We anticipate meeting later this year with the regulatory agencies in Canada, the U.S., as well as Europe to discuss the planned IND-enabling studies and the clinical development plan. To inform our clinical plan, we have engaged some of the world’s foremost clinicians and specialists is dysphagia to help develop the clinical platform. In addition, we are actively working with patient advocacy groups, so that patients that do have the disease know that they may have the opportunity to participate in the Benitec study.
To summarize, our key message for today’s call is that, we have two programs which are running to plan and will be in the clinic next year; our Phase 2 oncology program in quarter one 2018 and our OPMD orphan program in the second-half of the year.
I will now pass over to David Suhy to give you some background on our manufacturing strategy. David?
David Suhy
Thanks, Greg. As you’ve all just heard, Greg has provided an update on the advancement of our pipeline into human clinical studies. Furthermore, we’ve continuously emphasized the importance of being able to meet the developmental timelines that we have communicated to the market.
As a gene therapy-based company, the ddRNAi-based medicines that our scientific team have created are enormously complex drugs. And thus, the design and development of advanced manufacturing solutions early in the product development cycle are crucial to derisking the future development and being able to maintain those communicated timelines.
So within that context, I wanted to just spend a brief few moments to provide some color on our internal efforts to build in-house manufacturing capabilities and how we are using that exact same team to solve many of the challenges associated with scalable manufacturing of these complex medicinal products.
Approximately over two years, recognizing the importance of manufacturing to our long-term success, we strategically invested into in-house capabilities to be able to produce research grade materials, as well as optimize process development. The initial focus included both the acquisition of capital equipment to physically generate the materials, as well as hiring highly trained scientists to produce those materials.
The results have been immediately beneficial, allowing us to produce high-quality data in a timely manner to support much of the preclinical data that has been presented across our pipeline programs in the last 18 months. And I think you all agree that that some of the data has been quite impressive.
Now, as our attention has been turning to expanding the entry of several programs into the clinic, the focus of the group has likewise expanded into the enhancement of existing methodology, as well as the development of new scalable manufacturing processes for cost-efficient production of large quantities of our drugs. As we know, even the products with a strongest clinical data have failed to make it to market simply because they can’t be manufactured in adequate quantities and at a reasonable cost.
One specific example of how our thinking has influenced the development, our programs is the use of baculovirus-based manufacturing schemes to produce the clinical materials for the OPMD program that Greg just talked about. Production of similar products in baculovirus-based systems showed that the process can easily be scaled from one liter up to several 100 liters, or even 1,000 liters in a cost-efficient manner.
Ultimately, scalable manufacturing and that control over the long-term product supply are inherently linked to product costs, and these are really critical factors to determining the commercial viability of our products in the long-term. To be clear, Benitec will still require the transfer of these processes to third-party manufacturers to produce the rigorously qualified materials at its acceptable for use in human clinical studies.
Yet as we transfer our knowledge base to our preferred manufacturing vendors for the production in these clinical materials, we believe that this is a key element to ensure our future success as we engage with commercial partners on the journey to bring our products to patients worldwide.
So that’s just a brief overview of the story that’s not often told within these teleconferences. Back to you, Greg.
Greg West
Thanks, David. So turning to our fiscal fourth quarter earnings, our full - Benitec’s full-year loss for the 2017 financial year was A$5.7 million, as compared to A$24.8 million in the prior financial year. The A$19.1 million reduction in the loss was primarily the result of an increase in R&D grant income of A$6.92 million, a reduction in R&D development cost of A$6.4 million and a reduction in employee and share-based expenses of A$2.6 million.
Also in the 2017 financial year results for prior period items, which included the IPO costs of A$1.2 million and write-off of A$1.8 million clinical trial prepayment. We wrapped up the fiscal year 2017 with cash on hand of A$17.4 million. This was a decrease of A$0.9 million from June 30, 2016 and was represented by A$8 million in two placements during the year and operate - and operating cash outflow of A$8.3 million comprising expenditure of A$15.9 million, offset by the government R&D grant received of A$6.2 million and other cash receipts of A$1.4 million.
We had significant advancements in the last quarter across multiple programs, including, the OPMD orphan disease program; efficacy with a single vector system; and the Ocular program with initiated of in vivo proof-of-concept studies in a non-human primate model. In relation to infectious disease, we had a pre-IND submission with U.S. FDA administration for BB-103.
Looking forward, the upcoming financial year promises to be a pivotal year for Benitec with BB-401, our EGFR antisense therapeutic for the treatment of head and neck cancer, moving back into the clinic. Additionally, BB-301, our silence and replace ddRNAi therapeutic for the treatment of OPMD, will be progressing towards the clinic in later 2018. These milestones further our goal of becoming a multi-product, clinical-stage company by the end of calendar year 2018.
So at this time, I’ll ask the operator for questions.
Question-and-Answer Session
Operator
Thank you. [Operator Instructions] Your first question comes from Jason McCarthy with Maxim Group. Please go ahead.
Jason McCarthy
Hi, guys, thanks for taking the questions, a couple of questions. For the 401 study you talk about going into clinical trials early in 2018, is that going to be a Phase 2 trial in head and neck? And if so, how many patients do you think you need to enroll for a study like that? And what would the endpoints of the study be?
Greg West
Georgina, would you answer that?
Georgina Kilfoil
Yes. Hi, Jason, it is a Phase 2 study to gather more data about the activity of BB-401 as a single agent. We’re looking at an adaptive study design, it’s likely up to 50 patients as the maximum. And with this trial, we’ll be looking at objective response rate as the final endpoint.
Jason McCarthy
Okay. And if we could jump over Greg to BB-103, can you discuss what the plan is and have you been having partnering discussions and really what is the clinical path forward there?
Greg West
Well, I’d like just to get Georgina to talk about the clinical setting for that drug, and then I’ll come back to some of the other measures you just referred to.
Georgina Kilfoil
Yes. Hi, Jason, again. So from a clinical perspective, we have worked with hepatitis KOLs and have designed a clinical study, which is a study we discussed with the FDA, which is looking at BB-103 in combination with nucleoside analogue.
Greg West
So just on the other matter of the - what I essentially announced to the commercialization of this program, we’ve had discussions as you would expect with the leading Hepatitis B pharmas. And the important point here is that, of course, a large number of the pharmas are curious and interested in the type of technology that we have, because our results in these animal models have been quite extraordinary, 4 log drop in virus and a 2 log drop in S antigen is extremely impressive.
However, not all big pharma are interested in gene therapy and gene silencing activity. So the market is in - that context is relatively narrow.
Our attitude that we have commented on in our annual report and other earnings announcements over the last 24 hours is that, we are really looking for a partner. In order to advance this program, we will continue to do so. We’ve engaged some external specialists to help us do this in addition to our internal capabilities.
Jason McCarthy
Okay great. Thank you for taking the questions, Greg.
Greg West
Thank you. Thanks, Jason.
Operator
Your next question comes from David Blake with Bioshares.
Greg West
Hi, David.
David Blake
Good morning, everybody. I’ve got several questions. The first is, what are the clinical programs do you have - have you been able to develop budget for? And if you have, can you give us an indication of what you would be spending for those programs?
And secondly, with the OPMD program, can you just give us a more detailed description of the construct and explain what the point is of the second-half of the construct, which restores the wild-type PABPN1 [Indiscernible] body? And the other question with that is, what’s the patent situation with the OPMD program? Is that something that Royal Holloway has filed the patent on in Europe co-inventor on, or what’s the situation with that? Thanks.
Greg West
That’s good. David, I’d like to just pass over to you to talk about the OPMD construct and respond to David’s question there? And then I’ll deal with budgets and the patent situation, Georgina, you can do it. So over to you, David.
David Suhy
Sure. Thanks David for the question. So with the OPMD program the gene that we need to disrupt is not - is a gene that causes the disease through an autosomal dominant [like manner] [ph], which means that overexpression of this mutant protein is really what causes this disease pathology. I mean, it’s like a lot of genetic-based disease, a muscular dystrophy, so there’s an expansion disease that it means that protein essentiallyjust crashed out inside the cell [and form] [ph] back again this leads to fibrosis and fibrosis leads to tissue degradation.
The really key feature of the silence and replace based technology is the fact that it’s very difficult if not impossible to design shRNA or silencing [indiscernible] that simply only target the disease causing gene. So what we need to is, since we not only need to knockout the disease causing gene but also knock out a little bit of the wild-type type of protein. And in response, because there is additional vector capacity left in the ddRNAi construct, this allows us to co-express a healthy copy or wild-type copy of that same protein to restore functions.
Now we’ve made several modifications in that second-half that you’re asking about, such that the shRNA that we’re producing doesn’t itself attack that second disease or that second Codon optimized protein. So really in the basic sense, our construct is able to knockout disease causing genes and because in certain cases there’s enough vector packaging capacity left over we can re-express a healthy copy of that [Indiscernible]. So we like to call this silence and replace based technology.
In terms of traditional gene therapy, we don’t believe that there’s other technologies out there capable of doing this. Traditional gene therapy is either expressing proteins restore autosomal receptor diseases or if you think things like CRISPR-Cas9 or make a nucleotides to knockout protein, the problem with the lag areas effect, you often time have to knock in a huge protein complexes will be able to perform those genome editing techniques.
And because the Benitec technology is so compact and it fits within the vector so well it allows us to use a single vector system, which means that the manufacturing process is straight easier regulatory path and we believe it’s one of the few technologies that has the ability to knockout and silence within the single construct. So the application [Indiscernible] disease as well as [Indiscernible] diseases that have somewhat [Indiscernible].
Greg West
Thanks, David. So, David, just in relation to the patent situation, when we established our engagement with the Royal Holloway part of that was us securing the patents and ownership of the OPMD programs. So that’s part of the engagement that we have with them. And rather I’ll pass them over to Georgina, a fairly simple and direct answer.
In response to the budget position on this and all of the programs to that matter we did budgets for - extend for a couple of years. They’re upgraded quarterly just for your information and they are detailed. So we have a fairly good and clear picture of cash needs for each of our programs. And be aware that our existing burn as we described it in my earlier comments is about A$16 million before R&D grant.
So it’s probably down to about 10 or approaching that. So we’re saying that we’ve got sufficient cash to carry us for awhile. But of course, we - it goeswithout saying that in the absence of a deal, or in the absence of other fundraisings, we would have to access the market at sometime in the future. And when it comes to Capital Markets, the issue is to be ready to access when it suits us best rather than when we need to so.
In that context, [Indiscernible] have a performing share price be connected with the buy-side investors, notably in the U.S. and connected with the Australian investment banks and international investment banks, and we maintain relationships with all of those for that purpose so that when we choose to access capital markets, we will be positioned to do so. David, I think that probably covers where you’re heading with that question and hopefully that’s fairly full response.
David Blake
Yes. Look, I just wanted to maybe just extend that a little further just to find a bit more about BB-301. Another way to ask questions, what would it cost to take BB-301 to proof-of-concept in humans?
Greg West
Yes, we haven’t disclosed that to the market, so and we don’t disclose typically that information to the market. But this is, you can set it in a - position that in a normal setting for this type of therapeutic, it’s not a systemic application as it was in hepatitis C and you’re seeing the costs for that, it’s more a targeted treatment, so the costs are certainly less than what you shouldn’t experience to Benitec for the systemic application of that - about our therapeutics.
David Blake
Thanks for that.
Greg West
Thank you.
Operator
Your next question comes from Marc Sinatra with Lodge Partners.
Marc Sinatra
Hi, guys, good morning. Listen, just a couple from me. Probably the first one for David Listen, just going a little bit deeper into the OPMD vectors that you’ve been using, what sort of differences have you seen between the dual vector system and the single vector system? And are there any significant - significant performance and advantages with the single vector system?
Cliff Holloway
Yes, it’s great question, Marc. I would tell you from a performance perspective that in terms of how it impact the efficacy readout in that preclinical animal model there can be a 17 mice. If we see essentially no difference on the key parameters such as, restoration and muscle strength, reduction of intra-nuclear inclusions, reduction of fibrosis, all those parameters remain exactly the same.
I will tell you that one of the parameters that has changed from the dual vector system is that, we’ve been able to also now restore muscle weight back into those muscles of those diseased animal. So that’s a little bit of difference that we did not seen the dual vector system that the muscle still remain somewhat atrophy. But now with a single vector system, muscle weights have been essentially restored back to wild-type levels.
What I will tell you is that, as we mentioned in the press release we’re having significant knockdown of the disease causing gene almost 90% of that getting knockout. And we’re re-expressing upwards of 77% maybe, I can’t remember the exact number, but close to four activity in terms of the codon-optimized protein.
So it’s really a case where our genetic construct goes in and it wipes out the disease causing protein by and large and replace this with a healthy copy of the gene. So this is really novel in terms of gene therapy. In terms of how this benefits the program overall? I mentioned a little bit during my manufacturing piece. I talked about in the prepared comments.
We’re talking about that simply now the manufacturing of one clinical product. There have been gene therapy companies out there that are dealing with multiple AAV vectors going in at one. And I think enormously increases the complexity of those clinical trials that enormously doubles or triples depending upon how many vectors you use, your manufacturing cost, your inherent risk with one of those programs or one of those vectors not manufacturing. So that by the very nature of that, we’re essentially able to condense everything down through a very innovative design that our scientists have come up with really simplifies that process and makes this very efficient system moving forward not only for this program, but potentially for other rare monogenic diseases as well.
Marc Sinatra
What sort of penetration do you think its transduction in cells. You’re going to need to see a significant improvement in a human?
Cliff Holloway
It’s a great question and it’s one of the things as we move into our toxicology models to support design de-enabling study that we intend to work with. We’ve made no secret. We’re going to move into a larger animal model more specifically a sheep again depending upon regulatory review could be able to look to see how well the injections are tolerated in those animals, as well as the distribution.
I will tell you that the injections that we have locally, it is a local administered compound through direct intramuscular injection. And the injections that we’ve already had in the mouse model into the leg muscle, which is the largest muscle in that animal have produced the nominal result. So, we are working as we mentioned or Greg mentioned in his comments, we’re working with some of the world’s foremost experts not only on both AMD, but dysphasia in general and dysphasia to define a very complex word, this is the inability to follow.
So these are experts who are normally adjust at injecting compounds like both parts locally and to those quicker apparent to muscles. So that’s a type of expertise, that’s a type of clinical planning that we’re developing to ensure that we’re giving ourselves really the best chance of transduction and hoping, that that is sufficient in terms of the delivery to have a positive clinical outcome.
Marc Sinatra
Okay. What - I’m just going to switch just which is one question, quick question. With the vector - with the ocular vector program, is the first indication you’re going to go after going to be AMD, or is that not been settled yet, I was - I thought it had been 100% settled. And I was just wondering, if that - if the AMD have been chosen?
Greg West
On the preclinical animal model that we’re in right now, it’s a non-human primates. This is a dainty word for saying large monkeys. That is laser-induced model of choroidal neovascularization. So, again, that is probably the best animal model to be able to support the efficacy readout from those types of experiment.
So, that is the plan for the moment. We believe that the model we’re using, in fact, we know the model we’re using is the gold standard within the field. This is the same model used by companies like Regeneron and Genentech who basically get things like Eylea, Avastin and Lucentis on to the market.
So we believe that that is the most positive way to get a readout on the efficacy of these factors, as well as the efficacy of our clinical constructs. Once that data settles in and once we have a sneak peek at how the data rolls in and then if it meets those efficacy models, at that point, we’ll make that as appropriate determination of where we go from there.
Marc Sinatra
Okay, beautiful. Thanks. That’s it from me, guys.
Greg West
Thank you.
Georgina Kilfoil
We’ll now turn to webcast questions. The first question is, what are the implications of the CSL purchase of Calimmune?
Cliff Holloway
Yes. So just a little background. This is a transaction that occurred just a couple of days ago, where CSL acquired U.S. company, it’s a private company, Calimmune, for a little over US$400 million, at about US$19 million of that upfront. And our interaction with Calimmune has been that they have license ddRNAi for a HIV product, which they were developing that’s currently in the clinic.
Having said that the and the public domain and what we understand given CSL’s interest in hematology that their primary interest in this acquisition has been for the preclinical stem cell assets that Calimmune is developing for both Sickle cell anemia and beta-thalassaemia.
So I can’t really comment, given the fact that this transaction is very recent other than beyond what we understand from comments that we made in the public domain. There was an article in endpoints by John Carroll that refers to a CSL’s spokesperson who says that that they intend to look at their options around the clinical program in HIV as soon as possible, and that that may include looking for a licensing or partner to take that forward.
So beyond that, it’s difficult for us to comment on. Obviously, we’ll be maintaining an interaction with Calimmune and through them with the CSL folks to understand what will be the future trajectory of that program going forward.
Greg West
Thank you.
Georgina Kilfoil
The next question, what program is getting the most interest from potential partners, Greg?
Greg West
Well, the way programs get interest could probably be categorized into two ways; the financial sector that is the buy-side that is the major fund managers, and the sell-side which is the major investment banks have a strong interest really in notably our orphan program, OPMD and oncology, because they’re moving into the clinic. The novel nature of the IND program, which is the ocular program also creates a great deal of attention.
So I don’t know that there’s a distinct ranking, but the - just in the margin, the orphan disease would be most appealing to that group. I think, they can see that we can accelerate that to the market, get a financial benefit out of it in the immediate term and also prove about technology, some of what Mike was referring to about AMD and technology opportunities is that, when we prove our technology safe for the eye, it does invite us to have a look at other applications and maybe around orphan diseases.
Similarly, with the gene therapy that we use when we get results does invite us to have a look at other ways to expedite the commercial value of using our technology in the market. So but the point being then probably the areas of key interest. From a pharma perspective, I’ll just pass over to Cliff.
Cliff Holloway
Yes. So just as Greg said, obviously, pharma interest tends to obviously increase when programs get further towards the clinic or in the back of pivotal preclinical data. And we’ve had some pretty good announcements recently around obviously hepatitis B. You’re all familiar with the data around that and OPMD recently. And so, therefore, obviously, the interest level tends to increase on the back of those announcement and obviously, we intend to leverage that going forward.
So, we keep a pipeline of potential partner interest around each of our programs, quite a lot of these interactions now takes some time. It’s about timing relative to the partner of interest and our ability to know to get the right dataset in place. So that that obviously it leads to more meaningful interactions. So we continue to have a very built healthy pipeline of interactions, I would say, around most programs. On the AMD side, I think, now things are going to a little quiet and are waiting really for the outcome of the study that David referred to earlier. And should that come up positive, then I expect interest to substantially increase around that program, too.
Greg West
Thank you.
Georgina Kilfoil
Thanks. The last webcast question, what is happening with the work the company has done with CAR-T?
Greg West
David?
David Suhy
Yes, thanks, Greg, and thanks for the question. The CAR-T program, as many of you know, doesn’t necessarily show up on our “official pipelines” slide CAR-T. The work we’ve been doing has been around applying ddRNAi technology to be able to silence specific gene targets within T-cells for the ability to enhance the properties of those T-cells.
As many of you know, CAR-Ts and all the grades in terms of the clinical data and from the approvals that have come out recently with the Novartis drug And more recently, the Kite deal with Gilead, I guess, with Gilead snapping up Kite Pharmaceuticals.
Specifically, what we’ve been doing in a demonstration type of project has been working in selling that ddRNAi can be acquired thalassaemia-alpha T-cell receptor. On the surface of those T-cells, thereby creating what’s known as our allogeneic cell population, meaning that typically, there is an immune response or a series of proteins present within specific cells, which your immune system recognizes. The T-cell receptor is one of those proteins.
And what has been shown very nicely in a number of preclinical as well as now clinical studies is that by modifying our limiting expression of the T-cell receptor on those cells has the ability to produce a cell type that can be essentially used off-the-shelf. Meaning that, you don’t have to worry about an immune response to the source of their T-cells. So we’ve done something similar with ddRNAi technology. We continue to show and put out data supporting that this works with a T-cell receptor.
Now on the last quarterly call, we’ve mentioned establishing a number of collaborations and I will, again, I can’t develop specific at this point, but we’re still in the process of initiating a couple of those collaborations. What I can’t tell you is that the technology itself is not simply limited to reduction of T-cell receptor on the cell surface. And B, there’s a lot of problems, there are a lot of technology challenges that CAR-T methodologies in general need to overcome to be applied as some effect of we’re looking it as a cost-effective therapeutics.
And there are things like, for instance, the ability to expand T-cells once you transit some of the costs, how you’re going to enhance the activity can we now go after solid tumors as opposed to this simply single cell blood cancers, we’ve got all of that could be mediated through a series of genes or all those activities are mediated through a series of genes by modifying the activity of those genes, you can potentially enhance some of those properties of the CAR-T.
So, again, I won’t develop specific names and specific targets, but that’s where some of the interest around the CAR_T program growth-wise, and that’s where we’re finding a of traction in finding collaborators who want to buy their technology as sort of a bolt-on technology to enhance the activity of their CAR-T program.
Greg West
Thank you.
Georgina Kilfoil
That’s it for webcast questions, Greg.
Greg West
Thank you. Back to the operator?
Georgina Kilfoil
No, back to you for closing remarks.
Greg West
Okay. So in closing, I’d just like to say that the efforts and strategies of recent is now delivering with our orphan and ocular programs better into the clinic. With funding our other programs could be clinic ready around the end of 2019. We are transitioning to be - transitioning to become a clinical stage company once again, and we’re hopeful this will result in significant patient benefit and commercial value for Benitec. And thank you to all of our participants today, especially those shareholders and analysts who provided questions. I’d like to thank our investors for their continued support. Over to you, operator?
Operator
Thank you. That does conclude our conference for today. Thank you for participating. You may now disconnect.
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