Thank you and welcome to everyone joining us on the call to discuss our financial results for the second quarter and six months ended July 31, 2016. Earlier today, we issued a press release summarizing these results. If you have not had a chance to review, it is available on our website at www.summitplc.com. Joining me on the call today are our Chief Executive Officer, Glyn Edwards; our Chief Medical Officer, Dr. Ralf Rosskamp; and our Chief Financial Officer, Erik Ostrowski. Before we begin our discussion, I would like to remind listeners that we will be making forward-looking statements during this call. I refer you to our filings with the Securities and Exchange Commission for description of the risks and uncertainties associated with an investment in Summit Therapeutics. I would now like to turn the call over to Glyn for an overview of our co-production advantage.

Thanks, Richard and I thought you did very well considering you have got a bad cold. Thank you all for joining us on the call today and at Summit, we are perusing two key areas of focus with a goal significantly improving the current standard-of-care. One of these is Duchenne muscular dystrophy or DMD, a progressive muscle wasting disease that’s universally fatal. Our approach to utrophin modulation has the potential to slow or stop disease progression by substituting the missing dystrophin protein in these patients through the modulation of the expression of a related protein called utrophin. In contrast, other disease modifying treatments in DMD, utrophin modulation is potentially applicable to all the patients regardless of their underlying dystrophin gene mutation. A lead utrophin modulator is Ezutromid formally SMT C1100 and its currently in a Phase II proof-of-concept trials called the PhaseOut DMD study. We initiated this trial in June and are enrolling in dosing patients in the UK right now, with the US expected to begin enrollments shortly. With the trial underway, we are forecasting that the data from the first group of 24-week biopsies are expected to be available in the Q2, Q3 2017 timeframe. I will let Ralf go into a lot more detail on the trial, that these biopsy will be looking for a number of markers that could signal that Ezutromid indeed modulating utrophin and that this is having on impact on muscle health. In other words, this trial could provide proof-of-concept for Ezutromid and utrophin modulation in patients, we eagerly awaiting the data obviously. While we progress Ezutromid into Phase II, we are also working in parallel on the development of a new formulation of Ezutromid, which we call F6. Bio availability has historically been a challenge for this molecule, but now we believe…

Thank you, Glyn. In August 2016, we announced positive results from the Phase I clinical trial of a new formulation of Ezutromid, which we call F6. In this trial, we have served greater than six-fold increase in maximum plasma levels in patients with DMD compared to our current clinical formulation called F3 with only two fix of the dose. The trial was conducted in two parts the first part evaluated two new formulations in 16 healthy adult male volunteers. They provide pharmacokinetic and safety profile, formulation F6 was chosen to move into patients for the second part of the trial. In this portion of the trial, eight patients with DMD age between five to nine years old were enrolled at site in the UK. The trial tested the pharmacokinetics and safety of three fixed doses of the F6 formulation of Ezutromid. These doses were 250, 500 and 1,000 milligram. At the highest dose, the five evaluable patients achieved an average maximum plasma concentration of 390 nanograms per mL on day seven, the final days of dosing. By comparison, in an earlier Phase I clinical trial with the F3 formulation we observed an average maximum plasma concentration of 63 nanograms per mL on the final day of dosing, which was day 14. This increase in plasma levels with F6 was achieved with a reduced dose of Ezutromid compared to the F3 formulation. In both trials, patients followed a modified diet to include a balance of fat, protein and carbohydrates. Formulation F6 was generally well tolerated. One patient at the lowest dose had changes in liver parameters in laboratory findings. He showed no clinical symptoms, but was withdrawn from the trial as a precaution and the event was rectified as a serious adverse end. It is unclear what caused these abnormalities and…

Thank you Ralf , I will now provide an overview of our financial results for the second quarter ended July 31, 2016. We present Summit’s results in accordance with international financial reporting standards in British pound sterling, but for convenience purposes I will give U.S. dollar equivalents for certain key numbers. As we described in our earnings release today at July 31, 2016, we had cash and cash equivalents with £7 million tenants or $9.3 million compared to £16.3 million at January 31, 2016. Loss for the second quarter ended July 31, 2016 was £6.2 million or $8.2 million compared to a loss of £4 million during the second quarter of 2015. Other operating income was £17,000 during the second quarter ended July 31, 2016 as compared to £427,000 during the second of 2015. As noted in our press release, as of the end of the second quarter of 2016 all moneys in income from the Wellcome Trust has now been received and accounted for with the completion of our Phase II CoDIFy trial of Ridinilazole. Research and development expenses increase to £5.4 million or $7.2 million for the second quarter ended July 31, 2016 from £4.2 million for the second quarter of 2015. This increase reflected our increased investment in the DMD program and an increase in research and development related staffing costs driven by an increase in R&D headcount. General and administration expenses increased to £1.9 million or $2.5 million for the second quarter ended July 31, 2016 from £1 million for the second quarter of 2015. This increase was primarily due to continuing additional corporate costs associated with being a public traded company in the United States as well as in United Kingdom and an increase in staff related costs, offset by a favorable exchange rate variance. As stated in our release, we believe our cash on hand will allow us to fund our key program initiatives through January 31, 2017. We are evaluating various options to finance our cash needs including any or combination of equity offerings, collaborations and debt financing. I will now turn the call back over to Glyn for closing remarks. Glyn.

Yes, thank you. All right before we open the call for questions, I would just like to reflect on how far the company has come in a few short years. We are now in a mid stage from the contrail of DMD and approaching late-stage C. diff. We have overcome the bioavailability issue with Ezutromid and have two promising formulations to test in our PhaseOut DMD study and most importantly with the potential for two commercial products on the horizons. With that, I’ll open the line for questions. Thank you.

Thank you, sir. [Operator Instruction] We will now take our first question from Liisa Bayko of JMP Securities. Please go ahead.

Hi there, good morning or good afternoon, I guess wherever you are. Just wanted to ask sort of the change in tone with respect to the CDI trial. I know you have talked a lot of about partnering and was curiously about this update on how those conversations are going. I know you also talked on this call a little bit more about measures we are seeing with some government funding and wanted to just understand if that’s a kind of an evolution?

Not really an evolution. Thanks to your question. Our intension is to not ask our shareholders to do the heavy lifting on the Phase III costs for the C. diff. We are in a number of partnering discussions for partners to get marketing rights in exchange to some of the developments of the program. But antibiotics are also an area of great concern for a number of not-for-profits and also a number of government agencies and very substantial funds are available to push antibiotics through and we have been pursuing those options as well. And of course the two could be related in brining substantial non-profit funding into the program also changes the economics for partners as well and we would obviously like to benefit from that. So there is no real change in tone, we are pursuing both partners that who could fund the whole thing themselves, or government funding or partners together with government funding. Now the base is very, very strong and we are confident that we are going to find a way through to get this into Phase III, but it’s actually what the shape of that will have to wait for actual deal announcement.

Do you have any comments on what the appetite is for antibiotic transactions right now from maybe pharma and what not?

Yes, so in the past the appetite from pharma on antibiotics was not that great and we have seen a number pharma companies, AstraZeneca is what immediately comes to mind divesting of antibiotic assets, but that pendulum is definitely swinging back the other way now. Partly, society has a big need for new antibiotics and governments have been talking about this for some time. New antibiotic launches have done reasonably well and so we have had some mid-stage companies doing pretty well on antibiotics and that’s called in some of the big guys to start moving back in. We saw last year Merck buying Cubist and we just had the announcement from Pfizer that they were buying a number of other assets. So, as far as on the hottest item in with immune-oncology yet that there definitely is increasing interest from pharma companies in these antibiotic assets. So, I think something that is strong nature as we have got is going to find a good home at some point.

And when do you think you might have - turning now to the utrophin program. when do you think we might have a next generation candidate coming? I know you mean to stop the other one, it seems like that’s a medical need. So what would be the need I guess from developing something new with your collaborator? And then, what might be the timing for that?

Yes, I can’t really help you with the timing, but the aim is being the same with the pipeline products and we have seen quite profound improvements in outcomes in animal models using Ezutromid, but the core technology from which Ezutromid was found is really a number of years old now. And the geneticists and the team at Oxford have really made great strides in a more detailed understanding of what controls Ezutromid production. And so what we are looking for in our - whether it's a second or third or whatever the future products to come off Ezutromid would be things that are very material improvement in performance. And what we found was that having taken this portfolio approach of medicinal chemistry to come up with second generation compounds, which has been very successful and we published quite a bit on those second generation ones. But then, we had the big step forward with the F6 formulation with the data which we have announced fairly recently and that narrowed the gap, so the second generation were no longer a big step forward from that which we could achieve with Ezutromid using the F6 formulation, and so we have put those on ice for the time being while focusing our attention on the future generations which are coming out of the new streams they are in very different chemical space. And we hope we will be much more profound modulators of utrophin which might mean they can be given in smaller doses, or less frequently or indeed produce a greater clinical benefit. Obviously, we have got to see what the clinical benefit we get from Ezutromid is, but we feel as in common with lots of other therapies go that the first to market is transformational and then we hope it'd be a great benefit to these patients. But the next generations of compounds can build on that, and we have seen that with HIV, we have seen with Hep C, we have seen it with multiple sclerosis the whole host of things. The first ones are great and they really move the needle, but we want to show that something can be done and with more detail signs on the basic biology you can see better ways of doing it and that's our objective. So I am not giving any timelines for the future generation, but you'll expect to start seeing scientific data being published over the next 12 months from those future generations of products.

Our next question comes from Arlinda Lee of Canaccord. Please go ahead. Your line is open.

Can you maybe walk us through what the gating factors might be to include the F6 10 patients for the trial and then I guess how you think about, if it could add additional patients subsequently? And how you think about the Phase II registration directed one that you are - trial that you're planning to start next year? Thanks.

Yes those are two good questions Arlinda. So we just wind the clock back a little bit, when we started on the clinical trial with the new formulations for which we chose the F6 and the technology that was producing the F6 was really just very pilot scale it was to GMP but in really small equipments. And so we didn't think it was going to be possible to include any F6 there just wouldn't be enough production capacity to put - include any of that F6 in the current study. And so we planned that it would be available to go into the next randomized study. But once we got the preliminary data which looked so promising, we went back to talk to the manufacturers and they came up with a way to give us very limited amount so that we can include 10 patients while still working off a small scale, but to be quite frank it means this small scale equipment has been working flat out or nothing else just to do this. And it's a great testament to the team that they have managed to make that available. And 10 patients is going to be enough for us to do the comparison with the F3 and so we will get all the data we need from the PhaseOut study to be able to make a decision on whether, we are seeing utrophin modulation and the effect we want, and if we are which is the best material to take forward either the F3 or the F6 which obviously based on the balance of the safety and efficacy. We already have capacity and material to put the F3 formulation into the next randomized study and by the time we get data from the PhaseOut DMD, we will…

No thank you very much. I think you covered it very well Glyn, thank you.

Thank you. We will now take our next question from Michelle Gilson of Oppenheimer. Please go ahead. Your line is open.

I will just - a follow-up to that last question. Do you have the flexibility to switch boys to the F6 formulation in the extension study, if that is the formulation you are going forward with to add to the body of the data that you have for that molecule?

Ralf would you like to answer that one?

Well we will have interim results of the F3 formulation as we said in the second and third quarter of next year. And somewhat later we will have interim results based on the F6 formulation and then once we have the data on the table, we will make a decision with which formulation to go forward with. Yes and our expectation would be, first of all, if the PhaseOut DMD study will be continued, because we see target engagement, we see some positive trends in our MR parameters that actually will extend PhaseOut DMD and then it's really a matter of ramping up production, so that we not only can support the accelerated approval study with whatever formulation we choose or the PhaseOut extension.

So Michelle the answer is yes, we can.

Okay. And then can you also talk a bit on the biopsy data, 24 weeks some of the regeneration biomarkers that you are looking at? And also can you help us set for the expectation there for utrophin and what patterns are you looking for will it be a clear signal for you on Ezutromid or F6 for mechanism and efficacy?

Yes, that’s - I am glad that you have asked that because this is a key for us for early next year is when we get these biopsy data, what is it that would constitute a successful outcome. And it's a first of all looking at Ezutromid it's a bit more complicated for us than it would be for say a Sarepta, or a PTC who are looking at dystrophin because in their cases the boys have no dystrophin, if they see some dystrophin then that’s a proof of target engagement and things working. But with utrophin the situation is more complex because utrophin is going to be produced in these boys naturally when theirs break and repair. And what we are trying to do is additionally produce utrophin all the time when there isn’t breakdown and repair, and so that will be the difference. So in the pretreatment biopsies what we would expect to see as Ralf said in his discussion is and quite like this have used spotty, so if you look at the biopsy samples you will see some areas of high intensity utrophin but many areas with low intensity and many else with no utrophin so you get this spotty appearance. And what we would aim to see with treatment is that we have got more uniform utrophin on the fibre, so there are really no areas where there is no utrophin. But ultimately there could be no areas where there is very high intensity, because that would have indicated repair and what we trying to do is get to a position where there is no repair. So the first thing we would be looking for is a more uniform distribution of utrophin. And the second thing in the biopsies that we are looking for is…

And then just one more, when we are thinking about the MR data, you guys are looking at both at fraction and information. Can you talk about how much that fraction typically changes in a 24 week period for the age group that you are looking for? And what would constitute stabilization for you guys going forward?

Yes, I am sure we can. But I’ll hand over to Ralf, because he’s got deep into the weeks on the MRI?

Yes. And we are actually working together with the imaging DMD group out of Florida which has pioneered this work. They have natural history data and they have interventional data with steroids where they were able to demonstrate that at three or six months they were able to see a reduction in inflammation. So, after discussion with them so what they will do is actually they will look at our data and match the baselines of our patients, because this might slide off we have a 5P rolled who might still have a pretty low fraction and we might have a 9.5 year old who has a higher fraction. And as we know with the disease the rate of progression is different but what we believe is that if we stay a stabilization. So no further progression all the time that this really demonstrates that something is happening with the drug because according to their natural history data they always see some kind of progression but it's different of course from the baseline and therefore they will actually help us to analyze these data in the appropriate way.

Michelle did that help?

Yes. And then also when you are looking at the changes with inflammation, can you talk a little bit about how you are controlling for day-to-day variability in inflammation if a boy - after the day before which is not [Multiple Speakers].

I couldn’t get your question, the variability, the day before?

The day-to-day variability in inflammation in terms of boy [Multiple Speakers]?

Yes, day-to-day variability there is a paper from actually the same group who look at different sites and actually the sites get qualified by - they have the certain model where they have to scan it and analyze centrally. Everybody uses the same software, the same protocol, the data get uploaded, gets analyzed by the Florida Group and they have data around the variability or also from day-to-day. And the only which we require is that the boys don't have physical activity due to three days before the MRI because we know that this could affect especially the T2 inflammation, but other than this, this is a very reproducible measurement.

Thank you. We will now take our next question from Chad Messer of Needham & Company. Please go ahead.

Given that the biomarker data that we're looking for in PhaseOut is I think you just describe it, a little bit more complicated it is not as straightforward as some of the folks going after dystrophin directly, any thoughts as to what regulators might want in terms of a surrogate endpoint or is that too difficult to contemplate until you see PhaseOut results?

It's not too difficult to contemplate like all these things, if you see big differences then actually regulators are happy with that and we will all be happy with that. So I think if we see significant changes that makes it a whole lot easier. And those significant changes could be in utrophin or they could be in the fibre size or in an ideal world if we start seeing more mature fibres with utrophin then that would definitely be a very strong positive for us for the scientific community and for regulators, because in DMD boys you don’t see that. You only see utrophin in repairing fibers which are small and immature. So it is more complicated but I think provided you have got the good signs and you have got robust techniques of measuring it then that doesn't give you a big problem with the regulators, flipping it around the other way. The guys with the easy problem if you like are just showing dystrophin have - and it concerns not just showing some there has been big arguments about just how much dystrophin you need to see. So I would say it is more complicated, but it doesn't mean to say that it is not, it's going to be something that we could use as the basis for an accelerated approval. But as you point out you to see what the data is and how strong it is, how robust it looks. And our plan just to reiterate is not to take this data for approval but to use this data as the basis of designing a well controlled appropriate study for an accelerated approval.

And then just on that study you gave a little bit of potential timeline for an approval study starting if the data merits in the second half of 2016 for a 2019, I believe that or if you said filing your approval, just wondering that seems to be a little long if you just need six months data just wondering how you came up with that projected timeline?

Yes, so just broadly, let’s say we start in the second half of 2017 for recruitment, the last boys let’s say recruited at the end of the time period and his six months is the first half of 2018 then you have got to gather all the data and get it all crunched, so it is going to be in at the end of that year, which needed your approval and on the market in 2019 that is how it gets there.

[Operator Instructions] We will now take our next question from Samir Devarni of Rx Securities. Please go ahead.

Just a couple, just wondering whether there has been any impact on your C. diff. discussions following recent events at Seres Therapeutics?

No not really, so by the recent events you mean the failure of their SER-109 in its Phase II, I think all of us in the field think that that’s an anomalous result, because the data from fecal transplants has been so strong that’s, I think it’s a setback for them, but there will be an explanation for it. And it’s not a setback for the whole idea of both microbiome restoration for patients you have had severe CDI over many biopsy. And as such it doesn’t really affect our partnering discussions or the potential for Ridinilazole because, I think we all believe that fecal transplants or some form of them, whether it’s artificial or more uniform and predictable culture of ours going to the used in CDI particularly for the patients who seek microbiome is so sharp that is a drug like Ridinilazole is not going to help them. So in the, sort of third and fourth round and the later stages so then that will become the dominant treatment. The big opportunity for drug like Ridinilazole is in, first line or first recurrence this is the majority of cases, you need an antibiotic to treat the infection and the microbiome while it is being preserved is still capable of a restoration. And this is the huge volume, so it is about 500,000 patients who gets a C. diff. in the U.S. and a similar number in Europe. So, no it hasn’t and I think it would be unsafe to write the Seres product off or that approach off I think, the weighted evidence is that restoration of the microbiome in these patients who on their third and fourth recurrences is a very effective treatment. But it doesn’t really impact the huge potential for a drug like Ridinilazole in the earlier stages or even in combination with these things because you still need to manage the actual C. diff. infection.

And then just going back to the F6 formulation, you have made a protocol amendment. I am just wondering when we are likely to hear that that amendment has been accepted?

Ralf over to you for that.

Well, we haven't announced when the amendment will be accepted, and we are right now as you know we just got the results of the study and this would result in an IND amendment. So we have to put up the data altogether and the CMC information. And then we will then actually we have the regulatory approval start enrolling 10 patients in the U.S. which we expect to be this year. But we have made no more announcement around the exact timing of it.

And now we will take our final question from Liisa Bayko of JMP Securities. Please go ahead.

Just wanted to follow-up and ask you to give us a preview of what you might be presenting at World Muscle Society? Thank you.

Yes. We will have some data with Muscle Society, but once the abstracts are out then we will make an announcement of exactly what that’s going to be. And have you managed to get a ticket there because they are like gold dust.

I am working on the black market.

All I can tell you is it is going to be well worth your while being there.

Thank you. As there are no further questions, I would like to turn the call back to Glyn Edwards for any additional or closing remarks.

Thank you very much and thank you everyone first, and really good questions. So thanks for joining us today. And we look forward to providing you with further updates on our programs in DMD and C. diff. in the future. Thank you very much.