Ladies and gentlemen, before we begin, please note that Galmed will be making certain forward-looking statements on today’s call, including those regarding financial results, statements and forecasts regarding anticipated timelines and expectations with respect to regulatory and clinical development programs as well as other statements that relate to future events. These statements are based on the beliefs and expectations of management as of today and actual results, trends, timelines and projections relating to financial position and projected development programs and pipeline to differ materially. Galmed urge all investors to read carefully the risks and uncertainties disclosed in their filings with the SEC, including without limitation the risks under the heading Risk Factors described in the Annual Report on Form 20-F filed with the SEC and the risks and uncertainties included in the Form 6-K filed with the SEC earlier today. Galmed assumes no obligation to update any forward-looking statements or information which speak as of their respective dates only. Today’s conference is being recorded. I would now like to turn it to Allen Baharaff, President and CEO of Galmed. Please go ahead.

Thank you, Hannah. Good morning and thank you all for joining us on today’s conference call. I’m pleased to be here today with our CSO, Dr. Liat Hayardeny; our CMO, Dr. Tali Gorfine; and our CFO, Yohai Stenzler to provide you with an update on our development program and to report to you on our financial results for the Fourth Quarter and Full Year of 2016. As always, we will be happy to take any questions you may have at the conclusion of our prepared remarks. We are reporting today new and exciting data from our recently completed preclinical studies demonstrating Aramchol effect on liver fibrosis. Aramchol anti-steatosis effect was previously established and translated to humans in our phase IIa study. The new data suggests Aramchol also has the potential and direct effect on liver fibrosis by targeting the liver collagen producing cells. The data was accessed for presentation in the upcoming International Liver Congress event to be held from April 19 to 23rd 2017 in Amsterdam. We previously reported on an efficacy of Aramchol with HIV NASH intra-module which show the effect of Aramchol on fibrosis to be a down regulation of the sequence of events from steatosis to fibrosis and an improvement of fatty acid oxidation with an associated reduction in the generation of oxidizing agents [ph]. We now provide additional significant data on the effect of Aramchol on liver fibrosis. Aramchol has a direct impact on collagen producing cells which result in reducing fibrosis in a TAA animal model. TAA animal model is the gold standard to demonstrate direct anti- fibrotic effect. The importance of this finding is that we now understand Aramchol is targeting fibrosis via two pathways. First, by down regulating steatosis which is the main cause of inflammation and fibrosis; and secondly, by directly…

Thank you, Allen. Good morning and thank you for joining us today. This morning, I will be providing you with our financial results for the fourth quarter and the year ended December 31, 2016. For more information, please refer to our Annual Report on Form 20-F filed earlier today with the SEC, which, among other things, provides a summary of such financial results. Starting with our income statement. For the fourth quarter 2016, our net loss totaled 4.8 million or $0.40 per share compared with a net loss of 3.2 million or $0.29 per share for the corresponding quarter in 2015. For the full year 2016, our net loss totaled 17 million or $1.49 per share compared with a net loss of 10.6 million or $0.96 per share for 2015. Our revenue for the three and 12 months ended December 31, 2016 was 0.3 million and 0.5 million, respectively, compared to no revenue during 2015. The revenue relates to the amortization of the up-front payment under our license agreement with Samil Pharm. The remaining unamortized up-front payment of 1.6 million is reflected on the balance sheet as deferred revenue and will be amortized throughout the contractual term of the agreement. Research and development remains our largest expense which for the three and 12 months ended December 31, 2016 totaled 4.2 million and 14.3 million, respectively. This compares with 2.8 million and 7.6 million for the corresponding period in 2015. These expected increases primarily relates to our progress of the ARREST Study which reached total amortization [ph]. Turning now to G&A, our general and administrative expenses for the three and 12 months ended December 31, 2016 remains steady and totaled 0.8 million and 3.1 million, respectively, versus 0.6 million and 3.2 million for the corresponding period in 2015. The three months increase primarily resulted from an increase in non-cash stock-based compensation expenses while the decrease during the 12 months is due to a decrease in Investor Relations expenses. Now finally turning now to our balance sheet. As of December 31, 2016, our financial assets which include cash, cash equivalents and marketable securities totaled 15.4 million. During the full year 2016, our financial assets decreased by a total of 7.6 million. The decrease is mainly attributed to our 12.1 million cash flow used in operating activities, partially offset by the 4.5 million raised through our ATM offering. We believe that our existing cash balance will be sufficient to maintain our current operations through the first half of 2018 and will allow the company to complete the ARREST study as scheduled. With that said, operator, please provide instructions for the Q&A portion of our call.

Thank you. [Operator Instructions]. We’ll go first to Jason Kolbert with Maxim.

Hi, guys. Thanks for the update. Can you give us a little bit more granularity on the dynamics of the ARREST Study? How many patients are enrolled? Are you going to be opening any additional centers? And when do you project enrollment will be complete in this study? Thank you.

Okay. So 248 patients have been randomized and we completed a randomization, so the study is – of course we have no new centers are open and the study is ongoing. And as we said, we believe we will have the data at the beginning of the second quarter of 2018.

That’s terrific. Thank you. What other events outside of the ARREST Study will you be focusing us on in the interim period as we wait for solid results?

We are working on a number of preclinical data to support the data that we have just alluded on the TAA in the [indiscernible] model. And I would – basically I would let – this data is going to be presented first at EASL. Then of this work which is scheduled to be presented at the ASNB [ph] in November. And we believe that the result from our investigator-initiated study, the HIV lipodystrophy study which is run by Professor Loomba should be completed by the year end. But again this is an investigator-initiated study, so this is not in our hands. But we believe that this data will be available before ARREST Study.

And Allen, can you talk a little bit about your business development efforts? Obviously there’s going to be some nice licensing and partnership opportunities in parts around the world. How active are those discussions?

I can neither deny nor confirm of any discussion we are holding. We are as you know there [indiscernible] or Galmed really is in the unique position with a design; most advanced phase IIb study and you know the competitive landscape as good as I know. But we cannot discuss any research discussion that we are or we are not holding now.

Okay. Thank you.

We’ll go next to Thomas Yip with FBR.

Hi, everyone. Thank you very much for taking my questions. This is Vernon just asking a couple of questions for Vernon. First, we look forward to your EASL presentation next month. So for the ARREST national study, should we expect additional DSMB analysis between now until the top line reeval data is expected in 2Q '18?

[Indiscernible] which are ongoing as scheduled and we do not expect any major publish effect. The only interim was as I said 128 patients completed in six months and there will be no other data available before top line data.

Okay. So I just want to clarify, so 128 patients six months of treatment, so after this the trial will remain blinded but will there be an announcement to say the outcome of the DSMB analysis regarding whether to drop a phase and the trial will continue going forward without any changes?

This is a safety data, so there’s no – study continues as scheduled and there is no other – obviously it’s a blinded study, so we do not see any data and we do not report any data.

Okay. Thanks for the clarification. So one more question regarding your other study you mentioned HIV study. Should we expect – do you see some data from the ARRIVE Study?

As I said we hope – it’s an investigator-initiated study and we plan to have the data before ARREST by the end of 2017 but Professor Loomba is managing the study and we are basically at his hands, so we have no additional data on this.

Okay, thanks. I guess a follow-up question regarding the financial. So with the ARREST Study now fully enrolled, so how should we look at the R&D expenses until second quarter 2018?

As I mentioned, we believe that our existing cash balance will be sufficient until the end of the second quarter of 2018. I think R&D will be – will start pretty much close to what we have in this quarter, then would be reduced a little by the end of mid-'18. Of course this is according to our current cash balance.

Okay, sounds good. Thanks for the clarification and looking forward to – again looking for the EASL presentation next month. Thank you.

Thank you. Looking forward to seeing you.

We’ll go next to Ed Arce with H.C. Wainwright.

Hi. Thanks for taking my questions. Allen and team, I am also looking forward to the data at EASL next month. I was wondering if you could perhaps discuss a little bit more without obviously violating any sort of protocols with the data at EASL, but just discuss in broad terms how you view the mechanisms and particular the collagen formation data that you’ve seen with Aramchol? And I have a follow up. Thanks.

Maybe I will let our CSO --

Hi. Good morning. So we are actually I think into the collagen production and the effect of Aramchol on fibrosis, the effect of Aramchol on fibrosis the way we see it in animal models is first because there’s a sequence of events starting, so steatosis towards inflammation and fibrosis. The fibrosis is kind of an endpoint over sequential events and reducing the steatosis which we actually showed in few animal models and has been published in the literature for many, many times and a lot of papers is quite clear. The new data that we are currently showing is that Aramchol has a direct effect on collagen production from the cell itself which is the only cell in the liver that aren’t producing collagen which is the main cause of fibrosis. Once you actually directly affect these cells, the cell itself and you’re down regulating the Aramchol production, you are down regulating fibrosis. This is why we actually add two hour proof-of-concept of the TAA model. With this TAA, you don’t have the sequence of events and you don’t have the steatosis and inflammation and then you are actually inducing only fibrosis directly showing an effect on this model a very significant effect that Aramchol is actually showing. Together, it’s showing that Aramchol has a direct effect on fibrosis with regardless of the fact that it has on steatosis. So having said that, it shows that Aramchol has two ways as Allen just mentioned in the beginning of the talk, two ways affecting fibrosis. One of it is down regulating steatosis and the other one is affecting directly the collagen production. The way we show that the Aramchol effect [indiscernible] fibrosis is because we took those cells, human cells we put Aramchol on these cells and we are showing that upon [indiscernible], Aramchol is affecting the collagen production from these cells more than 50%. Having said that, we expect some effect on fibrosis in our studies as well.

That’s great. Thank you for that. And then just one last follow up around the mechanism directly impacting collagen production in fibrosis. Remind us what are the secondary endpoints with elucidate in ARREST? Thanks.

This is Tali. I’m the CMO. As Allen said, the secondary – the first key secondary endpoint in the OS is looking exactly at fibrosis improvement using the most value [indiscernible] effective definition.

Great. Thanks again. Look forward to seeing the team next month.

And you at the conference, Ed.

There are no further questions in queue.

Okay. So thank you very much. Thank you all for joining the call and looking forward to seeing you all at EASL.

This concludes today’s conference. Thank you for your participation. You may now disconnect.