Dr. Lan Huang
Thank you. Ladies and gentlemen, thank you for joining today’s call. With me today are Edward Liu, our recently appointed Chief Financial Officer who will discuss our first quarter 2018 financial results and recently announced registered direct offering; and Dr. Ramon Mohanlal, our Chief Medical Officer who will be available to answer questions during the Q&A portion of today’s call. This morning, I will begin by providing an update on our most current pipeline advances. As I noted on our last conference call in early April, 2018 promised to be an important year for BeyondSpring with significant milestones that have the potential to transform the Company and advance us on our trajectory to become a multinational commercial-stage oncology company. Already this year, we have made critical steps towards achieving this objective, advancing our late stage, lead asset Plinabulin in multiple clinical studies with ongoing data readouts that to date support our expectations for Plinabulin as a potentially superior new treatment for chemotherapy-induced neutropenia or CIN, and a new treatment candidate for non-small cell lung cancer. With additional interim data readouts expected beginning in the first quarter and assuming those data are positive, we plan to submit NDA to the China FDA soon thereafter, generating a steady flow of catalysts over the remainder of 2018 and into 2019. Specifically, in CIN, we expect number one, Phase 3 interim analysis data for Study 105, evaluating Plinabulin and docetaxel for prevention of CIN in the fourth quarter of 2018; number two, Phase 2 data for the primary endpoint of Study 106, evaluating Plinabulin and TAC also in the fourth quarter of 2018; number three, pending positive results from these two studies, we would expect to submit the NDA to the CFDA in late 2018 or earl y 2019 for Plinabulin for a broad target indication of prevention of severe, Grade 4 neutropenia induced by oral myelosuppressive chemotherapy. For non-small cell lung cancer, we expect to number one, announce Phase 3 interim data for Study 103, evaluating Plinabulin and docetaxel in early 2019 and contingent on positive interim data, submit an NDA to the China FDA in the first half of 2019. From our early stage pipeline, we plan to advance two Plinabulin triple-combo immuno-oncology programs into Phase 1 in the second half of this year and initiate in 2019 a Phase 1 study of BPI-002 some of our I/O program that we unveiled late last year as well as advance our ubiquitination program toward clinic. BeyondSpring has a truly robust drug development platform and strategy. And our first-in-class marine-derived small-molecular immune agent Plinabulin is itself a pipeline in a drug. However, for today’s call, I will be focusing my remarks on Plinabulin in the CIN indication, both because it’s our program nearest to regulatory advancement and commercialization, and because of its numerous developments in recent months. By way of background G-CSF drugs are the current standard of care in prevention of CIN, but they are characterized by second day dosing and overall safety limitations, including severe bone pain. One of the best known and most prescribed G-CSF is Neulasta. Despite indications limited to use principally in the high-risk febrile neutropenia segment, which represents around 20% of patients undergoing chemotherapy, G-CSF have reached $8 billion in global annual sales, dominated by sales of Neulasta and Neupogen. G-CSF therapy works by stimulating the expansion and proliferation of neutrophil precursors in the central part of bone marrow, an action that is believed to be the cause of bone pain associated with G-CSF use. Plinabulin works very differently by destabilizing the tubing network and releasing a protein called GEF-H1 of guanine nucleotide exchange factor. GEF-H1 activates downstream signal transduction pathways leading to the activation of protein c-Jun, which enters the nucleus of dendritic cells to up-regulate immune-related genes, leading to dendritic cell maturation, T-cell activation and other effects that prevent neutropenia by reducing the neutrophil breakdown. Results of our pre-clinical study were presented in April at AACR annual meeting and showed mechanistically Plinabulin’s ability to reduce CIN by protecting the normal transition of LSK to myeloid precursors in mice, providing further evidence of Plinabulin’s differentiated mechanism of action. This mechanism is important to understanding one of the key differentiating feature of Plinabulin, its potential for reduce incidence of bone pain in chemo treated patients, something that we are seeing bear out in clinical development, which I will explain in a moment. Early in the first quarter, we presented preliminary top-line clinical data from the Phase 2 portion of Study 105, our Phase 2/3 study looking at Plinabulin’s effect on preventing docetaxel CIN compared to Neulasta at the ASCO SITC Clinical Immunooncology Symposium. And early this month, at ASCO, we presented data, reflecting the full analysis of our Study 105 Phase 2 data in CIN. In the Phase 2 portion, which included a total of 55 patients with 14 treated with Plinabulin 20-miligram per meter square and 14 treated with Neulasta, patients given one dose of Plinabulin at 20-miligram per meter square 30 minutes after docetaxel dosing in the first cycle had following benefits. Number one, similar neutropenia reduction to those taking Neulasta; number two, two thirds lower rate of bone pain; and number three, neutrophil numbers in the normal range. This data demonstrates Plinabulin’s potential to be a product with the superior overall profile relative to Neulasta for treatment of CIN. With respect to neutropenia reduction, in this Phase 2 study, patients given Plinabulin just 30 minutes after first cycle docetaxel chemotherapy at a dose of 20-milligram per meter square, the dose that we subsequently selected for Phase 3, had the same 14% incidence of severe Grade 4 neutropenia as patients given 6-milligram of Neulasta the next day, consistent with its product label. Furthermore, the duration of severe neutropenia or DSN was also comparable at 0.5-day in both the Plinabulin and Neulasta arms. These findings are noteworthy indicating that even in a small sample size, Plinabulin performed comparably to Neulasta on key efficacy measures for CIN. And this is just part of the picture. We saw notable differences between the Plinabulin and Neulasta treatment groups on other key measures. As I mentioned earlier, while significant side effects in patients given G-CSF therapy to combat the neutrophil depletion associated with chemotherapy is bone pain. Bone pain that is so excruciating that it leads some patients to reduce or discontinue potentially life-saving chemo treatment. It is a significant issue and one that hasn’t been addressed by current available therapies. In our Phase 2 study, two thirds fewer patients given Plinabulin at 20-milligram per meter square reported bone pain compared to patients given Neulasta. Specifically, 11% given Plinabulin noted bone pain on their questionnaires, while 33% given Neulasta reported bone pain. While not unexpected given all we know about Plinabulin’s differentiated mode of action and the growing body of evidence that points to its ability to attenuate bone pain, these results are nonetheless meaningful and support our thesis that Plinabulin protects neutrophil precursors but does not induce their proliferation, an important distinction relative to the current standard of care. Incidence of bone pain will be a key secondary endpoint in Phase 3 and a meaningful lower rate of bone pain for Plinabulin treated patients would represent a very important, differentiating feature in the treatment of CIN. Our poster presentation at ASCO included data on another distinguishing factor for Plinabulin relative to Neulasta, a difference that was only partially expected. In the trial, Plinabulin performed as we had expected in maintaining absolute neutrophil numbers in the normal range, again, a theory that was supported by what we have observed in preclinical and clinical trials to date that have suggested as neutrophil protected properties. What was somewhat surprising was what was observed in Neulasta arm. In the study, the Neulasta treated patient group had a median neutrophil comps that were much higher than the normal range, which can potentially cause bone marrow exhaustion and suppressed immune system. Taken together, we believe that our Phase 2 results in CIN translate into distinct advantages for Plinabulin relative to the market leader Neulasta. The Phase 3 portion of Study 105 that we initiated in March is now well underway. The study will include a total of 150 cancer patients at 50 sites in the U.S., China, Ukraine, Russia and Hungary. The primary endpoint of Study 105 is the reduction of neutropenia as measured by DSN in the first cycle. Secondary endpoints include the incidence of neutropenia incidence of febrile neutropenia, incidence of and duration of hospitalization, and incidence of bone pain, among others. An interim analysis of 100 patients in this Phase 3 study is expected in the fourth quarter. This study is complemented by another ongoing late stage study evaluating Plinabulin in preventing high risk TAC chemo-neutropenia. This trial, Study 106 is currently in Phase 2 with breast cancer. Results from this study are expected late this year. In this study, we are planning for superiority in DSN in the first cycle. Our regulatory strategy for Plinabulin in CIN includes one global trial with patients for the U.S., China and Europe and with the combined package for the submissions for conditional approval to the China FDA first, then second to U.S. FDA. Together, studies 105 and 106 will serve as a basis for our NDA submission to the CFDA. We are preparing that NDA submission now working to compel in advance as much of the package as possible to enable us to submit it in late 2018 or early 2019, assuming a positive signal from the Phase 3 interim analysis of Study 105 and the positive results from Phase 2 of Study 106. Our plan is to follow the China submission with the NDA submission to the U.S. FDA, based on the full clinical development data package, following completion of the studies with a submission target for the second half of 2019. The regulatory strategy for Plinabulin in CIN is mirrored by a parallel strategy for Plinabulin non-small cell lung cancer indication. As with CIN, our non-small cell lung cancer program for Plinabulin is also a global Phase 3 clinical development with patients from the U.S., China and Australia. And we are looking to take a similar approach, targeting early 2019 for our pre-specified interim Phase 3 analysis from our ongoing 554 patients Phase 3 Study 103 with the primary endpoint of overall survival. The interim analysis is event-driven and will look at 146 patient tests. Assuming favorable trends comparing median OS from the two treatment arms, this interim data would serve as a basis for NDA submission to the CFDA targeted for the first half of 2019 followed by a U.S. FDA submission targeted for 2020, based on the full and final data readout from the non-small cell lung cancer program. For both of the CFDA submissions, efficacy data in each indication will be supplemented by a drug safety data base comprising data from the more than 300 cancer patients who have received Plinabulin in clinical trials. We have already met this requirement with Plinabulin treating over 300 cancer patients with good tolerability. Assuming we submit NDAs to CFDA as currently anticipated, we could be in a position to receive conditional approval in China within six months, following each submission. This is an important point and one that may not yet be fully appreciated by U.S. investors. The bar to achieve approval in China is already high long before a drug candidate reaches the submission stage. From a cultural standpoint, China and the Chinese government emphasize and advance initiatives that are believed to have a high likelihood of success, and that is true for new drug development. While nothing is absolutely certain, for a new medicine to reach the NDA stage in China, there has already been more rigor in the development process and dialogue with agency than is seen by the stages in the U.S., which significantly lowers the regulatory risk for drugs going through the approval process. As a result, we have a great deal of confidence in Plinabulin’s prospects. Rapid review can provide a significant market advantage and underpins the dual market strategy that is designed to expedite availability of our treatment candidates in the two largest pharmaceutical markets in the world, with the high incidence and unmet medical needs in CIN and non-small cell lung cancer in both China and the U.S. These two territories represent a logical starting point to introduce what we expect will be important new medicines for those two indications. Assuming favorable data and subsequent regulatory reviews, BeyondSpring has the potential to be a commercial stage company as early as the second half of next year. With that in mind, we have already started process of preparing ourselves for commercialization in both U.S. and China, including identifying and securing the resources and talent we need to put in place for commercial success for Plinabulin in both markets. We expect to have more to say on our progress on this front in the coming weeks and months as we make the transition toward a commercial stage company. With the business that integrates clinical and the manufacturing resources in the United States and China and led by a management team and world renowned KOLs with deep experience in our target therapeutic areas in each of these countries, we’re well-positioned to execute on our dual-market trend, first for Plinabulin followed by our pipeline of complementary earlier stage oncology assets. Our pipeline of early stage assets represents future growth drivers and comprises the next stage in the Plinabulin developed platform with Plinabulin in combination with I/O agents as well as Plinabulin plus chemotherapy plus I/O agents. And our early stage pipeline is further supplemented by our ubiquitination platform, a new area into discovery in which, I have a great deal of experience and passion, dear to my heart. I was the person who saw the first E2E3 ligase structure in the world, which was published in 1999 Science Magazine. In the second half of this year, we plan to submit INDs for two of our triple I/O combinations. And in 2019, we expect to advance BPI-002, an oral CTLA-4 inhibitor to IND stage and advance our ubiquitination platform toward the clinic for its effects on active-form mutant KRAS as the first target. This concludes my remarks today on our [technical development]. And I would like to now turn the call over to Edward Liu, our new CFO, for a review of our financials. Edward?
