Sesen Bio, Inc.

Thank you, Operator. Good morning and welcome to Eleven's First Quarter 2017 Financial Results Conference Call.

Earlier this morning, we issued our financial results and corporate highlights press release which is available at www.elevenbio.com. Today, on our call, Stephen Hurly, President and CEO, will provide an overview and update on Eleven and its TPT platform; John McCabe, Chief Financial Officer, will review the financial results.

And then, we will open up the call for your questions; Art DeCillis, Chief Medical Officer; and Glen MacDonald, Chief Technology Officer are also available for Q&A. Before we begin, I would like to caution you that during today's conference call, we will be making forward-looking statements regarding future events or the future performance of the Company, including statements about possible future developments regarding clinical, regulatory, commercial, financial and strategic matters.

Actual events or results of course could differ materially. We also refer you to the risk factors section of our annual report on Form 10-K, quarterly reports on Form 10-Q and other reports filed with the Securities and Exchange Commission.

With that, let me pass the call over to Steve.

Thank you, Michael, and thank you, everyone, for joining us today. As many of you know, Eleven acquired Viventia Bio back in September 2016.

That created a late-staged oncology company, focused on developing targeted protein therapeutics or TPTs that are designed specifically to improve upon and overcome the challenges of existing therapeutic options. TPTs are fully biologic, single protein molecules that are built by generally fusing a tumor-targeting antibody fragment to a cytotoxic or cell killing protein.

Our TPT platform emerged from the original concept of a smart missile, a front-end navigating molecule that selectively binds to an antigen or reception that's over-expressed on cancer cells. These binding targets are chosen not just for their selectivity of the cancer, but also for their internalization properties.

Once our agent binds to its target, it is internalized into the cancer cell where cytotoxic protein is released, driving targeted cancer cell death. Now for an update on the first quarter 2017 progress.

We made meaningful advances across our pipeline of rationally designed TPTs including advancing our Phase 3 registration trial of Vicinium and continuing development efforts with Proxinium. In addition, at the American Association for Cancer Research or AACR annual meeting in April, we presented new preclinical data which supports our belief that our TPTs not only directly kill tumor cells, but also operate via second mechanism of action - the induction of a host-immune cell mediated anti-tumor response.

This suggest our compounds are not only differentiated from existing treatments, but they may have real synergy with checkpoint inhibitors and other immuno-oncology compounds. Specifically in preclinical studies presented at AACR, VB4-845, the active pharmaceutical ingredient used to formulate our two lead TPTs for Vicinium and Proxinium infused the expression of HMGB1.

HMGB1 is one of three damage-associated molecular patterns or DAMPs, indicative of immunogenic cell death. This type of cell death is recognized by immunologists to actively engage the host immune system and promote anti-tumor immune responses.

This is especially meaningful because it builds on our prior research in which we observed two other DAMP markers, cell surfaced expression of calreticulin and extracellular release of ATP following treatment with VB4-845. The induction of these three DAMPs that comprise the hallmark of immunogenic cell death strongly suggests our TPTs are capable-inducing host anti-tumor immune responses that can promote the function of immuno-oncology agents like checkpoint inhibitors.

This was even further supported in preclinical data. We used patient-derived tumor xenograph bearing mice reconstituted with human immune system to assess the combination of intratumoral injection of VB4-845 with anti PD1 checkpoint inhibitor development.

VB4-845 suppressed the growth of injected tumors while Nivolumab alone had little effect. Growth delay of contralateral non-injected tumors in the same animals was more pronounced with the combination of VB4-845 and Nivolumab than either agent alone.

This data suggest that VB4-845 killing of tumor cells could facilitate and augment anti-tumor activity of checkpoint inhibitors. This data has important implications for our clinical development strategy.

Based on these results, we're exploring our lead TPTs and build monotherapies as well as combination agents. We're currently developing our lead drug Vicinium as a monotherapy for the treatment of non-muscle invasive bladder cancer.

Vicinium is a locally-administered single protein anti EpCAM antibody fragment genetically fused with Pseudomonas Exotocin A or EGA, a potent cytotoxic paylod. Vicinium is administered directly into the bladder where it seeks out the cancer tissue.

After binding to EpCAM on cancer cells, Vicinium is internalized into these cells where it releases ETA. ETA in turn interrupts protein synthesis and drive cell death.

Importantly, EpCAM is over-expressed or is expressed in more than 98% of high grade non-muscle invasive bladder cancer and is minimal to no expression or normal bladder cancer. Vicinium is currently in a Phase 3 registration clinical trial for non-muscle invasive bladder cancer.

Bladder cancer affects over 79,000 new patients in the U.S. annually, with non-muscle invasive bladder cancer making up 70% to 80% of all bladder cancer and carrying high per patient cost.

There have been no major advances in this space for over four decades. The first line standard of therapy BCG, which is initially very effective but offer some significant failure rates.

Upon relapse, unfortunately there are no good alternatives and patients typically undergo bladder removal, a major surgery or significant risk of complications, routine hospital stays, post-surgery and a major impact on quality of life. As a reminder in a Phase 2 study, Vicinium showed promising safety and efficacy in 46 post BCG refractory or intolerant Carcinoma in situ or CIS patients.

The study had two arms: one, where patients received one induction phase for six weeks and the other where they received one induction a week for 12 weeks. If the patient achieved a complete response, then move to maintenance dosing for up to 12 months.

At three months, 40% of the patients across both arms experienced a complete response, meaning no evidence of disease. At one year, 17% of the patients on the 12-week arm and 14% of the patients on the six-week arm remain disease-free.

Importantly, all the CR patients in the 12-week arm remained disease-free as of last follow up out to 25 months. Medium time to recurrence is 408 days for the 12-week arm and 274 days for the six-week arm.

Based on these results, we moved Vicinium into a Phase 3 trial. Importantly, in this Phase 2 trial, the majority of the patients had two or more courses of BCG as required by our Phase 3 protocol.

In fact, the response rates in those had two or more courses in the Phase 2 were actually better than the full trial. Specifically in the six-week treatment arm, cohort1, 10 of the 22 patients had two or more courses of BCG.

Four or 40% were CR at three months and two 20% were CR past 18 months. In the 12-week treatment arm, cohort2, 16 of the 23 patients had two or more courses of BCG, 43%, seven were CRs at three months and three or 18.8% were CRs past 18 months.

This is the patient population that best matches with our Phase 3 study. Our ongoing Phase 2 registration clinical trials enrolling 134 patients with BCG refractory or relapsed high grade non-muscle invasive bladder cancer.

At over 65 centers in the U.S. and Canada including 77 patients with Carcinoma in situ or CIS and the balance of the 134 will be the papillary [ph] tumor patients.

We plan on fully enrolling this trial by the end of 2017 and providing top line data in 2018. The primary end point of the study is complete response rate at one year in Carcinoma in situ subjects; secondary end points include timely disease recurrence and event-free survival.

Importantly, this trial design is in accordance with recently published FDA draft guidance on drug development in NMIBC. This draft guidance advises that our clinical trial is appropriate as a single arm clinical trial with complete response rate as the primary end point and can provide sufficient evidence of effectiveness to support a marketing application.

In fact, the guidance provide the opportunity to move from the potential for conditional approval to narrow [ph] the potential to receive full approval. I'll now turn it to our second program, Proxinium.

Proxinium is based on the data we received at AACR. In prior clinical experience with this drug, we decided to develop Proxinium in combination with the approved checkpoint inhibitors.

Like Vicinium, Proxinium is a single-chain in the EpCAM antibody fragment, genetically fused with ETA. We're developing Proxinium for patients with head and neck cancer or Squamous Cell Carcinoma of the Head and Neck of SCCHN.

SCCHN affects more than 650,000 patients annually. Surgery to treat this disease is highly invasive and is associated with significant morbidity.

The five-year survival rate is only 40% - 40% to 50% depending on the stage of advancement and the majority of patients present with advanced disease. We remain on track to initiate a Phase 1/2A study for Proxinium in combination with checkpoint inhibitors in the second half of 2017.

Beyond Vicinium and Proxinium, we are developing a pipeline of de-immunized systemically administered TPTs, which utilize our next generation proprietary payload deBouganin. DeBouganin is a highly potent plant toxin which has picomolar killing, avoids multi-drug resistance and may potentially induce an effect against cancer stem cells.

Moreover, its safety profile provides a broad therapeutic window which suggest that deBouganin-based therapies may be effective against a wide spectrum of different cancers. At AACR, we presented preclinical data suggesting that deBouganin is capable of effectively killing tumor cells that are resistant to treatment with certain antibody drug conjugates, composed of the anti-mitotic payloads DM1 and MMAE when conjugated to the same monoclonal antibody.

We believe that this in part is due to deBouganin's lack of sensitivity to both the multi-drug resistance pumps and changes in status approachings involved in self-proliferation and survival that allows some cancers to escape action of anti-mitotic ADCs. Based on these results, we believe that deBouganin-based therapies may be capable of overcoming mechanisms of resistance employed by cancer cells against ADC payloads and that they may therefore represent a more effective treatment option.

We intend to finalize preclinical development this year and file an IND with the FDA in Q1 2018. Before I turn the call over to John McCabe, our CFO to review the financial results, just a brief comment on the team here at Eleven.

In the first quarter, we welcome two new hires to our clinical team including Gary Conboy as Executive Director in Clinical Sciences and Mary Rohrer, an Associate Director in Clinical Operations to support our continued clinical development. Together, Mary and Gary bring extensive experience overseeing clinical operations and clinical study planning within the biopharmaceutical industry and I look forward to the contributions as we continue to advance our clinical programs including progressing our ongoing Phase 3 study of Vicinium and initiating our study with Proxinium.

With that, I'll pass the call over to John.

Thank you, Steve, and good morning to everyone. For the first quarter of 2017, we reported a net loss of approximately $6.1 million or $0.25 per share, compared to a net loss of $7.6 million or $0.39 per share for the same quarter last year.

Total revenue for the first quarter of 2017 was $0.4 million, compared to $0.2 million for the same period last year. This increase was related to revenue recognized under our license agreement with Roche.

Research and development expenses for the first quarter of 2017 were $2.9 million, compared to $4.6 million for the same period in 2016. This decrease was primarily due to a reduction in [indiscernible] and EBI-031 related development expenses, partially offset by an increase in Vicinium-related development expenses.

General and administrative expenses for the first quarter of 2017 were relatively flat at $2.2 million, compared to $2.1 million for the same period in 2016. Cash and cash equivalents were $20.3 million at the end of the first quarter of 2017.

Based on our current operating plans, we believe that we have sufficient cash and cash equivalents defined our operating expenses into early 2018. Now I'll turn the call back over to Steve for concluding remarks.

Steve?

Thanks, John. I'd like to take a brief moment the recap the key program milestones we anticipate for the remainder of the year which will continue to enhance our pipeline forward.

Starting with the lead product Vicinium. Later this year we expect to complete enrollment in our Phase 3 registration clinical trial for BCG refractory or relapsed high grade non-muscle invasive bladder cancer patients and expect to have top line data in 2018.

For Proxinium, we plan to initiate a Phase 1/2A trial, clinical trial in combination with checkpoint inhibitors in the second half of the year in head and neck cancer; and finally in our earlier stage pipeline, we plan to finalize preclinical development later this year and file an IND for the first de-immunized systemically-administered TPT VB6-845d in the first quarter of 2018. Taken together, we believe these programs have the potential to bring meaningful new treatment options to patients and we're excited to continue advancing them through development.

We look forward to updating you further as we continue to progress. With that, I'd like to thank you all for your time and open up the call to any questions.

Operator?

Thank you, Operator. And again, I'd like to -- on behalf of the entire team at Eleven, thank you all for your time.

We look forward to continue to providing you updates as we progress in our clinical development and balance of this year. Thank you again.

Bye, bye.