Jennifer McNealey – Senior Director, Investor Relations Susan Molineaux – Founder, President and Chief Executive Officer William Waddill – Senior Vice President and Chief Financial Officer

Paul Matteis – Leerink

Good day, ladies and gentlemen, and thank you for standing by. Welcome to the Calithera Biosciences’ First Quarter 2016 Earnings Conference Call. At this time, all participants are in a listen-only mode. Later, we will conduct a question-and-answer session and instructions will follow at that time. [Operator Instructions]. I would now like to introduce your host for today’s presentation, Ms. Jennifer McNealey, Senior Director, Investor Relations. Ma’am, please begin.

Good afternoon, everyone and welcome to Calithera’s first quarter conference call. Joining me today are Susan Molineaux, our Founder, President and CEO; and Will Waddill, our Senior Vice President and CFO. Before we begin, I would like to remind you that today’s discussion will include statements about the company’s future expectations, plans, and prospects that constitute forward-looking statements for the purposes of the Safe Harbor provisions under the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by these forward-looking statements as a result of various important factors including those discussed in the Risk Factors section of our Annual Report on Form 10-K, on file with SEC. In addition, any forward-looking statements represent our views only as of today and should not be relied upon as representing our views as of any subsequent date. While we may elect to update these forward-looking statements at some point in the future, we specifically disclaim any obligation to do so even if our views change. Please note that this call is being recorded. With that, I will turn the call over to Susan.

Thanks, Jennifer. Good afternoon everyone and thank you for joining us today on our quarterly conference call. During the first quarter, we continued to advance our development pipeline by recruiting patients into clinical studies of CB-839, preparing for an investigational new drug application or IND for CB-1158 and expanding our clinical development leadership team. For CB-839 our glutaminase inhibitor we are currently enrolling multiple expansion cohorts in combination therapy with standard of care agents. We look forward to the initiation of novel combination trials in the near term, including an investigator sponsored trial with more details on these trials to follow. For CB-1158, our arginase inhibitor we are on track to file an IND application mid-year. As we plan for multiple drug candidates in the clinic by the end of 2016, we’ve been driving expansion of our clinical developments and operations team. And so, we’d like to start out today’s call by extending a warm welcome to Dr. Sam Whiting as Vice-President of clinical development who just joined Calithera. Most recently, Dr. Whiting served as Vice-President of Research and Clinical Development at Gradalis and previously Dr. Whiting was a member of the Fred Hutchinson Cancer Research Center and assistant professor at the University of Washington, where he was clinical director of gastrointestinal oncology. Dr. Whiting received his M.D. and Ph.D. degrees and completed his internal medicine residency at the University of Washington and his medical oncology fellowship at the Fred Hutchinson Cancer Research Center. In addition, we would like to congratulate Keith Orford, M.D., Ph.D for his promotion Senior Vice President of Clinical Development. At Calithera, our three programs targeting glutamine, arginine and glucose metabolism are interrelated with each program targeting a different aspect of tumor-specific metabolism. Tumor metabolism and immune-oncology have emerged as promising new fields for cancer drug discovery and recent clinical successes with therapeutic agents in each field have demonstrated the potential to create fundamentally new therapies for cancer patients. We are developing agents to take advantage of the unique metabolic requirements of tumor cells and of cancer fighting immune cells such as cytotoxic T-cells. With these programs, we believe that we have multiple opportunities to positively impact clinical outcomes for cancer patients by building a pipeline of novel therapeutic product candidates. Now an update on the pipeline. CB-839 is a first-in-class selective and potent inhibitor of glutaminase and we believe it is the only glutaminase inhibitor currently in clinical development. CB-839 has demonstrated single agent solid tumor clinical benefit across a variety of solid tumor types. We have seen an objective response in a renal cancer patients treated with CB-839 as the monotherapy as well as signs of durability and continuation of a positive safety profile. We now have ongoing studies of CB-839 in combination with standard of care agents that target tumor signal transduction pathway. And in addition, we have preclinical data showing that you can combine CB-839 also with I-O agents. At AACR in April, we presented preclinical data showing that the combination of CB-839 and anti-PD-L1 or anti-PD-1 substantially increased the number of tumor regressions seen in a mouse syngeneic colon carcinoma model. Synergistic effects with CB-839 and anti-PD-L1 were also observed in a mouse melanoma model. Interestingly, both of these agents are known to affect metabolism in the tumor microenvironment. Treatment with anti-PD-1 or PD-L1 increases glucose metabolism into T-cells. And CB-839 increases the amount of glutamine available for T-cells because it inhibits the average metabolism of glutamine by the tumor itself. T-cells require adequate levels of these two key nutrients in order to expand and mount a strong anti-tumor response. Based on these preclinical results, we remain on track to initiate a checkpoint inhibitor of combo trial in the second quarter. Checkpoint inhibitors promote the activation and tumor killing properties of the patient’s own immune cells such as cytotoxic T-cells. And CB-839 could potentially have a one-two punch in the treatment of cancer by first starving the tumor cells and by second, facilitating the activation of T-cells in the nutrient deprived tumor microenvironment. We are also looking forward to the initiation of an investigator sponsored trial in a biomarker selected colorectal cancer cohort. This trial is expected to begin in the second half of 2016 at Case Western Reserve University, overseen by Dr. Jennifer Eads, Alok Khorana, and Neal Meropol. The trial will enrolling colorectal cancer patients with a PIK3CA mutation for treatment with a combination of CB-839 and capecitabine. Research group at Case Western Reserve University has demonstrated that single agent CB-839 inhibits the growth of colorectal tumors with PIK3CA mutations in immunocompromised mice but colorectal tumors with a normal PIK3CA were not inhibited. Remarkably, the combination of CB-839 with 5-fluorouracil induced complete and long-lasting tumor regressions in animals bearing PIK3CA mutant colorectal tumors but not tumors with normal PIK3CA, suggesting that this combination therapy may be a unique and effective approach in the clinic. We also announced in the quarter that data from two of our solid tumor combination cohorts have been accepted for presentation at the 2016 American Society of Clinical Oncology or ASCO, Annual Meeting. Initial results of CB-839 in patients with triple-negative breast cancer those in combination with paclitaxel will be presented in a poster and poster discussion on Sunday, June 05, 2016. And initial renal cell carcinoma results of CB-839 alone and in combination with everolimus will be presented in a poster on Monday, June 6th. ASCO has communicated that the abstract which was submitted in January will become available at the ASCO website on May 18th and we intend to update our results in our ASCO poster presentation with more patients and longer follow ups in what we published in the abstract. We will also be hosting a briefing for analysts and investors on Monday evening, June 6th and we look forward to seeing you there. For our immune-oncology program, CB-1158 which is our oral inhibitor of arginase, we recently presented additional preclinical data at the AACR meeting where the presentation garnered great interest. CB-1158 is a small molecule inhibitor of human arginase with the potential to treat cancer by blocking immune-suppression in the tumor microenvironment. Our data demonstrated that inhibition of tumor growth was accompanied by an increase in the local concentration of arginine, and the induction of multiple pro-inflammatory changes in the tumor microenvironment. CB-1158 also increased CD8+ T-cell infiltrates in a lung tumor model. The addition of CB-1158 to anti-CTLA-4 and anti-PD-1 therapies significantly inhibited tumor growth and reduced metastases in a mouse model that was resistant to dual checkpoint inhibitor therapy. CB-1158 was well tolerated as a single agent and in combination with checkpoint inhibitors in animal studies. We are very excited about the significant progress we have made on our CB-1158 program and we remain on track to file an IND application in mid-2016. We are planning initial trials as a monotherapy with the ability to move into combination therapy as quickly as possible. Similar to the IDO inhibitors, there is a rationale for combined CB-1158 with other immune-oncology therapies that target T-cell activation like CTLA-4 and PD-1 antibodies. So, our near term anticipated milestones included the following; for CB-839, our RCC and TNBC combination data to be presented at the ASCO meeting in June; continued enrolment of CB-839 of combination expansion cohorts; initiation of the checkpoint inhibitor combination trial in the second quarter; and initiation of IST in colorectal cancer later this year. For CB-1158, we plan to file an IND for our arginase inhibitor in mid-2016 and begin clinical study soon after. With that, I’ll pass it over to Will for an update on our financials.

Thank you, Susan and good afternoon everyone. Calithera remains in a strong financial position at the end of the first quarter, with sufficient resources to drive our first in class tumor specific metabolism programs forward. As for our financials, our cash, cash equivalents and investments as of March 31, 2016 was $68.3 million compared to $71.9 million as at December 31, 2015. Research and development expenses for the first quarter 2016 were $7.1 million compared with $5.6 million in the prior year, an increase of $1.4 million which was primarily attributed to increased development activities in our arginase inhibitor program as we plan to file our IND in mid-2016. This is partially offset by a decrease of $0.4 million compared to the company licensing arrangement. General, administrative expenses for the first quarter 2016 were $2.6 million compared to $2.2 million in the prior year. The increase of $0.4 million was primarily due to higher employment related expenses including stock-based compensation expenses. Loss from operations for the first quarter 2016 was $9.6 million. And with that, I will now turn the call back over to Susan.

Thank you, Will. And with that operator, we are happy to open the line for questions.

[Operator Instructions]. Our first question or comment comes from the line of Paul Matteis from Leerink. Your line is open.

-- my questions congratulations in all the progress. I’m wondering with regards to CB-839 combination data that you are going to have in June at ASCO. How far along are you in these different tumor types, triple negative breast and renal cell carcinoma, for having enough data to make a go no-go decision for further investment in these contacts?

Thank you for that question, Paul. We will have sufficient data at ASCO to further comment on where the steps in development will take place in the company.

Okay. That’s great. And are there other combination studies that we should be expecting to read out over the course of the summer that will also inform strategic plans?

In the very near future, so the next couple of quarters, it will be primarily focused on RCC and TNBC and the next one to read out will be AML probably at the end of the year.

Okay. And -- that’s great, okay. And then separately on 1158, I know Susan you’ve said historically that you see them most clinical potential for this compound and the combination setting, how rapidly do you think you could move into combination studies with this drug? And how quickly could you go through phase 1a?

Our current plan is to do a standard dose escalation and then once we’ve established a safety profile and a dose to move forward, we have built into the protocol the ability to add a checkpoint inhibitor at that point in time. So, we do plan on focusing for combination therapy as soon as possibly once you have sufficient monotherapy safety information and potentially efficacy information.

Okay, great. And may be just one more if you don’t mind, the Case Western study, do you think that there could be some data for that next year, in 2017, or is that too soon?

That would be our intention and the investigator’s intention to have data some time in 2017, yeah.

Okay, great. Thanks for taking my questions.

Sure. Thanks, Paul.

Thank you. [Operator Instructions]. Our next question or comment comes from the line of Jim Birchenough from Wells Fargo Securities. Your line is open.

This is actually Yanon [ph] in for Jim. Question on 1158, have you talked about whether this molecule is a self-permeable or does it work exclusively outside the cell in a plasma?

Yes, we have talked about that. It has variable permeability in different cell tissues. So we believe in our animal studies that it works as a combination of intracellular or extracellular, but in mouse the arginase targeted cells are primarily intracellular. In humans, we expect to easily inhibit the extracellular enzyme and also to be able to inhibit some of the intracellular enzyme as well.

And – so do you think the extracellular component is sufficient? There will be intracellular activity, but if we’re just relying on the extracellular component of it, would that be sufficient to fleet arginine to the level that’s desired given that the cell may still continue to -- inside the cell will still new arginine being made?

We do expect it to be sufficient to inhibit both the systemic intracellular stores of arginase which we do see and we have published in our rodent model, causes an increase in systemic arginine. So we inhibit intracellular arginase sufficiently to cause a systemic rise in the plasma level of arginine that’s quite significant. And in addition, had there been extracellular arginase in our mouse model, we would have inhibited that as well. And we expect for our human dose to be able to do the same that is, cause sufficient intracellular arginase inhibition to cause a rise in systemic arginine in the plasma of the patient as well as to inhibit extracellular arginase. So it is actually a two-pronged approach to providing T-cells with sufficient levels of arginine, both by inhibiting any extra-cellular arginase in the tumor microenvironment, and also by raising the arginine levels in the plasma to replete the missing level of arginine.

Yeah. Great. Then another question on, because arginase is involved in the urea cycle which is important for the excretion of ammonium, and nitrogen waste, does the drug have any impact on the urea cycle?

Not at the dosage that we were just discussing. We do know from the data that we have published on hepatocytes and other cells that it requires a very significant increase in the dose, but we can, at very high levels eventually inhibit the urea cycle. And there’s about a hundred-fold difference to inhibit standard arginase as opposed to the ability to inhibit the arginase in the urea cycle in hepatocytes. And the reason for that in the urea cycle, the arginase enzyme is basically being exposed to an infinite concentration of arginine because the urea cycle enzymes are very tightly coupled.

Right. I see.

And this is the competitive inhibitor of arginase so it does compete with arginine to bind at the arginine binding site.

Got it. Another question on the PIK3CA mutation, do you know the prevalence of that mutation in CRC patients?

Yes, it’s about 15% to 20%.

Got it. Great. Thank you.

Thank you. [Operator Instructions]. I’m showing no additional audio questions at this time. I would like to turn the conference over to Ms. Molineaux for any closing remarks.

Once again, thank you all for joining the call today. And in closing, we look forward to seeing you at ASCO and in particular, at our Analyst Meeting on Monday night. Thank you and have a good day.

Ladies and gentlemen, thank you for participating in today’s conference. This concludes today’s program. You may all disconnect. Everyone, have a wonderful day.