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

Matthew Andrews – Wells Fargo Securities

Good day, ladies and gentlemen, and welcome to the Calithera Biosciences Second Quarter 2015 Earnings 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] As a remainder, this conference is being recorded. I would now like to introduce your host for today’s conference, Jennifer McNealey, Senior Director Investor Relations. Ma’am you may begin.

Thank you. Good afternoon everyone and welcome to Calithera’s second quarter 2015 conference call. Joining me today are Susan Mano, 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 factor section of our quarterly report on Form 10-Q, which is on file with the 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, and good afternoon everyone. Thank you for joining us today on our quarterly conference call. The second quarter was a dizzy and exciting time at Calithera as CB-839 data was selected for presentation at three key medical meetings, the American Association of Cancer Research, or AACR, the American Society of Clinical Oncology, or ASCO, as well as the European Hematology Association. These data included the first clinical update to the program since our initial public offering in October of last year. CB-839 is the only targeted allosteric inhibitor of glutaminase that has reached human testing in clinical development. For our lead immuno-oncology program, we have made significant progress. We selected a clinical candidate, CB-1158, a small molecule arginase inhibitor with the potential to treat cancer by blocking the immunosuppression in the tumor micro-environment and thus enabling the activation of cytotoxic T cells. At Calithera, we have three interrelated programs, each targeting a different aspect of tumor-specific metabolism. Two of our programs are aimed at depriving tumor cells of nutrients essential for their growth and survival, namely glutamine and glucose, and one program that's aimed at restoring the nutrient, arginine, which is required for immune cell activation in tumors. With this integrated approach, we can continue to leverage our expertise in tumor metabolism and focus multiple drug discovery efforts in parallel on targets in the metabolic pathways that enable tumors to grow and evade the immune system. We remain dedicated to creating and developing first-in-class drugs, small molecule inhibitors of innovative targets. So let's begin with an update on CB-839, our most advanced product candidate. At the AACR meeting in Philadelphia, in April, we had data highlighting significant preclinical insights into glutamine metabolism in tumors. These new findings will bear directly on the design of our clinical trials for CB-839, our glutaminase inhibitor currently in Phase 1b testing. Key data included the identification of two new potential biomarkers, namely KRAS and EGFR mutations, in lung cancer; also the demonstration of synergy between CB-839 and diverse series of targeted inhibitor including: mTOR, MEK, EGFR, and PARP; and finally, data confirming our earlier observations of single-agent activity with CB-839 in animal tumor models. At the American society of clinical oncology, in May of 2015, we presented data that demonstrated the clinical activity, tolerability and unique mechanism of action of CB-839 as a single agent in patients with solid tumors. Robust inhibition of glutaminase was observed in platelets and tumor biopsies, with the magnitude of inhibition correlated with CB-839 exposure. Among evaluable patients, stable disease which reported a 19% that the patients on our initial clinical dosing regimen of three times a day on a fasting schedule, and 41% of patients on our amended standard dosing regimen of twice daily feeding. Patients who met the criteria were stable at least three cycles or 63 days. As a reminder, all of the patients in this trial were heavily pre-treated and have failed therapies with multiple approved drugs. We continues to enroll four CB-839 single agent solid tumor expansion cohorts in patients with triple negative breast cancer, renal cell carcinoma, KRAS-mutated non-small cell lung cancer, and tumors harboring TCA cycle mutations. In addition, a combination expansion cohort with CB-839 and paclitaxel in triple negative breast cancer has initiated enrollment, two other combination cohorts are planned: CB-839 plus everolimus in renal cell carcinoma, and CB-839 plus erlotinib in KRAS-mutated non-small cell lung cancer. We look forward to presenting additional Phase I solid tumor monotherapy data in the fourth quarter of 2015 as well as combination data in the first half of 2016. At the European Hematology association in June 2015, we presented data that demonstrated the clinical activity and tolerability of CB-839 in patients with acute leukemia. Among 18 acute leukemia patients, including 16 with acute myeloid leukemia, or AML, one patient achieved a complete response in the bone marrow with incomplete recovery of peripheral counts or CRi. Five of 18 efficacy-evaluable patients across dose levels remained on therapy for at least 4 cycles. Monotherapy and combination AML expansion cohorts are planned, including a combination of CB-839 with azacitadine. In multiple myeloma, we continue to enroll patients; everolimus has not been attracted as our other indication. A combination expansion cohort with pomalidomide and dexamethasone is also currently enrolling. Across hematological indications, we plan to present and update later this year as well as having combination data by the first half of 2016. Next is our arginase inhibitor immuno-oncology program. As a bit of background, a key way that tumors evade recognition by the immune system is through the suppression of cytotoxic T-cells, the cells that would normally attack and kill tumors. Without the amino acid arginine, tumor-associated cytotoxic T-cells fail to express a fully functional T-cell receptor on their surface, and as a result, are unable to be activated to mount an effective anti-tumor response. Myeloid-derived suppressor cells, or MDSCs, reside in tumors and secrete the enzyme arginase. Elevated arginase activity in the tumor depletes arginine, resulting in immunosuppression. In June, we selected CB-1158, as our lead clinical candidate. This orally active arginase inhibitor has shown inhibition of tumor growth in immunocompetent syngeneic mice. This inhibition of tumor growth is accompanied by a rapid increase in the local concentration of arginine, resulting in a rise in the number of CD3 positive T-cells within the tumor. This is similar to what happens when indoleamine 2,3-dioxygenase, or IDO, inhibitors block the degradation of tryptophan by IDO, leading to restoration of tryptophan levels in the tumor and activation of tumor-associated T-cells. CB-1158 has the potential for anti-tumor activity in renal cell cancer, non-small cell lung cancer, acute myeloid leukemia, and several other tumor types where arginase-secreting MDSCs are known to play an immunosuppressive role. CB-1158 may also have the ability to combine with other immuno-oncology therapies that target T-cell activation, such as CTLA-4 and PD-1 antibodies. We expect to present pre-clinical data on the arginase inhibitor program in the second half of 2015. In addition, we plan to file an investigational new drug application, or IND, for our lead first-in-class oral, selective arginase inhibitor in the first half of 2016. And with that I will pass it over to Will for an update on our financials.

Thanks, Susan. Calithera continues to be in a strong financial position today and remains on tract with current capital to advance our three programs to what we believe will be meaningful value inflection points for our shareholders. As for our financials, our cash, cash equivalents and investments as of June 30, 2015, were $88 million compared to $102 million as of December 31, 2014. The decrease was mainly driven by cash used to fund operating activities and clinical development of our lead program CB-839. Research and development expenses for the second quarter in 2015 were $5.5 million compared with $4.2 million in the prior year, an increase of $1.3 million which was primarily attributed to higher expenses again associated with the advancement of CB-839 into Phase 1 clinical trials and investments in the company's arginase inhibitor program. General and administrative expenses for the second quarter of 2015 were $2.3 million compared with $1.3 million in the prior year. The increase of $1 million was primarily due to higher employment-related expenses including stock-based compensation expenses and professional service fees related to the company's costs associated with operating as a publicly traded company. Loss from operations for the second quarter was $7.8 million resulting in a loss per share for the quarter of $0.44. Lastly, we continue to expect our cash position to be at least $65 million at the end of 2015 exclusive of any licensing milestone payments or funds arising from any additional equity financings, collaborations, or other new sources of capital. And with that, I will turn it back over to Susan.

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

Thank you. [Operator Instructions] Our first question comes from Matthew Andrews of Wells Fargo Securities. Your line is open.

Hi, good afternoon everybody, a couple of questions from me. Susan is the plan still to study 839 with dex. I noticed that you mentioned pom-dex study [indiscernible] the cohort with dex still in the works or eliminated? And then I know the translating results from pre-clinical studies to humans are of course challenging and have some monotherapy signals of efficacy. But could you just give us a sense in which tumor types for pre-clinical studies you think you’ve seen the greatest activity for the combination studies that you’ve run in vitro or in animals to date?

Certainly, so to answer your first question, there is a dex cohort as well as a pom-dex cohort, both combination therapies with CB-839 are currently enrolling.

Okay.

To answer your second question about the pre-clinical data that we have seen and how it translates to clinical data, I would say that our best pre-clinical data was for triple negative breast cancer for non-small cell lung cancer and for multiple myeloma because in those cases we were able to show regressions of tumors or certainly threat lining of the growth of the tumors with some regression. For all of those tumor types in the case of triple negative breast cancer, we saw regressions with paclitaxel added and we have a current combination arm and I think rolling right now in that indication. Also two for multiple myeloma with pomalidomide and dexamethasone and as we just said, we have an arm enrolling of that combination. In non-small cell lung cancer, we saw interesting results with EGFR inhibitors, again tumor regression. And we are planing to very shortly and open an EGFR inhibitor erlotinib plus CB-839 combination in the new combination arm again very shortly.

And then just one more sort of about a strategic 10,000 foot view level if you will for the arginase inhibitor program. I want you to establish a proof of concept, as the goal to immediately move it into a combination studies with checkpoint inhibitors for example, [indiscernible] inside approach with IDO inhibitor? Thanks.

Yes, that is the current plan.

Thank you. Our next question comes from Kennen Mackay with Citi. Your line is open.

Hi, this is actually [indiscernible]. I have a question for arginase inhibitor 1158 and could you please comment on more on your development plan and what kind of combination therapy could jump out as synergistic for the drug candidate? Thank you.

Sure. Any indicator – any drug that is involved in directly activating T-cell would be of interest to combine within arginase inhibitor because myeloid-derived suppressor cells are essentially a resistance mechanism or a block to allowing T-cells to move forward. So PD-1, PD-L1, CTLA-4 and most likely many new therapies coming down the path will all be able to release T-cells allow them to respond to antigenes and allow them to activate. However, if you have sufficient myeloid suppression, those T-cells will not be able to proliferate and then attack tumors because they have a block in their activation step. So it is the same step were IDO act at insufficient arginine level the T-cell receptor will not fully formed and the data chain of the TCR will not insert into the receptor at the membrane and therefore there will be no T-cell signaling. So it is a last step right before the T-cell is armed to go and kill a cancer cell. And that’s why it would have biologically a lot of synergy potentially with anything that just liberated the T-cell at another point in the pathway.

Thanks.

Thank you. [Operator Instructions] We have a follow-up question from Matthew Andrews with Wells Fargo Securities. Your line is open.

Hi, thank you for additional questions. So, Susan, you discussed this at the ASCO investor even, but can you just remind us how efficacy is being assessed going forward for your combination studies and I guess for the cohort expansion as well this Simon Two-Stage, will the hurdle be objective response or PFS for the efficacy hurdle to take the combinations forward? Thanks.

In differs in terms of the different combination arms. There are cases where we are expecting essentially no objective responses. And so in the first part of the Simon Two-Stage design, the hurdle is just seeing responses of above very low single-digit. In the case of combinations, which already have an inherent objective response, we’ve built in both the higher objective response hurdle and an assessment of progression fee survival, so compared to historical control, we wrote in the statistical hurdle that would allow us to go significantly above, what we knew for historical controls of the combination drug without CB-839.

Okay, great thank you.

Thank you. I'm showing no further questions. I would like to turn the call back to Susan Molineaux for closing remarks.

Thank you. And once again thanks everyone for joining the call today. In closing, we look forward to seeing you at multiple investor conferences in early autumn. In addition we plan to present multiple scientific presentations and medical meetings, including the first presentation of the arginase preclinical data as well as clinical and scientific updates on CB-839 in the second half of the year. We will be in our office to take calls this afternoon. Thank you and have a good day.

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