Targeting cancer, differently. Susan M. Molineaux, Ph.D. | Founder, President & Chief Executive Officer Exhibit 99.1

Forward-Looking Statements This presentation and the accompanying oral commentary contain “forward‐looking” statements for purposes of the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. We may, in some cases, use terms such as “believe,” “will,” “may,” “estimate,” “continue,” “anticipate,” “intend,” “should,” “plan,” “might,” “approximately,” “expect,” “predict,” “could,” “potentially” or the negative of these terms or other words that convey uncertainty of future events or outcomes to identify these forward‐looking statements. All statements other than statements of historical facts contained in this presentation and the accompanying oral commentary are forward‐looking statements, and such forward‐looking statements include statements regarding our intentions, beliefs, projections, outlook, analyses or current expectations concerning, among other things: plans regarding anticipated clinical trials for our product candidates, including CB-228 (sapanisertib), CB-659 (mivavotinib), CB-280, INCB001158 and CB-708, the potential safety, efficacy and other benefits of and market opportunity of product candidates, the timing of and our ability to make regulatory filings and obtain and maintain regulatory approvals for our product candidates, statements relating to future royalties and the development, regulatory and sales milestone payments of INCB001158 and CB-708 in connection with our collaborations with Incyte and Antengene, respectively, and of CB-228 and CB-659 in connection with our asset purchase agreement with Takeda, our intellectual property position and cash needs. Forward‐looking statements involve known and unknown risks, uncertainties, assumptions and other factors that may cause our actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward‐looking statements. The potential product candidates that we develop may not progress through clinical development or receive required regulatory approvals within expected timelines or at all. In addition, clinical trials may not confirm any safety, potency or other product characteristics described or assumed in this presentation and the accompanying oral commentary. Such product candidates may not be beneficial to patients or be successfully commercialized. The failure to meet expectations with respect to any of the foregoing matters may have a negative effect on our stock price. We discuss many of these risks in greater detail under the heading "Risk Factors" contained in our Quarterly Report on Form 10‐Q for the quarter ended September 30, 2021, filed with the Securities and Exchange Commission on November 9, 2021. Forward‐looking statements are not guarantees of future performance and our actual results of operations, financial condition and liquidity, and the development of the industry in which we operate may differ materially from the forward‐looking statements contained in this presentation and the accompanying oral commentary. Any forward‐looking statements that we make in this presentation and the accompanying oral commentary speak only as of the date of this presentation. We assume no obligation to update our forward‐looking statements whether as a result of new information, future events or otherwise.

Calithera Today Core expertise in oncology, discovering and developing novel small molecule enzyme inhibitors Primary focus is on precision oncology Nimble and well-versed in conducting biomarker-driven early and late stage clinical trials Recent addition of two mature mid-stage clinical assets to our pipeline With this acquisition from Takeda Pharmaceuticals, we fully own all development and commercial rights We have developed a new biomarker-driven clinical strategy for both compounds Potential for rapid approval paths in genetically-defined patient populations Robust discovery engine creating a preclinical pipeline of synthetic lethal targets Experienced leadership team across a fully-integrated biopharmaceutical company Expected cash runway into 2023 sufficient to reach next clinical milestones on both new programs

Strong Management Experienced Leadership Stephanie Wong Chief Financial Officer & Secretary Eric Sjogren, Ph.D. Senior Vice President of Drug Discovery Susan Demo, Ph.D. Senior Vice President of R&D Operations Matthew Gross Vice President of Business Development Susan Molineaux, Ph.D. Founder, President & Chief Executive Officer Christopher Molineaux, Ph.D. Senior Vice President of Development Frank Parlati, Ph.D. Senior Vice President of Research Allison Dillon, Ph.D. Senior Vice President of Commercial & Portfolio Strategy Emil Kuriakose, M.D. Chief Medical Officer Sumita Ray Chief Legal & Administrative Officer Board of Directors Sunil Agarwal, M.D. Chief Development Officer, Sana Biotechnology Jonathan G. Drachman, M.D. CEO, Neoleukin Therapeutics Scott Garland CEO, PACT Pharma Suzy Jones Founder & Managing Partner, DNA Ink Susan Molineaux, Ph.D. Founder, President & CEO, Calithera Keith Orford, M.D., Ph.D. CMO, FogPharma Deepa Pakianathan, Ph.D. Managing Member, Delphi Ventures Blake Wise CEO, Novome Biotechnologies H. Ward Wolff Former CFO, Sangamo Therapeutics

New Clinical and Preclinical Pipeline Synthetic Lethality VPS4A/VPS4B (ATPases) Preclinical program: paralogs Inhibitor to target tumors with one deleted paralog NGS biomarker defined Potential for large market SYK inhibitor Biomarker-defined clinical activity in ABC DLBCL Ph 2A/2B trial in ABC DLBCL initiating in 1Q22 Ph2a single agent data expected 4Q22-1Q23 Mivavotinib Sapanisertib mTORC1/2 inhibitor Biomarker-defined clinical activity in NRF2m sqNSCLC Ph 2A/2B trial in NRF2m sqNSCLC initiating in 1Q22 Ph2a single agent data expected in 4Q22-1Q23

Calithera Pipeline: Focus on Precision Oncology Program Target Indication DISCOVERY PRE-IND PHASE 1 PHASE 2 PHASE 3 MivavotinibSYK ABC DLBCL Sapanisertib mTORC1/2 NRF2 mutated sqNSCLC VPS4A VPS4B mutated solid tumors CB-280 Arginase Cystic Fibrosis Partnered Programs ‘1158 Arginase Solid tumors ATG-037 CD73 Solid tumors

Mivavotinib SYK inhibitor for NHL

Mivavotinib Overview SYK Inhibitor Entering a Phase 2 Trial in Diffuse Large B-Cell Lymphoma (DLBCL) 2Schmitz, N Engl J Med 2018;378:1396-407 3Wilson, Cancer Cell 2021;39:1-11 1Gordon, Clin Cancer Res 2020;26:3546-56. C34001 and C34004 CSRs (Unpublished data on file) In NHL trials mivavotinib was active, with durable single agent responses in DLBCL 1 Our initial development is in ABC DLBCL where BCR signaling and SYK activation are central drivers of tumor growth, and mivavotinib is most active ~50% 2,3 of ABC DLBCL have MYD88 and/or CD79b mutations that hyperactivate SYK and are predicted to have enhanced sensitivity to mivavotinib Fast-to-market opportunity in a biomarker-defined DLBCL population Biomarker-specific clinical data expected in 4Q22-1Q23

Mivavotinib has Durable Single Agent Responses in R/R DLBCL 1C34001 and C34004 CSRs (Unpublished data on file) *Mivavotinib 100 mg QD Response evaluable population Probability of Maintaining a Response Months mDOR not reached (95% CI: 7 mos-NE) Pts N* CR ORR R/R DLBCL 81 16% (13/81) 33% (27/81) Mivavotinib is an orally dosed, potent and selective SYK kinase inhibitor IP protection through 2036 US/2035 EU assuming full 5-year patent term extension In NHL trials1, mivavotinib had impressive single agent activity in late stage DLBCL patients Responses were durable over several months, with mDOR not reached Duration of Response Response Rate in DLBCL

Mivavotinib is Differentiated from Other SYK Inhibitors SYK Inhibitor ORR Mivavotinib1 33% (27/81)* Entosplentinib2 0% (0/43)** Fostamatinib3 3% (2/68)** Cerdulatinib4 8% (1/12)** Assay Species Mivavotinib Entospletinib Vol of Distribution (L/kg) Rat 9.5 0.55 Dog 6.7 1.45 Tumor/Plasma AUC Ratio Mouse 3.6* - Protein Binding Human 54.9% 97.1%5 Plasma Half-Life Human 38 hrs 9-15 hrs6 *Plasma and tumor concentrations of mivavotinib following oral dosing in MV411 tumors Mivavotinib has higher response rates in DLBCL Mivavotinib achieves higher tissue and tumor exposure *Response evaluable, 100 mg QD **ITT Higher clinical activity could be due to higher tissue penetration and duration of target engagement 1Gordon, Clin Cancer Res 2020;26:3546-56. C34001 and C34004 CSRs (Unpublished data on file) 2Burke, Clin Lymphoma, Myeloma & Leukemia 2018;18:e327-e331. 3Flinn, Eur J Cancer 2016;54:11-7 4Coffey, Clin Cancer Res 2019;25:1174-84. 5Currie et al, J of Med Chem 2014; 57: 3856-73 6Ramanathan Clin Drug Investig 2017 37:195-205

Safety Profile of Mivavotinib in DLBCL is Favorable For Development as Monotherapy or in Combination with Other Drugs >300 patients with heme malignancies treated with mivavotinib Favorable safety profile Most common AEs were asymptomatic and reversible laboratory abnormalities Mivavotinib is combinable with bendamustine-rituximab, ibrutinib, venetoclax2, and R-CHOP3 1Safety data from 89 DLBCL patients in the C34001 study 2Data from C34005 3Karmali, ASH Poster 2021 TEAEs ≥ 10% in DLBCL patients (N=89)1

Current DLBCL Treatment Landscape R-CHOP Standard treatment for newly diagnosed DLBCL patients Salvage chemotherapy Stem cell transplant CAR-T therapies ADCs (Polatuzumab, Loncastuximab) Antibodies (Tafasitamab) Selinexor Relapse/Refractory Remission High unmet need remains for patients who are ineligible for, or relapse after, CAR-T or transplant Currently no defined patient selection strategies to optimize therapy for patients with R/R DLBCL A fully oral regimen with enriched efficacy in a biomarker-defined subset of DLBCL meets a key unmet need

DLBCL Disease Characteristics ABC (Activated B-Cell) ~50% GCB (Germinal Center B-cell) ~40% Unclassified ~10% DLBCL treatments are the same for all patients, despite the fact that it is a biologically heterogeneous disease3 DLBCL is the most common form of lymphoma, representing ~30% of all NHL diagnoses1 ~30,000 people diagnosed in the US each year, with ~60% 5 year survival1,2 1Decision Resources Group, epidemiology, DLBCL incidence 2021 2https://seer.cancer.gov/statfacts/html/dlbcl.html 3Mareschal, Haematologica 2011;96:1888-90. 4Schmitz, N Engl J Med 2018;378:1396-407 Chronic activated BCR signaling ABC patients have a poorer prognosis Fewer curative responses to R-CHOP and shorter OS3,4 Currently no approved treatments specific for ABC patients

SYK Controls Central Activation Pathways in ABC DLBCL The ABC DLBCL subgroup is defined by chronic activation of the BCR signaling pathway In ABC DLBCL, SYK activates NF-kb and PI3K pathways, driving both proliferation and survival In contrast, in GCB DLBCL SYK activates the PI3K pathway Pathway biology predicts SYK inhibition to be active in both ABC and GCB, with higher activity in ABC Efremov, Cancers 2020;12:1396-1434.

Mivavotinib Activity is Highest in ABC DLBCL *Response evaluable population Patients of unknown cell-of-origin are excluded Cell of Origin N* ORR ABC (non-GCB) 15 53% GCB 45 22% Retrospective analysis of ORR by cell of origin shows enriched activity in ABC patients R/R DLBCL Unpublished data; combined analysis of Takeda studies C34001 and C34004 *3 pts with PD as best response not graphed (target lesions not recorded) *

MYD88 and CD79b Mutations Hyperactivate SYK ~50% of ABC DLBCL tumors have one or both mutations1,2 3Munshi, Blood Cancer J 2020;10:12 4Phelan, Nature 2018;560:387-391. 5deGroen, Haematologica 2019;104:2337-48 6Wilson, Nat Med. 2015; 21(8): 922–926 1Schmitz, N Engl J Med 2018;378:1396-407 2Wilson Cancer Cell 2021;39:1-11. 1 2 In ABC DLBCL, the BCR pathway is chronically activated, and SYK is key for activating NFkB NFkb CD79m SYK is hyperactivated Drives BCR signaling MYD88m SYK is hyperactivated Drives BCR and TLR signaling3,4,5 CD79m and CD79m/MYD88m BTK inhibitors active6 MYD88m (~70%) BTK inhibitors not active6 BTK Mivavotinib expected to be active in CD79b and MYD88 mutated DLBCL In a retrospective analysis, 2 out of 3 patients with known CD79b mutations had CRs (1 DLBCL, 1FL)

Trial Design for Mivavotinib in R/R ABC DLBCL Objectives Further define patient population and refine RP2D dose** Safety and tolerability Anti-tumor efficacy Biomarker validation Enroll biomarker defined cohorts for potential accelerated approval study Primary endpoint: ORR Safety and tolerability Secondary endpoints: DOR, PFS, OS MYD88m and/or CD79m ABC (non-GCB) R/R DLBCL WT ABC (non-GCB) R/R DLBCL ABC (non-GCB) R/R DLBCL and/or *ctDNA based liquid NGS performed in parallel to enroll a pre-specified number of patients harboring MYD88/CD79b mutations ** Doses: 100 mg QD or 120 mg QD for 2 wks, 80 mg QD FPI expected in 1Q22 Enroll ABC DLBCL MYD88m and/or CD79m ABC (non-GCB) R/R DLBCL NGS* Phase 2a Population Defining Phase 2b Registration Enabling

Clinical Expansion of Mivavotinib Into Other Indications Earlier Stage DLBCL and Other Heme Malignancies Monotherapy (R/R DLBCL) ABC (including MYD88/CD79bm) GCB (biomarker exploration) Combination Mivavotinib + SOC DLBCL drugs Monotherapy (R/R WM) MYD88 mutant (95%) Combination (earlier lines of therapy) Mivavotinib + SOC WM drugs DLBCL Waldenstrom’s Macroglobulinemia Potential for further development In FL, CLL and AML

Mivavotinib Summary DLBCL projected to be ~$8B market by 2026 High unmet need in R/R for treatments with biomarkers to identify patients most likely to benefit Potential to expand beyond initial line of therapy and indication based on activity as a single agent and combinability as a tolerable, oral agent Market Opportunity and Unmet Need Deep and durable single agent activity in DLBCL and other NHL Mivavotinib has enhanced activity in ABC DLBCL, where unmet need is high, and potential in MYD88 and CD79b patients DLBCL provides a near term clinical readout and a fast-to-market strategy Potential to be the first biomarker-driven drug in DLBCL

Sapanisertib mTORC1/2 Inhibitor for NRF2-mutated Squamous NSCLC

Sapanisertib Overview mTORC1/2 Inhibitor Entering a Phase 2 Trial in NRF2-Mutated Squamous NSCLC (sqNSCLC) *NFE2L2 1Paik, J Clin Oncol 2020;38 15 suppl: 9607 A recent Ph 2 trial showed durable single agent activity of sapanisertib in a NRF2m* subset of sqNSCLC patients, a genetically defined group with poorer prognosis 1 Sapanisertib has a well-established and manageable safety profile Possible future expansion to NRF2m populations in other tumor types Initial development of sapanisertib will be in R/R NRF2m sqNSCLC Potential to be the first approval in a NRF2m patient population

Sapanisertib has Durable Single Agent Activity in NRF2m R/R SqNSCLC Patients Paik, J Clin Oncol 2020;38 15 suppl: 9607 Mutation Indication ORR * mPFS NRF2m SqNSCLC 27% (3/11) 8.9 mo KEAP1m SqNSCLC 17% (1/6) KEAP1m + KRASm Adeno NSCLC 0% (0/5) *Sapanisertib at 3 mg QD Response evaluable population NRF2m sqNSCLC KEAP1m sqNSCLC KEAP1m/KRASm adenoNSCLC Sapanisertib is a potent and selective oral inhibitor of mTORC1/TORC2 IP protection through 2036 US/2034 EU assuming full 5-year patent term extension Sapanisertib has single agent activity (27% ORR) in heavily pre-treated NRF2m sqNSCLC patients Responses were durable with a mPFS of 8.9 months (95% CI 7 mo-NR)

NRF2 or KEAP1 mutant tumors constitutively activate the oxidative stress pathway to support survival NRF2 activation upregulates mTOR activity Sapanisertib inhibits mTORC1/2, blocking proliferation and inducing cell death Sapanisertib is More Active than Other mTOR Inhibitors in NRF2m sqNSCLC Animal Models Paik, J Clin Oncol 2020;38 15 suppl: 9607 Shibata, Cancer Res. 2010;70:9095-105. Bendavit, J Biol Chem 2016;291:25476-88. Sapanisertib Sapanisertib (MLN0128) NRF2m LK-2 Xenograft Several mTOR inhibitors (sapanisertib [MLN0128]), everolimus, AZD2014 (vistusertib), and deforolimus) were dosed in a NRF2m sqNSCLC xenograft Sapanisertib was the only inhibitor to have strong single agent efficacy TORC1 inhibitors (everolimus and deforolimus) were not active

Sapanisertib was Well-tolerated in R/R Solid Tumor Patients Grade ≥3 Adverse Events of any Cause in ≥2% of Patients 1 Paik, J Clin Oncol 2020;38 15 suppl: 9607 (NSCLC) 2 Moore, ESMO Open 2018;3:1-11. (Solid tumors) 3 Phase 1 CSR INK128-001 and Voss et al., Brit J Cancer 2020;123:1590–8. (Solid tumors) Sapanisertib on a QD schedule (3-5 mg QD) was evaluated in 3 separate trials in NSCLC and other solid tumor patients Predominantly Gr1/2 TEAEs Most commonly observed TEAE was hyperglycemia Well controlled with oral hypoglycemic therapy and home glucose monitoring Only one discontinuation (1/93) for hyperglycemia at these QD doses Ph 2 Studies of Sapanisertib in Patients With Solid Tumors Adverse Event 3 mg QD1 3 mg QD2 4 mg QD2 4 mg QD3 5 mg QD3 Total (N=30) (N=11) (N=6) (N=7) (N=39) (N=93) Hyperglycemia 14 (47) 1 (9) 1 (17) 2 (29) 5 (13) 23 (25) Rash macular 4(13) 1 (9) 1 (17) 0 3 (8) 9 (10) Fatigue 0 0 2 (33) 0 5 (13) 7 (8) Hypophosphatemia 0 0 0 0 4 (10) 4 (4) Stomatitis 0 0 1 (17) 0 3 (8) 4 (4) Abdominal pain 0 1 0 0 3 (8) 4 (4) Hyponatremia 0 1 (9) 1 (17) 1 (14) 1 (11) 4 (4) Hyperkalemia 0 0 0 1 (14) 2 (5) 3 (3) Dyspnea 0 0 0 0 2 (5) 2 (2) Acute kidney inj. 0 0 0 0 2 (5) 2 (2) Thrombocytop. 0 0 0 0 2 (5) 2 (2) Hematuruia 0 0 0 0 2 (5) 2 (2) Pneumonia 0 0 0 0 2 (5) 2 (2)

Squamous NSCLC Landscape https://seer.cancer.gov/statfacts/html/lungb.html Data from TCGA BioPortal https://www.cbioportal.org/ https://www.cancer.gov/types/lung/hp/non-small-cell-lung-treatment-pdq#_359 NCCN NSCLC guidelines June 2021 Garon, Lancet 2014;384:665-73. Rizvi, Oral Abstract OA04.07: World Conference on Lung Cancer, 2019 for all NSCLC 50,000-60,000 patients diagnosed in the US each year 25-30% of NSCLC 1 Only 1-5% of tumors have actionable mutations such as EGFR , KRAS, etc. 2 Five year survival rate is 6% 1 1L SOC anti PD-1 and chemo 3 2L SOC Salvage chemo 3 (mPFS 3-4.5 mo) 5 15% NRF2 mutants 2 Prognosis is poorer in patients with these mutations 6

Clinical Development Plan for Sapanisertib Objectives Refine RP2D* and validate NRF2m patient selection strategy Safety and tolerability Anti-tumor efficacy Validate NRF2m biomarker Enroll NRF2m sqNSCLC expansion cohort for single arm or randomized study Primary endpoint: ORR (potential accel approval) Secondary endpoints: DOR, PFS, OS Primary endpoint: PFS (full approval) Safety and tolerability Expansion in NRF2m sqNSCLC at RP2D for potential accelerated approval Randomized study versus SOC for full approval and/or FPI expected in 1Q22 NRF2m R/R sqNSCLC WT R/R sqNSCLC NGS screen for NRF2 mutations 2 mg BID or 3 mg QD Phase 2a Population Defining Phase 2b Registration Enabling

Potential to Treat NRF2/KEAP1 Mutations in Other Tumor Types Many patients could potentially benefit from treatments specific to this pathway Data from TCGA BioPortal https://www.cbioportal.org/ Histology NRF2 mutation frequency KEAP1 mutation frequency Total mutation frequency NSCLC squamous 15% 12% 27% NSCLC adeno 2% 19% 21% Bladder 9% 3% 12% Esophagus 9% 3% 12% HNSCC 5% 4% 9% HCC 4% 5% 9% Cholangiocarcinoma 3% 6% 9% Uterine 6% 2% 8% Cervical 6% 0.5% 6.5% Gastric 0.5% 2.5% 3% papRCC 2% 1% 3% CRC 1% 2% 3% ccRCC 1.5% 0.5% 2% Melanoma 1% 1% 2% Pancreatic 0% 1% 1% Breast 0.3% 0.4% 0.7%

Sapanisertib Summary SqNSCLC is expected to be a $4.5B market by 20261 NRF2 mutations account for 15% of all sqNSCLC patients High unmet need for biomarker-driven treatments in sqNSCLC patients NRF2m SqNSCLC Market Opportunity and Unmet Need Sapanisertib Potential 1DRG Nov 2021 Single agent activity with durable responses in NFR2m sqNSCLC Safety profile favorable for development as monotherapy and/or in combination Potential first-in-class treatment for NRF2m sqNSCLC patients Potential to expand into NRF2 mutant populations in other cancers

CB-280 Arginase Inhibitor for Cystic Fibrosis

Rationale for Arginase Inhibitors in Cystic Fibrosis Despite recent advances with CFTR modulators, many patients still have impaired lung function Arginase plays a critical role in CF airway disease1, 2, 3 Decreases nitric oxide (NO) production4, increases production of polyamines and proline Inhibition of arginase should increase NO, increasing anti-microbial activity and improving airway function5 Potential for additional benefit when combined with standard of care therapies6 Potential benefit in all CF patients, regardless of CFTR genotype CB-280 is an investigational first-in-class orally-dosed arginase inhibitor in Phase 1b trials supported by a grant from the Cystic Fibrosis Foundation Grasemann et al., Am J Respir Crit Care Med 172: 1523-1528, 2005 Grasemann et al., Respiratory Research 7: 87, 2006 Jaecklin et al., J Appl Physiol 117: 284-288, 2014 Grasemann et al., Eur Respir J 25: 62-68, 2005 Mermis et al, NACF-2020-CX-280-202-TIP-POSTER-08Sep2020 Wu, Mol Pharmacol 96:515-525, 2019

Ongoing Randomized Double Blind Ph1b Trial in CF Interim Analysis Key Conclusions CB-280 was well-tolerated, showed linear PK and demonstrated robust dose-related PD effects Encouraging trends seen in disease biomarkers including increased FeNO and decreased sweat chloride Early positive trend seen in FEV1, a safety endpoint Cohort 4 (300 mg) enrollment is complete with analysis ongoing Additional dose cohort to enroll in 2022 if warranted Ph1b Interim Data Presented at North American Cystic Fibrosis Conference Boas et al. Abstract 529 North American Conference for Cystic Fibrosis, November 2021. Primary Endpoint: Safety Secondary Endpoints: PK/PD: arginase inhibition and arginine increase assessed in plasma and sputum Exploratory Endpoints: FENO, sweat chloride, sputum colonization

Synthetic Lethality in Solid Tumors VPS4A Program

Synthetic Lethality Research Pipeline: VPS4 VPS4A and VPS4B are paralog ATPases essential for remodeling intracellular organelle membranes1,2 Loss of function of both paralogs is lethal VPS4B homozygous deletion occurs in 1-3% of several solid tumor types3 VPS4B heterozygous deletion is common across solid tumor cancers2,3 Most notably in CRC and PDAC (~65%) Occurs frequently because of proximity to tumor suppressors SMAD2/4 Heterozygous or homozygous loss of VPS4B in cancer cells makes them vulnerable to inhibition of VPS4A2 Calithera has identified small molecule inhibitors of VPS4 VPS4 is our most advanced synthetic lethality program Adell FEBS Journal 283 (2016) 3288-3302 1Szymanska EMBO Molecular Medicine 2020 12:e10812 2Neggers Cell Rep 2020 33 (11): 108493 3Data from TCGA BioPortal https://www.cbioportal.org/

Calithera Today: Significant Value Creation Three clinical stage programs Biomarker-defined clinical development for our two oncology drugs Upcoming Milestones Data for mivavotinib and sapanisertib expected in 4Q22-1Q23 Leveraging an experienced management team Research pipeline for synthetic lethality targets in biomarker defined patient populations