NASDAQ: MRTX Targeting the genetic and immunological drivers of cancer Corporate Presentation April 2019 1
Safe Harbor Statement Certain statements contained in this presentation, other than statements of fact that are independently verifiable at the date hereof, are "forward-looking" statements, within the meaning of the Private Securities Litigation Reform Act of 1955, that involve significant risks and uncertainties. Forward looking statements can be identified by the use of forward looking words such as believes, expects, hopes, may, will, plan, intends, estimates, could, should, would, continue, seeks, pro forma, or anticipates, or other similar words (including their use in the negative), or by discussions of future matters such as the development of current or future product candidates, timing of potential development activities and milestones, business plans and strategies, possible changes in legislation and other statements that are not historical. Forward-looking statements are based on current expectations of management and on what management believes to be reasonable assumptions based on information currently available to them, and are subject to risks and uncertainties. Such risks and uncertainties may cause actual results to differ materially from those anticipated in the forward-looking statements. Such risks and uncertainties include without limitation potential delays in development timelines, negative clinical trial results, reliance on third parties for development efforts, changes in the competitive landscape, changes in the standard of care, as well as other risks detailed in Mirati's recent filings on Forms 10-K and 10-Q with the U.S. Securities and Exchange Commission. Except as required by law, Mirati undertakes no obligation to update any forward-looking statements to reflect new information, events or circumstances, or to reflect the occurrence of unanticipated events. 2 April 1, 2018
Mirati Therapeutics Answering Cancer s Challenges with a Targeted Approach We Are Experienced: A Team of Knowledgeable Oncology Drug Developers with a Track Record of Success in Rapidly Developing Multiple Therapies from Preclinical to the Market Oncology Experience Applying Proven Approaches to the Development of Sitravatinib and KRAS We Are Focused: Addressing Areas of Unmet Need for Patients in Large Patient Populations > Treating cancer progression after checkpoint inhibitor therapy > Targeting previously undruggable KRAS mutations across multiple tumor types Utilizing our Knowledge to Expedite Development of our Novel Approaches 3
Mirati s Development Programs Indication Preclinical Phase 1/1b Phase 2 Phase 3 Current Status NSCLC Phase 3 Expected to be Initiated 1H 2019 Immuno-oncology Sitravatinib + checkpoint inhibitor Bladder Phase 2 Initiated September 2018 Sitravatinib Oral Multi Kinase Inhibitor MOA Trials RCC, Head & Neck Mechanism of Action Trials Initiated September 2018 BeiGene Sitravatinib + Tislelizumab (anti-pd-1) NSCLC, RCC, HCC, Gastric, Ovarian, other BeiGene-led Trials Initiated November 2018 Targeted Single Agent CBL mutations NSCLC Melanoma Ongoing Phase 1b Focused on CBL in NSCLC and Melanoma KRAS Oral KRAS Inhibitors Targeted Single Agent MRTX849 G12C mutations Targeted Single Agent G12D mutations NSCLC CRC Pancreatic CRC, NSCLC, Pancreatic 1 st Patient Enrolled January Clinical Candidate Identification Underway 4 NSCLC = non-small cell lung cancer; CRC = colorectal cancer; RCC = renal cell cancer; HCC = hepatocellular cancer; IND = Investigational New Drug application; Tislelizumab (BeiGene s anti PD-1) MOA = Mechanism of Action
Immuno-Oncology Combinations Sitravatinib + Checkpoint Inhibitors 5 5
6 Sitravatinib in the Tumor Microenvironment May Restore Immune Response
Sitravatinib + Checkpoint Inhibitors Phase 2 Trial of Sitravatinib + Nivolumab in Checkpoint Refractory NSCLC MRTX-500 Trial Phase 2 Trial Design Checkpoint Refractory NSCLC Expansion Criteria (PRs) Stage 1 Stage 2 Expansion Criteria (PRs) Stage 3 Key Inclusion Criteria: Advanced/metastatic NSCLC Documented radiographic progression on prior checkpoint inhibitor therapy Checkpoint Refractory NSCLC Documented Tumor Progression Prior Clinical Benefit No Prior Clinical Benefit 1 PR 3 PR n=9 n=8 n=40+ 1 PR 3 PR n=9 n=8 n=40+ Key Exclusion Criteria: No intervening therapy following progression on checkpoint inhibitor therapy No significant immune-related AEs with prior checkpoint therapy Exclude patients with known driver mutations Endpoints: Primary: ORR Secondary: Safety and tolerability, duration of response, PFS, OS, PK 7 Sitravatinib: Dose 120mg daily Nivolumab: Dose 3mg/kg every 2 weeks (full labeled dose) Study cycles of 28 days, with disease assessment scans every 2 cycles
Sitravatinib + Checkpoint Inhibitors Phase 2 Trial of Sitravatinib + Nivolumab in Checkpoint Refractory NSCLC Maximum % Change from Baseline 70% 60% 50% 40% 30% 20% 10% 0% -10% -20% -30% -40% -50% -60% -70% -80% -90% -100% * On study as of 27-Aug-18 Complete response (1 target lymph node) BEST RESPONSE 1 (Evaluable Patients, N=56) Confirmed Response Stable Disease Progressive Disease 42/56 (75%) Clinical Benefit (SD+PR+CR) 18/56 (32%) Tumor Regression >30% * 11/56 (20%) Confirmed CR/PR 8 Study cycles of 28 days, with disease assessment scans every 2 cycles 1. Data cut-off: 27-Aug-2018; presented at ESMO 2018 Congress. Response data per investigator assessment, response confirmations updated after data cut-off.
Sitravatinib + Checkpoint Inhibitors Phase 2 Trial of Sitravatinib + Nivolumab in Checkpoint Refractory NSCLC DURATION OF TREATMENT (Evaluable Patients, N=56) 50 * Confirmed Response Stable Disease Progressive Disease 40 Response first achieved 30 on study On study as of 27-Aug-18 Off study Complete response (1 target lymph node) 20 * Preliminary Kaplan-Meier Estimate of Median Duration of Response: 9.2 months 10 9 0 4 8 12 16 20 24 28 32 36 40 44 48 52 56 60 64 Weeks Study cycles of 28 days, with disease assessment scans every 2 cycles 1. Data cut-off: 27-Aug-2018; presented at ESMO 2018 Congress. Response data per investigator assessment, response confirmations updated after data cut-off.
Clinical Practice in 1 st Line NSCLC has Changed The checkpoint refractory population is now in 2 nd line Sitravatinib + Checkpoint Inhibitors Prior Standard of Care No/Low PD-L1 High PD-L1 Stage IV Non-Squamous NSCLC Treatment Paradigm New Standard of Care No/Low PD-L1 High PD-L1 1L Platinum Doublet PD-1 1L PD-1 + Chemo PD-1 2L PD-(L)1 Platinum Doublet 2L Checkpoint Refractory Patients Platinum Doublet 3L Checkpoint Refractory Patients Docetaxel 3L 3 rd line population is diminishing Docetaxel By 2022 It is estimated that >50,000 patients in US/EU will be 2 nd line Checkpoint Refractory 1 10 1. Kantar Health CancerMPact Treatment Architecture, Kantar Health projections. Excludes patients with addressable driver mutations
Sitravatinib + Checkpoint Inhibitors Phase 3 Randomized Trial in 2 nd Line NSCLC Two Opportunities for Approval in 2 nd Line NSCLC Interim Analysis: ORR, for Accelerated Approval Primary Analysis: OS, for Full Approval Preliminary Study Design Key Inclusion/Exclusion Criteria: Advanced, Non-Squamous NSCLC Checkpoint Refractory 2 nd Line NSCLC Documented Tumor Progression RANDOMIZATION 1:1 Sitravatinib + Nivolumab Docetaxel Primary Analysis OS N:~620 pts Progression on or following first line combination of PD-(L)1 inhibitor plus chemotherapy Excludes patients with known driver mutations Endpoints: Interim: ORR (for potential Subpart H accelerated approval) Primary: OS (for potential full approval) Secondary: PFS, duration of response, safety, tolerability Interim Analysis ORR Projected Phase 3 Timing: Study Initiation: 1H 2019 Interim ORR Analysis: Year End 2020 Primary OS Analysis: Year End 2021 11
Sitravatinib + Checkpoint Inhibitors Docetaxel: An Efficacy Comparator Used in Prior 2 nd Line NSCLC Trials Advanced NSCLC 2 nd Line or Subsequent Therapy Trial Compound Pts ORR, % DOR, Mos PFS, Mos (Range) SD, % CBR, % (CR+PR+SD) OS, Mos (Range) 057 [1] Docetaxel n=290 12% 5.6 4.2 (3.5-4.9) 42% 54% 9.4 (8.1-10.7) CheckMate Nivolumab n=292 19% 17.2 2.3 (2.2-3.3) 25% 44% 12.2 (9.7-15.0) Checkpoint Naïve Patients Atezolizumab n=425 14% 16.3 2.8 (2.6-3.0) 35% 49% 13.8 (11.8-15.7) Docetaxel n=425 13% 6.2 4.0 (3.3-4.2) 42% 55% 9.6 (8.6-11.2) Not yet Pembrolizumab n=345 18% KEYNOTE reported 3.9 (3.1-4.1) 10.4 (9.4-11.9) 010 [3] Docetaxel n=343 9% 6.1 4.0 (3.1-4.2) 8.5 (7.5-9.8) Checkpoint Refractory Patients MRTX-500 [4] Sitravatinib + Nivolumab n=56 20% 9.2* 6.8* 55% 75% 15.1* 12 1. Borghaei H, et al. N Engl J Med. 2015;373:1627-1639. 2. Rittmeyer A, et al. Lancet. 2017;389:255-265. 3. Herbst RS, et al. Lancet. 2016;387:1540-1550. 4. Mirati ESMO 2018 Congress Data presented is from separate studies and does not reflect results that might have been obtained from head-to-head studies. Results from Mirati's planned Phase 3 trial comparing sitravatinib + nivolumab to docetaxel may differ materially from prior studies presented. ORR = Overall Response Rate DOR = Duration of Response CBR = Clinical Benefit Rate (CR + PR + SD>14 weeks) * Preliminary Kaplan-Meier Estimate
Sitravatinib + Checkpoint Inhibitors Sitravatinib Value Creation and Expansion Strategy Mirati Development Activities 1 Advance Sitravatinib Towards Registration NSCLC Phase 3: 2 nd line checkpoint refractory Interim Analysis for Potential Accelerated Approval End of 2020 2 Extend Proof of Concept into Other Tumor Types Bladder Phase 2: checkpoint refractory Initial Proof of Concept Clinical Data Expected 2H 2019 3 Expand Mechanism of Action Data RCC Pre-surgical study HNSCC Pre-surgical study Early Mechanism of Action Data Expected 2H 2019 13 NSCLC = non-small cell lung cancer; RCC: renal cell cancer; HNSCC: head & neck squamous cell cancer Note: HNSCC pre-surgical mechanism of action study is investigator-sponsored
BeiGene / Mirati Collaboration: Expanding the Value of Sitravatinib Sitravatinib + Checkpoint Inhibitors BeiGene Development Activities 1 Generate Additional Proof of Concept Data in New Indications and With Another PD-1 Inhibitor BeiGene-Sponsored Clinical Trials 2 (in China and Australia) NSCLC: checkpoint naïve & refractory Independent confirmation in NSCLC with another PD-1 inhibitor RCC: checkpoint naïve & refractory Ovarian: checkpoint naïve HCC: checkpoint naïve & refractory Gastric: checkpoint naïve Initial Proof of Concept Clinical Data Expected 2H 2019 Initial Proof of Concept Clinical Data Expected 1H 2020 BeiGene will Fund and Conduct Multiple I/O Combination Trials with Sitravatinib 250+ Patients Across 5 Tumor Types in Initial Proof of Concept Trials Leverages BeiGene s Considerable Clinical Development Capabilities Access to Difficult-to-Enroll Patient Populations in China Provides Further Proof of Concept with Another PD-1 Inhibitor: Tislelizumab 14 1. Sitravatinib is licensed to BeiGene, Ltd. in China, Asia (less Japan, Russia and India), Australia and New Zealand 2. In BeiGene s combination trials, Sitravatinib will be tested in combination with BeiGene s PD-1 inhibitor, tislelizumab NSCLC = non-small cell lung cancer; RCC: renal cell cancer; HNSCC: head & neck squamous cell cancer
Sitravatinib + Checkpoint Inhibitors Sitravatinib IO Combinations Summary Positive Interim Phase 2 Efficacy Data in Checkpoint Refractory NSCLC 1 (n=56) 42/56 (75%) demonstrated Clinical Benefit (Stable Disease, Partial Response or Complete Response) 11/56 (20%) achieved a confirmed Partial or Complete Response Preliminary Kaplan-Meier estimates Median Duration of Response: 9.2 months Median Progression Free Survival: 6.8 months Median Overall Survival: 15.1 months Registration Path: FDA Agrees to Phase 3 Design with Potential for Accelerated Approval Phase 3 randomized trial with potential for accelerated approval based on interim ORR analysis Phase 2 Clinical Trials in Expanded/Other Indications Checkpoint Refractory Bladder Cancer: Initial Phase 2 Proof of Concept data expected in 2H 2019 BeiGene-funded Phase 2 Trials: Initial Phase 2 proof of concept data expected in 2H 2019 / 1H 2020 15 1. Data presented at ESMO 2018 Congress; Data cut-off: 27-Aug-2018; Response data per investigator assessment, response confirmations updated after data cut-off.
Targeted Oncology Sitravatinib Single Agent: CBL Loss of Function Mutations 16 16
Single Agent Sitravatinib Sitravatinib: CBL Loss-of-Function Mutations in Cancer 17 Loss-of-function mutations in CBL result in increased target RTK activation in tumor cells that may act as oncogenic drivers
Single Agent Sitravatinib Phase 1b Trial of Single Agent Sitravatinib in Patients with CBL Mutations Summary of On-going Trial Initial Clinical Activity 1 in CBL Mutations is Encouraging 1/2 confirmed Partial Response in NSCLC 1/2 confirmed Partial Response in Melanoma (mucosal) (non-uv form which does not respond well to other treatments) Phase 1b Expansion Trial Design Patients with CBL Loss of Function Mutations Expansion Criteria (PRs) Stage 1 Stage 2 Expansion Criteria (PRs) Stage 3 Single Agent Sitravatinib Has Been Well Tolerated with Manageable Side Effects NSCLC Melanoma CBL Loss of Function Mutation (via NGS) n=8 2 PR 7 PR n=16 n=46 Single Agent Sitravatinib Program Focused on CBL in NSCLC and Melanoma Circulating tumor DNA assay (liquid biopsy) is now available to identify CBL loss of function mutations Clinical update expected in 2H 2019 to define single agent registration pathway Key Inclusion Criteria: Malignancy harboring loss of function CBL mutation Advanced metastatic or unresectable solid tumor malignancy Adequate bone marrow and organ function Key Exclusion Criteria: Symptomatic or uncontrolled brain metastases Endpoints: Safety, PK/PD Clinical Activity (ORR, DR, PFS, OS) 18 1. Presented at ESMO 2018 Congress; data cut-off 4-Sep-2018
Targeted Oncology MRTX849: KRAS G12C Inhibitor 19 19
MRTX849 KRAS G12C Inhibitor KRAS: The Holy Grail of Mutated Oncogene Targets KRAS Signaling Drives Growth and Survival KRAS: The Most Frequently Mutated Gene in Human Cancer KRAS Mutations are Prevalent in High Mortality Cancers Pancreas Colorectal NSCLC 90% 44% 30% KRAS First Identified in 1980 s 1. Image from Genetics Home Reference 20 2. Zehir A et al, Mutational landscape of metastatic cancer revealed from prospective clinical sequencing of 10,000 patients. Nat Med. 2017;23(6):703-713.
MRTX849 KRAS G12C Inhibitor Mutant KRAS is an Oncogenic Tumor Driver KRAS mutations occur early in tumor genesis and do not overlap with other tumor drivers Mutational Prevalence and Overlap in 1,357 Lung Adenocarcinomas 1 Mutant KRAS signaling is required for tumor cell survival Sensitivity of Cancer Cell Lines to shrna Knockdown of KRAS 2 HER2 (44) RET Fusion (20) KRAS G13 (37) EGFR L858R (109) BRAF (65) KRAS G12 (346) EGFR Exon 19 Deletion (102) KRAS Q61 (18) MET (47) ROS1 (29) ALK Fusion (42) Sensitivity Score 0-1 -2-3 -4 Wild Type KRAS Cancer Cell Lines Mutant KRAS 21 1. Zehir A et al, Mutational landscape of metastatic cancer revealed from prospective clinical sequencing of 10,000 patients. Nat Med. 2017;23(6):703-713. 2. McDonald et al, Project DRIVE: A Compendium of Cancer Dependencies and Synthetic Lethal Relationships Uncovered by Large-Scale, Deep RNAi Screening, Cell 2017
KRAS G12C Mutations Occur Frequently in Multiple Tumor Types MRTX849 KRAS G12C Inhibitor KRAS G12C Mutation Frequency 1 G12C (14%) NSCLC adenocarcinoma Colorectal G12C (4%) Pancreatic G12C (2%) U.S Addressable Patients 2 : ~24,500 22 1. Mirati frequency estimates based upon the following sources and underlying databases: Zehir A et al, Mutational landscape of metastatic cancer revealed from prospective clinical sequencing of 10,000 patients. Nat Med. 2017;23(6):703-713.; Campbell et al, Nature Genetics 2016 Distinct patterns of somatic genome alterations in lung adenocarcinomas ; Bailey P et al, Nature 2016 Genomic analyses identify molecular subtypes of pancreatic cancer ; MSKCC Cancer Hot Spots database; NIH TCGA: The Cancer Genome Atlas 2. Mirati estimate based upon frequency data from sources above and epidemiology data from Globocan 2022 incidence projections (accessed January 2019) ; Total includes additional histologies
MRTX849 KRAS G12C Inhibitor KRAS G12C Mutations are Prevalent in a Large Population of Patients No Targeted Treatments Available for Patients with KRAS G12C+ Tumors 30,000 U.S. Patient Populations 2 KRAS G12C vs. ALK, RET and TRK Significant Commercial Opportunity 3-4x size of the ALK mutation population ($1.8B worldwide market in 2018 1 ) Diagnosed by Approved Assays Both tissue and liquid biopsy tests are commercially available Testing common in NSCLC and CRC U.S. Patient Population 25,000 20,000 15,000 10,000 5,000 0 KRAS G12C ALK RET TRK NSCLC CRC Other 23 1. 2018 major-market sales (projected) for ALK inhibitors (Decision Resources NSCLC Forecast published Dec 2017) 2. Mirati estimates based on epidemiology data reported in Globocan 2022 (accessed January 2019) and frequencies by mutation; RET estimate does not include thyroid cancer
MRTX849 KRAS G12C Inhibitor Mirati s KRAS Program: Targeting KRAS G12C Mutations Targeting KRAS Historically Undruggable Shallow Binding Pocket GTP pocket 1. KRAS G12C has a cysteine present in its inactive form Switch II pocket KRAS G12C Can Be Inhibited Covalently 3. Inhibitor covalently binds to the cysteine and the induced Switch II pocket Cysteine KRAS Picomolar Affinity for GTP KRAS G12C 2. Binding to the cysteine opens an adjacent Switch II pocket KRAS G12C Inactive 4. KRAS G12C is irreversibly locked in the inactive state KRAS tumor cell death 24
MRTX849: A Potent and Selective Investigational KRAS G12C Inhibitor MRTX849 KRAS G12C Inhibitor Potent Selective Antiproliferation IC50s MRTX849, 3D format Cysteine Selectivity in H358 Cells MRTX849 (3 µm) IC50 (um) 10 1 0.1 0.01 0.001 KRAS G12C cell lines Treated/Control Peptide Ratio 5,700 other cysteine peptides Ratio of significance Only modified cysteine is KRAS G12C 0.0001 Cervix Colon Pancreas Urinary Lung Peptide 25
MRTX849: Promising In Vivo Antitumor Activity Complete tumor regressions observed following oral administration in preclinical models MRTX849 KRAS G12C Inhibitor Tumor Volume(mm 3 ) 1250 1000 750 500 250 MRTX849 Oral Administration CDX pancreatic model (MIA PaCa-2) Vehicle 1mg/kg 3mg/kg Vehicle 1 mg/kg Vehicle 1mg/kg 3mg/kg 10mg/kg 30mg/kg 100mg/kg 3 mg/kg 10 mg/kg 30 mg/kg 100 mg/kg 10mg/kg Dose-Dependent Regressions Observed In Vivo Durable and complete responses seen at 30mg/kg and 100mg/kg doses Tumor response continued after cessation of treatment MRTX849 Tested in More than 20 In Vivo Models Tumor regressions observed in ~80% of all KRAS G12C in vivo models tested Similar activity seen in both cell-derived and patientderived tumor models 0 0 10 20 30 40 50 S tart D osing End Dosing Day 30 & 100mg/kg* Preclinical Data Predicts Single Agent Activity Supports pursuit of an accelerated single agent development pathway based on response rate * Tumors did not recur despite cessation of treatment, indicating durable and complete responses 26
MRTX849 KRAS G12C Inhibitor Phase 1/2 Clinical Trial of MRTX849 in KRAS G12C+ Tumors Accelerated Dose Escalation Design Wide preclinical therapeutic index supports starting dose close to predicted active exposure Single patient cohorts 150mg starting dose with planned 100% escalations Intra-patient dose escalations Stage 1 Stage 2 Phase 1b Expansion Cohorts Opportunity to enroll additional patients based on early efficacy signals while still escalating to maximum tolerated dose (MTD) Advanced solid tumor types (lung, CRC and others) with G12C+ mutations only Single patient Cohorts 100% dose escalations until MTD reached Example: Pt 1 150mg Pt 2 300mg Pt 3 600mg Dose expansion when RP2D reached Registration-Enabling Protocol Design supports single arm registration from expansion cohorts without the need for a new protocol 27 ClinicalTrials.gov Identifier: NCT03785249
MRTX849 KRAS G12C Inhibitor MRTX849: Summary Summary Potent: 1-20 nm potency in cellular assays Selective: 1,000 fold selective for KRAS G12C mutations over KRASwild type Orally Bioavailable: PK profile consistent with once daily oral dosing Highly Active in vivo: Complete durable regressions in KRAS G12C models Wide Therapeutic Index: Preclinical toxicology studies suggest a favorable safety profile Strong Patent Estate: First program patent issued in December 2018 Phase 1/2 Clinical Trial Open: Potential for initial efficacy data in 2H 2019 28
Targeted Oncology KRAS G12D Program 29 29
KRAS G12D Discovery Program Mirati s Next KRAS Program: KRAS G12D KRAS G12D is a Driver Mutation Early oncogenic event Non-overlapping with other driver mutations, including KRAS G12C Large Patient Population Highly prevalent in pancreatic cancer (ductal adenocarcinomas) No targeted treatment options for patients with KRAS G12D+ tumors Leveraging Learnings from G12C Applying knowledge gained from designed targeting KRAS G12C Identified KRAS G12D leads G12D (35%) G12D (5%) KRAS G12D Mutation Frequency 1 Pancreatic Endometrial Colorectal NSCLC adenocarcinoma U.S Addressable Patients 2 : ~46,000 G12D (12%) G12D (5%) 30 1. Sources: Zehir, Ahmet et al. Nature Med 23 2017 Mutational Landscape of Metastatic Cancer ; Krakstad et al. PLoS One 2012, High-Throughput Mutation Profiling of Primary and Metastatic Endometrial Cancers ; NIH TCGA: The Cancer Genome Atlas 2. Mirati estimate based upon frequency data from sources above and epidemiology data from Globocan 2022 incidence projections (accessed January 2019)
Mirati Therapeutics: Potential Value-Driving Catalysts in 2019 Sitravatinib Initiating Phase 3 Registrational Trial in NSCLC Sitravatinib + Nivolumab in Checkpoint Refractory NSCLC Phase 3 Trial Initiation 1H 2019 Extending Proof of Concept into Additional Tumor Types Sitravatinib + Nivolumab in Checkpoint Refractory Bladder Phase 2 Initial Proof of Concept Data Sitravatinib + Tislelizumab in NSCLC, RCC, Ovarian Phase 2 Initial Proof of Concept Data (BeiGene) 2H 2019 2H 2019 Expanding Clinical Mechanism of Action Data Sitravatinib + Nivolumab in Pre-Surgical RCC, HNSCC Initial Mechanism of Action Data 2H 2019 MRTX849 KRAS G12C Generating Clinical Data with Potential Best-in-Class KRAS G12C Inhibitor MRTX849 in KRAS G12C+ Tumors Phase 1/2 Early Proof of Concept Data 2H 2019 KRAS G12D Program Expanding KRAS Franchise into KRAS G12D KRAS G12D Program Lead Candidate Identification Q4 2019 31
Company Financials NASDAQ MRTX Cash (Q4 18)* $222.8M Shares Outstanding** 46.4M * Reported cash and investments as of December 31, 2018. Does not include $107.9 million of net proceeds from January 2019 offering ** As of February 22, 2019, includes 35.3 million shares of common stock and pre-funded warrants to purchase a total of 11.1 million shares of common stock. The pre-funded warrants have a per share 32 exercise price of $0.001.
NASDAQ: MRTX Targeting the genetic and immunological drivers of cancer Corporate Presentation March 2019 33