Targeted Cancer Therapies ASCO Presentation, June 6th, 2016 Safe Harbor Statement Except for statements of historical fact, any information contained in this presentation may be a forward-looking statement that reflects the Company’s current views about future events and are subject to risks, uncertainties, assumptions and changes in circumstances that may cause events or the Company’s actual activities or results to differ significantly from those expressed in any forward-looking statement. In some cases, you can identify forward-looking statements by terminology such as “may”, “will”, “should”, “plan”, “predict”, “expect,” “estimate,” “anticipate,” “intend,” “goal,” “strategy,” “believe,” and similar expressions and variations thereof. Forward-looking statements may include statements regarding the Company’s business strategy, potential growth opportunities, clinical development activities, the timing and results of preclinical research, clinical trials and potential regulatory approval and commercialization of product candidates. Although the Company believes that the expectations reflected in such forward-looking statements are reasonable, the Company cannot guarantee future events, results, actions, levels of activity, performance or achievements. These forward-looking statements are subject to a number of risks, uncertainties and assumptions, including those described under the heading “Risk Factors” in documents the Company has filed with the SEC. These forward-looking statements speak only as of the date of this presentation and the Company undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date hereof. Certain information contained in this presentation may be derived from information provided by industry sources. The Company believes such information is accurate and that the sources from which it has been obtained are reliable. However, the Company cannot guarantee the accuracy of, and has not independently verified, such information. Trademarks: The trademarks included herein are the property of the owners thereof and are used for reference purposes only. Such use should not be construed as an endorsement of such products. 2 ProNAi Therapeutics A drug development company advancing targeted cancer therapies • We are an ambitious oncology drug development company oriented towards registration and commercialization. NASDAQ: DNAI • We have a world-class management team with a proven track record in oncology drug development. Headquarters: Vancouver, BC Development: San Francisco, CA Research: Plymouth, MI IPO: July 2015 Shares: 30.2M outstanding 34.3M fully diluted Cash on hand (31/3/16): $140.9M • We intend to build a broad and diverse pipeline of promising oncology assets against emerging targets on the leading edge of cancer biology. • We have a healthy cash balance, that we expect will allow us to achieve meaningful development milestones. 3 Proven Leadership in Oncology Development Nick Glover, PhD President and CEO Barbara Klencke, MD Chief Development Officer Angie You, PhD Chief Business & Strategy Officer; Head of Commercial Sukhi Jagpal, CA, CBV, MBA Chief Financial Officer Keith Anderson, PhD Senior Vice President, Technical Operations Wendy Chapman Senior Vice President of Clinical Operations Diane Gardiner Senior Vice President of Human Resources Chris Hassig, PhD Senior Vice President of Research Chandra Lovejoy Senior Vice President of Global Regulatory Affairs and Head of Quality Emma McCann Senior Vice President of Program Management Gregg Smith, PhD, MBA Senior Vice President of Preclinical 4 PNT2258 Program Update PNT2258: DNAi Drug Candidate PNT2258 • Proprietary formulation of multiple copies of PNT100 encapsulated within a lipid nanoparticle, delivered systemically via infusion. PNT100 DNAi • A single stranded 24-base DNAi oligonucleotide rationally designed to bind to a specific regulatory region associated with the BCL2 oncogene. 6 PNT2258: Development Program - Status PNT2258-01 Solid Tumors 22 subjects Initiated Sep. 2010 PNT2258-02 r/r NHL 13 subjects Continuation/Follow Up Initiated Jan. 2013 PNT2258-03 Wolverine r/r DLBCL 45/61 subjects Initiated Jan. 2015 Interim -02 Data (ASH) ProNAi Updated Appoints -02 Data Dr. Glover (ASH) Crossover ProNAi $60M Appoints Raised Dr. You 2010 2012 2013 2014 PNT2258-04 Brighton Richter’s 5/50 subjects Initiated ProNAi Appoints Oct. 2015 Dr. Klencke IPO $158M Raised 2015 Interim -03 Data 2016 7 Final Results of PNT2258-02: A Pilot Phase 2 Study of PNT2258 for r/r NHL PNT2258-02: Pilot Phase 2 Trial in r/r NHL Primary Objective • To characterize pilot antitumor activity and collect safety data on subjects with recurrent or treatment refractory (r/r) NHL receiving single-agent PNT2258. Population • 13 subjects with metabolically active recurrent or treatment refractory B-cell NHL were enrolled from three centers. • All subjects were required to have received prior therapy with rituximab and cytotoxic therapy. Dosing Regimen • Administered PNT2258 as a single agent IV, Days 1-5, every 21-days for 6 to 8 induction cycles or until progression. • Subjects with ongoing benefit were allowed to receive continuation therapy at a modified dose and schedule until progression. Efficacy Evaluation • Antitumor activity according to the Cheson criteria (2007). • FDG-PET and CT imaging evaluation were conducted at baseline, at the end of Cycle 2, and after 6 to 8 cycles. 9 PNT2258-02: Demographic and Baseline Characteristics Disease Status (Relapsed or ECOG PS Refractory)* No. Prior Lines of Therapy Best Response on Last Prior Therapy Time to Treatment Failure with Last Prior Therapy (months) Refractory 2 SD 9.4 2 Relapsed 2 PR 21.6 65 1 Refractory 4 SD 5.5 MCL 65 0 Relapsed 4 PR 23.7 9 3 7 4 FL FL FL FL 54 55 73 56 1 1 1 1 Refractory Relapsed Relapsed Relapsed 5 1 2 2 SD CR PR CR 5.1 21.2 35.2 48 1 FL 71 0 Relapsed 1 CR 57.9 13 11 12 10 DLBCL-B DLBCL-RT DLBCL DLBCL 61 78 80 40 1 1 1 1 Relapsed Relapsed Relapsed Refractory 1 2 1 1 CR PR CR PD 19.9 6 87.6 2.3 Subject No. Diagnosis Age (years) 5 CLL 51 0 8 CLL/SLL 65 2 MCL 6 Legend B = Burkitt’s-like CLL = chronic lymphocytic leukemia DLBCL = diffuse large B-cell lymphoma FL = follicular lymphoma MCL = mantle cell lymphoma RT = Richter’s Transformation Legend ECOG PS = Eastern Cooperative Oncology Group Performance Status Legend CR = complete response PR = partial response SD = stable disease PD = progressive disease * Disease status classified per internal clinical review of baseline data. 10 PNT2258-02: Final Progression-Free Survival 8 2 PD 7 SD FL SD 4 CR 1 PR 13 PR 11 PR 12 10 On treatment Subject off treatment but in follow-up without progression 1.3 Months SD 3 3 Years PFS duration 2.4 Months PD SD 2 Years 1.2 Months SD 9 DLBCL Subject Number 6 MCL 5 CLL/SLL 1 Year 14.2 Months 4.0 Months Subject is still on treatment or active follow-up without progression Disease progression 8.9 Months 32.8 Months* 27.4 Months 16.7 Months** 9.1 Months 9.5 Months CR 26.0 Months CR 30.3 Months 0 CLL = chronic lymphocytic leukemia DLBCL = diffuse large B-cell lymphoma FL = follicular lymphoma 12 Months MCL = mantle cell lymphoma SLL = small lymphocytic leukemia 24 36 Note: Response per investigator assessment (Cheson 2007). * Subject remains on PNT2258 therapy. ** An additional 17.8 months of follow-up without progression has been censored pending data entry 11 PNT2258-02: Outcome with Last Therapy vs. PNT2258 Best Response with Last Prior Therapy and Time Interval from Start of Last Prior Therapy 2 6 CLL/SLL 8 PD SD SD PR SD PR SD SD FL CR CR PR * CR 1 CR 13 12 SD PR 4 11 SD CR 3 PR PR DLBCL Subject Number 9 7 PD SD MCL 5 Time to Progression and Best Response with PNT2258 PR CR CR CR PD 10 96 -96 84 -84 72 -72 60 -60 48 -48 36 -36 24 -24 12 -12 0 12 24 36 48 Months * An additional 17.8 months of follow-up without progression has been censored pending data entry. 12 PNT2258-02: Final Efficacy Summary PNT2258-02 (N = 13) n (%) Best response (Investigator assessment; Cheson 2007) CR 3 (23.1) PR 3 (23.1) SD 5 (38.5) PD 2 (15.4) Overall response rate (best response ≥ PR) (n [%], 95% CI) 6 (46.2%) (19.2, 74.9) Disease control rate (best response is ≥ SD) (n [%], 95% CI) 11 (84.6%) (54.6, 98.1) Duration of response Median months (min, max) 95% CI 23.4 m (3.0, 26.1*) 13, NE * Indicates censored value. 13 PNT2258-02: Overview of Safety • 12 of the 13 subjects have discontinued PNT2258 therapy. • Median treatment duration on PNT2258 was 8.9 months (range: 1 to 33+ months). • No subjects discontinued treatment due to AEs. • One subject required a dose reduction. • The majority of AEs were Grade 1 or 2 in severity. • 85% of subjects experienced Grade 3 or 4 AEs. • No Grade 5 AEs were observed. • Most common AEs were nausea, chills, diarrhea, fatigue, headache, and vomiting. • 31% of subjects experienced an SAE. • 8% of subjects experienced a treatment-related SAE. 14 PNT2258-02: Conclusions PNT2258 as a single-agent resulted in clinically significant, durable responses in recurrent or treatment refractory NHL, including in four subjects with DLBCL. • Overall response rate of 46.2% in the entire study population of 13 subjects. • Noteworthy responses (CR, PR) and durable SD was also observed in follicular lymphoma subjects. Six subjects were progression free at 12 months; PFS extended to 2 years and beyond in four subjects. • Five of the six subjects who were progression free at 12 months with PNT2258 were relapsed (not refractory) at study entry and had responded with their last prior therapy with a median time to treatment failure (TTF) of 48 months (4 yrs), range 23.7-87.6 months. • All four responding DLBCL subjects had received 1 or 2 prior therapies. PNT2258 was safe and well tolerated in these NHL subjects and was administered for extended periods without evidence of cumulative toxicity for 2 years and longer. 15 A Phase 2 Study of PNT2258 in Patients with r/r DLBCL: An Initial Report from the Wolverine Study PNT2258-03: Wolverine Phase 2 Trial in r/r DLBCL Primary Objective • Overall response rate (ORR). Secondary Objectives • DCR, DOR, TTR, OS, PFS. • Safety. • Identify predictors of outcome. Population • Previously treated subjects with metabolically active (r/r) DLBCL, defined as refractory to prior therapy or relapsed after prior therapy. • Prior exposure to CD20-targeted therapy, an alkylating agent, and a steroid. Dosing Regimen • Administered PNT2258 as a single agent IV, Days 1-5, every 21-days for up to 8 induction cycles. • Subjects with ongoing benefit were allowed to receive continuation therapy at a modified dose and schedule until progression. Efficacy Evaluation • FDG-PET/CT imaging evaluations (Lugano) conducted at baseline and after Cycles 3, 5, 8. 17 PNT2258-03: Interim Study Populations Safety Population* N = 37 Subjects who received at least 1 dose of PNT2258 Eligible Population* n = 27 ECOG PS 0-1 and 1-3 lines of prior therapy Additional Subjects* n = 10 ECOG PS 2 and/or ≥ 4 prior therapies Response Evaluable Population* n = 19 At least 8 doses of PNT2258 within 35 days of starting therapy Excluded from Response Evaluable Population Due to Early Discontinuation* n=8 • Analysis performed on all subjects enrolled as of February 29th, and included all available data as of April 25th • This is an ongoing study with an open and active database, with outstanding, unresolved queries. * Interim. 18 PNT2258-03: Biomarker Assessments Wolverine is designed to explore the correlation between various patient baseline characteristics and response rate. Performance of the Lymph2Cx Assay as Previously Published IHC: • BCL2, c-MYC, Ki-67, BCL6. FISH: • BCL2, c-MYC, Ki-67, BCL6. Cell of Origin (COO) in DLBCL • Utilizes the Lymph2Cx assay (NanoString), a digital 20 gene-expression based test for COO assignment in formalin-fixed paraffin-embedded tissue. Blood. 2014;123(8):1214-17 19 PNT2258-03: Demographic and Baseline Characteristics Clinical Characteristics Age (median years [min, max]) ECOG PS 0 1 2 Patient Outcome with Prior Therapy Number of prior lines (median [min, max]) PNT2258-03 (N = 37) n (%) 64 (26, 84) 6 (16.2) 25 (67.6) 6 (16.2) 3 (2, 7) Refractory to most recent prior therapy 19 (48.6) Best response to last prior therapy CR + PR SD PD Other 15 (40.5) 2 (5.4) 17 (45.9) 3 (8.1) Time to Treatment Failure on last prior therapy (median months [min, max]) Biomarker Results FISH+ for MYC and BCL2 and/or BCL6 (Double hit) 3.9 (1.1, 71.5) IHC+ for MYC and BCL2 (Double expressor) 16/29 (55.2%) 2/22 (9.1%) 20 PNT2258-03: Interim Efficacy PNT2258-03 (N = 37) n (%) Subjects with PS 0-1 and ≤ 3 Prior Therapies (n = 27) n (%) Response Evaluable Subjects (n = 19) N (%) 3 (8.1) 4 (10.8) 11 (29.7) 19 (51.4) 2 (5.4) 17 (45.9) 3 (8.1) (1.7, 21.9) 7 (18.9) (8.0, 35.2) 3 (11.1) 4 (14.8) 8 (29.6) 12 (44.4) 1 (3.7) 11 (40.7) 3 (11.1) (2.4, 29.2) 7 (25.9) (11.1, 46.3) 3 (15.8) 4 (21.1) 7 (36.8) 5 (26.3) 0 5 (26.3) 3 (15.8) (3.4, 39.6) 7 (36.8) (16.3, 61.6) 1.5 (0.07, 8.6) 0.03** - 5.3 1.9 (1.3, 2.4) 1.5 (0.07, 8.6) 0.03** - 5.3 2.0 (1.7, 3.6) 1.5 (0.85, 8.6) 0.03** - 5.3 2.0 (1.9, 3.6) Best Response ≥ Partial Metabolic Response (PMR) No Metabolic Response (NMR) Progressive Metabolic Disease (PMD*) N/E Still on treatment Discontinued treatment Overall Response Rate (n [%], 95% CI) Disease Control Rate (n [%], 95% CI) Durability Treatment Duration (median months [min, max]) DOR (range months) PFS (median months, 95% CI) * ** One additional PMR incorrectly remained in the database at the time of the 25 April 2016 data cut-off date. This was subsequently corrected to PMD in the database and thus, is displayed above as PMD as best response. Indicates censored value. 21 PNT2258-03: Interim Data Summary for Responders Characteristics of Responders: • 3/3 male. • 3/3 ECOG PS of 1. • Median age 63 years (range: 63-68). • 2/3 had received 2 prior lines of therapy. • 1/3 had received 3 prior lines of therapy. • 1/3 had a partial response to their last prior therapy. • 2/3 progressed as their best response to prior therapy. • One subject remains on therapy. Biomarker Results: • Cell of origin: • 1 ABC, 1 GCB, 1 unknown. • 1/3 MYC(+) by ICH, 0/3 MYC(+) by FISH. 22 PNT2258-03: Overview of Safety • Median treatment duration on PNT2258 was 47 days (range: 2-263). • Median treatment duration was 15 days in the 10 subjects with ECOG PS of 2 and/or ≥ 4 prior lines of therapy. • 33 subjects (89%) have discontinued PNT2258 therapy. • All 37 subjects experienced one or more AE. • 65% of subjects experienced one or more Grade 3 or 4 AEs. • Most common AEs were fatigue, nausea, pyrexia, anemia, diarrhea, hypotension, and thrombocytopenia. • 43% of subjects experienced an SAE. • 35% of subjects experienced a treatment-related SAE. • 22% of subjects died within 30 days of their last dose of PNT2258. • 50% of subjects with ECOG PS of 2 and/or ≥ 4 prior lines of therapy died within 30 days of their last dose of PNT2258. 23 PNT2258-03: Conclusions - Interim Efficacy PNT2258 showed modest single-agent activity in r/r DLBCL patients. Response Evaluable (n= 19)(%) Safety Population (N=37)(%) Overall response rate (n% [95% CI]) 3 (15.8) (3.4, 39.6) 3 (8.1) (1.7, 21.9) Disease control rate (n% [95% CI]) 7 (36.8) (16.3, 61.6) 7 (18.9) (8.0, 35.2) • All three responses were observed in subjects with PS 0-1 and ≤ 3 prior lines of therapy. • Currently, 45 subjects have been enrolled. • No additional responses seen to date in eight subjects enrolled after data cutoff. • 39 subjects have discontinued treatment. • Six subjects remain on PNT2258. • one with an ongoing response after 10 cycles of therapy. • five yet to be evaluated (on study for <9 weeks). 24 PNT2258-03: Conclusions - Interim Safety Overall, the safety profile of PNT2258 appears acceptable in subjects with PS 0-1 and ≤ 3 prior lines of therapy. Subjects with PS 0-1 and ≤ 3 prior lines of therapy (n = 27) Subjects with PS 2 and/or ≥ 4 prior lines of therapy (n = 10) 47 days 15.5 days SAE rate 37% 60% Grade 5 AE rate 11% 50% Median duration of therapy on study • We determined that the most advanced subjects, with PS 2 and/or having received ≥ 4 lines of therapy, did not respond to therapy, and experienced higher rates of serious adverse events and Grade 5 events. 25 The Brighton Phase 2 Trial: PNT2258-04 Richter’s Transformation PNT2258-04: Brighton Phase 2 Trial in Richter’s The Brighton Phase 2 Trial PNT2258-04 Richter’s Transformation [NCT02378038] • A multicenter, single-arm, open-label study of PNT2258. • PNT2258 administered as a 4-hour IV infusion on Days 1-5 of a 21-day cycle. • Adults with Richter’s transformation. Efficacy Evaluation • FDG-PET/CT imaging evaluations conducted at baseline and after Cycles 3, 5, and 8. • Antitumor activity interpreted according to the revised 2014 IWG criteria for lymphoma (Lugano classification). Primary Objective • Overall response rate (ORR). Secondary Objectives • DCR, DOR, TTR, OS, PFS. • Safety. • Identify predictors of outcome. 27 PNT2258-04: Current Study Status Five subjects enrolled to date. • No responses have been observed to date. Four subjects have discontinued study treatment. • One subject received one dose and died on Study Day 2 (intracranial hemorrhage). • One subject received one cycle and discontinued therapy on Day 24 for progressive disease and died on Day 38. • Two subjects discontinued for progressive disease after receiving three cycles of PNT2258. One subject continues on study treatment. • Subject has completed two cycles of therapy. 28 PNT2258: Next Steps PNT2258: Overarching Conclusions • We have designed and run an appropriate, well-executed study, and have sought to optimize the conduct of Wolverine in real-time in order to focus on the most appropriate patient populations for treatment with PNT2258. • Advanced DLBCL and Richter’s Transformation are challenging diseases to treat, and PNT2258 did not markedly improve outcomes in these indications. • Modest efficacy has been observed in Wolverine, with mostly limited duration of response. No responses have been observed in Brighton. • Clinical data in Wolverine are not trending to an outcome that supports the likelihood of registration as monotherapy in late line DLBCL. • In the Brighton study, although only a few patients have been enrolled to date in this ultra-orphan indication clinical trial, we have also noted generally poor outcomes in this advanced patient population, with limited signs of activity. • In context of the interim Wolverine data, our emerging view is that Brighton is unlikely to support registration of PNT2258. 30 Next Steps for PNT2258 and DNAi Programs • On the basis of these interim assessments, we have decided to close the Wolverine and Brighton studies to further enrollment of new subjects. On behalf of ProNAi, we would like to thank the patients and their families, investigators and staff involved in these studies for their participation and support. • Considering these data in context of the broader development of PNT2258, we have decided to suspend all development of PNT2258 pending further review of data in order to determine next steps for the asset. • Similarly, we have halted all further investment in our DNAi research program at this time given our emerging view that this research is unlikely to yield additional ProNAi development candidates. • We continue to maintain a strong balance sheet that we will manage prudently as we focus our resources and activities on the advancement of PNT141 and future assets. We plan to secure additional assets towards building a broad and diverse pipeline of oncology assets under development. 31 PNT141: Targeting Cdc7 ProNAi Therapeutics: Focused on Building a Pipeline of Promising Oncology Assets • We are an ambitious oncology drug development company oriented towards registration and commercialization. • We have a world-class management team with a proven track record in oncology drug development. • We intend to build a broad and diverse pipeline of promising oncology assets against emerging targets on the leading edge of cancer biology. • We have a healthy cash balance, that we expect will allow us to achieve meaningful development milestones. On May 26, 2016, we announced our first transaction: AS141 (PNT141), a Cdc7 inhibitor licensed from Carna Biosciences. • Initial upfront payment of $0.9 million. • Aggregate additional potential payments upon achievement of certain developmental, regulatory and commercial milestones of up to $270 million. • ProNAi will also pay Carna single-digit tiered royalties on the net sales of any product successfully developed. 33 PNT141: Selective Small Molecule Targeting Cdc7 PNT141 (formerly AS-141) • A highly-selective and potent Cdc7 inhibitor, with favorable development characteristics. • Cdc7 is a key regulator of both DNA replication and DNA damage response, making it a compelling emerging target for the potential treatment of a broad range of tumors. • Broad development scope in solid and liquid tumors; mono- and combo- therapy. • PNT141’s selectivity profile offers possible differentiation and potential safety and efficacy advantages. • First-in-class and/or best-in-class opportunity. Attractive Asset and Deal Terms • Licensor: Carna Biosciences, Japan: expertise in kinase screening and chemistry drug discovery (first validating deal with J&J in 2015). • Attractive cost of entry, and ongoing deal and development costs typical for a smallmolecule oncology drug. Intellectual Property • PNT141 covered by composition of matter (2032 plus extensions) and combination patents. 34 PNT141: Cdc7 Plays an Essential Role in Two Vitally Important ‘Hallmarks of Cancer’ Cdc7 is a serine/threonine kinase with essential roles in both DNA replication initiation [proliferation] and subsequent S-phase cell cycle checkpoint control [genomic instability]. • Responsible for the “firing” of replication origins leading to initiation of DNA synthesis, and is the final critical step in growth regulatory control. • Phosphorylates and activates (i) the helicase complex MCM2-7 (leading to the unwinding of dsDNA during the G1/S transition), (ii) claspin, a Chk1 activator, and (iii) RAD18 to mediate TLS. Cellular Energetics Replicative Immortality Invasion / Metastasis Proliferation Evading Growth Inhibition Tumor Inflammation Immune Evasion HALLMARKS OF CANCER Angiogenesis Genome Instability Cell Death Resistance 35 PNT141: Tumor Cells are Predisposed to Cell Death in Response to Cdc7 Inhibition Normal cells activate a p53-dependent cell cycle arrest in response to transient Cdc7 inhibition, whereas tumor cells undergo apoptosis via checkpoint failure – opportunity for a favorable therapeutic window. Cdc7 Inhibitor Adapted from Carna Biosciences website. 36 PNT141: Clinical Development Opportunities and Patient Selection Strategy • Preclinical data and published literature suggest a variety of indications with potential for response to Cdc7 inhibitors. • Solid tumors – breast, ovarian, pancreatic, melanoma, colorectal, uterine, thyroid, etc. • Hematological malignancies – AML, DLBCL, etc. • A patient selection, biomarker-driven strategy focusing on drivers of replication stress, genomic instability and proliferation (e.g. p53, BRCA, MYC, KRAS, H2AX expression) will help facilitate clinical trial execution. • Potential to exploit tumor-specific genetic defects and/or combination therapies to effect cancer cell death via ‘synthetic lethality’. • ProNAi plans to pursue a robust program of preclinical studies to further evaluate tumor responses across a variety of indications and dosing regimens to inform clinical development plans and patient selection strategies. 37 PNT141: Summary • Cdc7 is a key regulator of both DNA replication and DNA damage response, making it a compelling emerging target for the potential treatment of a broad range of tumor types. • PNT141’s promising pharmaceutical properties, combined with target utility, IP runway (to 2032 plus extensions) and patient selection strategies, afford broad development scope in solid and liquid tumors as both mono- and combination therapy, with opportunity for first and/or best-in-class positioning. • Deal metrics are highly competitive, with an attractive upfront, and ongoing licensing and development costs typical for a small-molecule oncology drug. • Importantly, there exists opportunity for ProNAi to add significant value to the program, via its world-class preclinical and clinical development team. • We anticipate filing an IND for PNT141 in H2 2017, with clinical studies expected to begin by the end of 2017. 38 ProNAi Therapeutics: Focused on Building a Pipeline of Promising Oncology Assets • We intend to build a broad and diverse pipeline of promising oncology assets. • PNT141 is our first transaction. • We are actively engaged in ongoing business development activities, with two additional promising assets under exclusive option to enable further validating studies under MTA. • These assets are consistent with our strategic in-licensing focus, namely: • Orally bioavailable small molecules and next generation biologicals with exemplary target selectivity. • Assets with a foundation of strong, cancer-critical biology. • Assets against emerging targets, where there is an opportunity to be first-in-class or fast follower/best-in-class. • Assets with potential as monotherapy and in combinations, across a variety of cancer indications. • Assets that could possibly form proprietary combinations with each other. 39 Targeted Cancer Therapies