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TERN - 701 Investor Educational Webinar NASDAQ: TERN September 3, 2025
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Forward-Looking Statements and Disclaimers This presentation contains forward-looking statements about Terns Pharmaceuticals, Inc. (the “Company,” “we,” “us,” or “our”) and its industry within the meaning of the federal securities laws that involve substantial risks and uncertainties. All statements other than statements of historical facts contained in this presentation, including any statements regarding the Company’s strategy, future operations, future results, future financial condition, projected costs, prospects and plans, objectives of management, and expected industry and market trends, are forward-looking statements. Forward-looking statements in this presentation include statements related to or in connection with expectations, timing and potential results of the clinical trials and other development activities for TERN-701, including with respect to the CARDINAL trial; the therapeutic potential of TERN-701; the potential for the mechanism of action of TERN-701 to effectively target CML; the potential utility and progress of TERN-701 for the treatment of CML, including the clinical utility of the data from and the endpoints used in the Company’s clinical trials; the applicability of expected parameters and benchmarks on which to assess clinical trial results for TERN-701; the Company’s clinical development plans and activities for TERN-701, including potential future trial designs, milestones and the results of any interactions with regulatory authorities; the Company’s expectations regarding the profile and potential beneficial characteristics and therapeutic effects of TERN-701, including with respect to efficacy, tolerability, safety, pharmacokinetic profile and convenience and potential differentiation as compared to competitive products or product candidates; the best-in-class potential of TERN-701; the Company’s plans for and ability to continue to execute on its current development strategy for TERN-701; the market potential for TERN-701; the anticipated regulatory pathway for TERN-701; and possible future regulatory approval and commercialization of TERN-701. In some cases, you can identify forward-looking statements by terminology such as “aim,” “anticipate,” “assume,” “believe,” “contemplate,” “continue,” “could,” “design,” “due,” “estimate,” “expect,” “goal,” “intend,” “may,” “objective,” “plan,” “position,” “potential,” “predict,” “seek,” “should,” “target,” “will,” “would” and other similar expressions that are predictions of or indicate future events and future trends, or the negative of these terms or other comparable terminology. The Company has based these forward-looking statements largely on its current expectations, estimates, forecasts and projections about future events and financial trends that it believes may affect its financial condition, results of operations, business strategy and financial needs. In light of the significant uncertainties in these forward-looking statements, you should not rely upon forward-looking statements as predictions of future events. Although the Company believes that it has a reasonable basis for each forward-looking statement contained in this presentation, it cannot guarantee that the future results, levels of activity, performance or events and circumstances reflected in the forward-looking statements will be achieved or will occur at all. These risks are not exhaustive. For a detailed discussion of the risk factors that could affect our actual results, please refer to the risk factors identified in our reports filed with the Securities and Exchange Commission, including but not limited to our Annual Report on Form 10-K for the year ended December 31, 2024 and subsequent Quarterly Reports on Form 10-Q. New risk factors emerge from time to time and it is not possible for our management to predict all risk factors, nor can we assess the impact of all factors on our business or the extent to which any factor, or combination of factors, may cause actual results to differ materially from those contained in, or implied by, any forward-looking statements. Except as required by law, we undertake no obligation to update publicly any forward-looking statements for any reason after the date of this presentation. This presentation discusses product candidates that are investigational only and have not yet been approved for marketing by the FDA. No representation is made as to the safety or effectiveness of these product candidates for the use for which such product candidates are being studied. Data presented for our product candidates and other agents are not based on head-to-head trials and are based on publicly available data, which include cross-trial and/or cross-phase data and information. 2
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Agenda and Presenters ▪ Opening Remarks / Amy Burroughs, CEO ▪ Recapping TERN-701’s Best-in-Class Potential / Emil Kuriakose, MD, CMO ▪ Calibrating and Assessing CML Phase 1 Data / Emil Kuriakose, MD, CMO ▪ Future of CML and Development Path Ahead / Scott Harris, CDO ▪ Closing / Amy Burroughs, CEO 3
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The First Allosteric Inhibitor is Rapidly Becoming the Preferred Therapy of Choice in CML 1. Novartis ASCO Investor Event | June 2, 2024. 2. Novartis Q2 2025 Results Presentation | July 17, 2025 Allosteric Inhibitors Represent a Significant Advancement Over All Active-site TKIs1 Superior SuperiorEfficacy Safety/Tolerability Profile Approved CML Therapies 2G/3G active-site TKIs dasatinib, nilotinib, bosutinib, ponatinib 1G active-site TKI imatinib Allosteric TKI asciminib 35% 15% $3B+ ‘New to brand’ Rx share across all lines Share of front-line Anticipated peak sales Asciminib Use is Rapidly Increasing in 1L and Beyond2 4
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However, Asciminib Leaves Opportunities for Improvement Across Efficacy, Safety and Convenience 1. Hochhaus A, et al. N Engl J Med 2024;391:885-898. 2. Atallah E. et al. Blood 2024; 144 (Supplement 1): 479. 3. Rea D et al. Blood 2021; 138 (21): 2031–2041. 4. SCEMBLIX® (asciminib). Prescribing information, 2024. Accessed August 2025. Hypertension Pancreatic Toxicity 19% 16% Adverse Event Profile of Asciminib4 Patient Adherence4 Can’t be taken with food do not reach MMR at 48 weeks1 Asciminib Patients Who Fail to Reach Efficacy threshold ( ) - 32% - - 57% - do not reach MMR at 24 weeks2 1L 2L 3L+ - 75% - do not reach MMR at 24 weeks3 5
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Our Goal for TERN-701 is to be the Best Allosteric TKI in CML Improved Efficacy Improved Convenience Improved Safety BCR-ABL 6
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Recapping TERN - 701’s Best - in - Class Potential Emil Kuriakose, MD Chief Medical Officer
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160 mg N ≥ 3 320 mg N ≥ 3 400 mg N ≥ 3 500 mg N ≥ 3 Chronic phase 2L+ CML patients w/wo BCR-ABL1 mutations who have had: • Treatment failure/suboptimal response OR intolerance to >1 TKI • Prior asciminib treatment failure/intolerance allowed • Myristate pocket resistance mutations excluded Part 1 Dose Escalation Part 2 Dose Expansion TERN-701 Once-daily Monotherapy (N≈80) R Endpoints For Part 2 • Primary: Efficacy • Secondary: Safety/tolerability, PK 500 mg N = 40 320 mg N = 40 RDE Selection CARDINAL Phase 1 Study of TERN-701 in Chronic Myeloid Leukemia Upcoming 4Q25 data will include patients from dose escalation and expansion cohorts ClinicalTrials.gov identifier: NCT06163430 PK: pharmacokinetics; TKI: tyrosine kinase inhibitor Endpoints For Part 1 • Primary: Safety/tolerability • Secondary: PK, Efficacy Study Population TERN-701 Once-daily Monotherapy (N= up to 80 via backfill) 8
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Early Data Showed TERN-701 has Potential to Achieve Best-in-Class Efficacy and Safety Note: No head-to-head clinical studies have been conducted comparing TERN-701 with asciminib. Differences exist in study designs and conditions, and caution should be exercised when comparing data across studies. ✓ Rescue of response in asciminib failure ✓ Rapid deep molecular response in asciminib naïve patient ✓ Trends towards improved safety over asciminib at higher doses High target selectivity with greater potency than asciminib Potential for best- in-class MMR achievement rates and safety + + = 1 Better in vivo target coverage than asciminib Wider therapeutic index 2 3 Observed in early CARDINAL data Emerging Potential Differentiators for TERN-701 Based on Early Data 9
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Allosteric BCR-ABL Inhibitors are Inherently More Selective than Active Site Targeting Inhibitors Kinase domain (KD) consists of: 1. active site (shared with other kinases) 2. myristate pocket 3. myristoyl group (unique to ABL kinases) Myristoyl binding to the myristate pocket in WT ABL turns off kinase activity Wild-type (WT) ABL Active site inhibitors have low selectivity for BCR-ABL because of its shared active site with WT ABL and other kinases1,2,3 1. Rix U, et al. Blood 2007;110:4055–63. 2. Remsing Rix LL, et al. Leukemia 2009;23:477–85. 3. O'Hare T, et al. Cancer Cell 2009;16:401–12. 4. Adrián FJ, et al. Nat Chem Biol. 2006 Feb;2(2):95-102. BCR-ABL fusion in CML Allosteric inhibitors (bind to the myristate pocket) have 1. high selectivity for BCR-ABL due to its open myristate pocket that is unique to BCR-ABL4 ; and 2. low risk of WT ABL inhibition due to myristoyl group blocking access to the pocket BCR replaces myristoyl group of ABL leaving myristate pocket open → kinase stays on 10 Active Inactive Active 1
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High Selectivity of Allosteric Inhibitors Allows Targeted, Potent BCR- ABL Inhibition Without Interfering with Activity of Normal Kinases Less off-target kinase inhibition allows improved safety compared to non-selective active-site TKIs 1. Moslehi Javid J. Journal of Clinical Oncology, 2015, Vol 33 (35), 4210-4218. 2. BCR-ABL1 potency derived from KCL22-s cytotoxicity assay (n=3); 3. ELVN-001 selectivity data derived from Enliven Company Overview, April 2024. • Off-target inhibition of wild-type kinases including ABL1, ABL2, SRC, VEGF is linked to cardiovascular and other toxicities1 • >10,000X better selectivity for BCR-ABL with allosterics over the closest related wild- type kinases (ABL1, ABL2) and over 450 other kinases compared to active-site TKIs • Higher target selectivity of allosterics drives the improved safety profile of asciminib vs. active-site TKIs in randomized clinical trials TERN-701 & asciminib Selectivity of Allosteric TKIs (TERN-701 & Asciminib) vs Active-Site TKIs2 11 3 1
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TERN-701 has Numerically Greater Potency than Asciminib Against Multiple BCR-ABL Variants in Preclinical Assays In vitro IC50 values determined via cytotoxicity assay (BaF3 cell line for mutations) * denotes myristoyl mutations or mutations indicated in resistance to allosteric inhibition of BCR-ABL1 Cell-Based Potency (IC50, nM) TERN-701 asciminib In cell proliferation assays, TERN-701 demonstrated numerically greater potency vs. asciminib against several BCR-ABL variants, including active site and myristoyl site mutations 12 1
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TERN-701 Clinical Doses Appear to Achieve Multiple Times Higher Target Coverage Than Approved Dose of Asciminib TERN-701 Clinical Doses Likely Achieve 2X - 7X Greater Target Coverage than Asciminib 80mg 80 mg QD 160 mg QD 320 mg QD 400 mg QD 500 mg QD 0 5 10 15 20 Target Coverage (Cave Ratio) 4.5 9.2 12.2 14.3 2.3 TERN-701* Asciminib* Mean Cave Ratio [Clinical dose : Effective KCL22 xenograft dose] * For TERN-701, the Cave ratio compares Cave in humans (steady state PK from CARDINAL Ph1 study) to Cave in KCL22 mouse xenograft at which >90% inhibition of tumor growth and downregulation of BCR-ABL signaling was seen. Asciminib Cave ratio is Cave in humans at 80mg QD to efficacious exposure (121ng/ml) in KCL-22 mouse xenograft as previously reported1. Preclinical PK-PD Clinical PK Dose TKI Dose TKI KCL-22 mouse model Exposure at efficacious dose in mouse model Exposure at clinical dose Asciminib 80mg Dose Informed by Clinical Exposures Relative to Efficacious Exposures in KCL-22 Mouse Model1 Target coverage is the ratio of exposure at clinical doses in patients to maximally efficacious exposures in a reference mouse model 1. Hughes TP et al. NEJM. 2019;381(24):2315-2326. 13 2
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Improved Target Coverage Hypothesis is Supported by Rescue of Response in Asciminib Failure by the Lowest Dose of ‘701 MR2 in 4L patient treated with 2G TKI, 3G TKI and asciminib with baseline BCR-ABL1 >1% Note: Data previously presented in December 2024 (October 2024 cutoff) * Hypertriglyceridemia/elevated liver function tests MR1: at least 1-log reduction; MR2: at least a 2-log reduction (i.e., BCR-ABL1 ≤ 1%); cycle = 28 days CML diagnosis Loss of response Suboptimal response Suboptimal response/ Intolerance* dasatinib x 6 yr ponatinib x 1yr asciminib x1yr TERN-701 -2 -1 0.01 0.1 1 10 100 Years BCR::ABL1 transcripts (IS, %) Baseline TERN-701 160mg QD deepened response to MR2 160 mg x 5 cycles80 mg45 mg 30 mg Patient Characteristics Age 35 years Gender Male # of prior TKIs 3 BCR-ABL1 Mutations None Efficacy MR1 to MR2 BCR-ABL1 transcripts (IS, %) Years Met ELN criteria for treatment failure/suboptimal response 14 2
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Hughes TP, et al. N Engl J Med 2019;381:2315-2326. Note: No head-to-head study has been conducted with TERN-701 against asciminib. Differences exist in study designs and conditions, and caution should be exercised when comparing data across studies. Data previously presented in December 2024. Asciminib Dose Dose Limiting Toxicities 40 mg BID Grade 3 lipase elevation (n=2) 80 mg BID Grade 2 myalgia & arthralgia (n=1) 150 mg BID Grade 3 acute coronary syndrome (n=1) 200 mg QD Grade 3 clinical pancreatitis (n=1) Grade 3 lipase elevation (n=1) Grade 3 abdominal pain (n=1) 200 mg BID Grade 3 bronchospasm (n=1) TERN-701 Dose Dose Limiting Toxicities 160 mg QD No DLTs 320 mg QD No DLTs 400 mg QD No DLTs 500 mg QD No DLTs Incidence of Dose Limiting Toxicities (DLTs) During First 28 Days of Treatment Wider TI enables administration of higher doses that achieve maximal target coverage and potentially improved efficacy Trend Towards Improved Safety Relative to Asciminib in Dose Escalation Supports Potential Wider Therapeutic Index (TI) 15 3
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Calibrating and Assessing CML Phase 1 Data Emil Kuriakose, MD Chief Medical Officer
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Phase 1 CML Studies Enroll Patients With or Without Baseline MMR MMR achievement is the regulatory endpoint in pivotal studies which only enroll patients without baseline MMR Wang R et al. Medicine (Baltimore). 2019 Apr;98(15):e15222; Saussele S et al. Leukemia. 2018 May;32(5):1222-1228; Shah NP et al. Journal of the National Comprehensive Cancer Network 2024, 22(1), 43-69; Talpaz M et al. Cancer. 2018 Apr 15;124(8):1660-1672 IS: international standard; MR: molecular response 1013 1012 1011 109 108 107 106 105 BCR-ABL1 (%) 100% <10% <1% <0.1% <0.01% <0.0032% 1010 MR Levels MR1 MR2 MR3 MR4 MR4.5 <0.0001%MR5 IS baseline Deep Molecular Response (DMR) Leukemic Burden Approximate number of leukemic cells Major Molecular Response (MMR) Patients without baseline MMR enroll due to treatment failure or intolerance Patients with baseline MMR or better enroll due to intolerance Reason to Enroll Treatment Goal Achieve MMR Maintain MMR Clinical Endpoints MMR Achieved MMR maintained Overall (cumulative) MMR 17
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Interpreting CML Phase 1 Data: Key Parameters and Questions Parameter Key Questions Baseline Demographics - # of prior TKIs; prior asciminib; prior ponatinib - Lack of efficacy vs intolerance to last TKI - Baseline BCR-ABL transcript distribution - Is the CARDINAL population comparable to recent Ph1 studies in CML? Key Measures of Molecular Response - MMR achievement: - at 6 months - across baseline transcripts - within key patient subgroups - Is MMR achievement at 6 months competitive with asciminib and other novel agents? - Are MRs occurring across the range of baseline BCR-ABL transcripts? - Meaningful MMR achievement within difficult to treat patient subsets? Safety and Tolerability - Treatment discontinuation, dose reduction, etc. - Gr 3 or higher and all grade hematologic and non-hematologic AEs - Are majority of patients staying on treatment? - Are safety differentiators seen early in dose escalation holding at higher doses with longer follow up? 18 TKI: tyrosine kinase inhibitor; MMR: major molecular response; MR: molecular response; AE: adverse events
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Majority of Patients in Phase 1 CML Trials Have High Baseline Transcripts and Lack of Efficacy on Prior TKI Hughes TP, et al. N Engl J Med 2019;381:2315-2326. Hochhaus A et al. HemaSphere 2025; 9(S1), pg 155-156. Jiang Q et al. Blood 2023; 142, Supplement 1, pg 867. Baseline characteristics in Ph1 CML studies over the last decade Baseline transcript >1% >50% Baseline MMR or Better (%) <20% Lack of efficacy to last TKI >60% Resistance mutations (%) T315I 7-25% Other ~10% T315Im and non-T315I mutant patients are historically separated for efficacy reporting 19
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CARDINAL Enrolls Patients Who Have Had Treatment Failure/Intolerance to Asciminib and Other TKIs 1. Hughes TP, et al. N Engl J Med 2019;381:2315-2326. 2. Rea D et al. Blood 2021; 138 (21): 2031–2041. 3. Pamuk et al. Clin Cancer Res. 2024 Oct 1;30(19):4266-4271. 4. Hochhaus A et al. HemaSphere 2025; 9(S1), pg 155-156. 5. ClinicalTrials.gov identifier: NCT06163430. 2014 Ph1 study of asciminib 2017 Asciminib Ph3 study approved in 3L+ CP-CML3 2021 20242022 Ph1 ENABLE study of ELVN-001 (active-site TKI) Ph1 CARDINAL study of TERN-701 (allosteric TKI) Enrolled population Asciminib naïve1,2 Imatinib / 2GTKI / ponatinib failure/ intolerant1,2 Asciminib failure / intolerant4 Imatinib / 2GTKI / ponatinib failure / intolerant4 Primarily 3L+ patients1,2 Primarily 3L+ patients4 enrolling a similar population as ENABLE5 20
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MMR Rates from Completed Asciminib Trials and Ongoing Ph1 Trials Provide Informative Efficacy Benchmarks Response rates of non-T315Im patients who achieved at or by 6 months. *BCR ABL1 > 0.1% was required at screening. DMR= deep molecular response. Included patients achieving MR4, BCR-ABL1IS ≤0.01%; MR4.5, BCR-ABL1IS ≤0.0032%; and MR5, BCR-ABL1IS ≤0.001; N/A = not applicable Hughes TP, et al. N Engl J Med 2019;381:2315-2326. Mauro M et al. Leukemia 2023; 37:1048-1059. Rea D et al. Blood 2021; 138 (21): 2031–2041. Hochhaus A et al. HemaSphere 2025; 9(S1), pg 155-156. 6-month timepoint Asciminib ELVN-001 Ph1 ’X2101 (N=99) Ph3 ASCEMBL (N=157) Ph1 ENABLE (N=53) MMR Achievement 24% 25% 32% Overall (cumulative) MMR 37% N/A* 47% DMR Achievement 14% 10% Not disclosed • Additionally, it is important to look at MMR achievement and cumulative MMR in key patient subgroups which reflect more refractory patients (responses are strong indicators of efficacy): ‒ Patients with prior asciminib ‒ Patients with prior ponatinib ‒ Patients with lack of efficacy to last TKI 21
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The Response Shift Table Can Be Used to Comprehensively Assess Depth and Quality of Molecular Responses In general, the goal is to shift patients ‘upwards’ into lower BCR-ABL1 MR categories Hughes TP, et al. N Engl J Med 2019;381:2315-2326. • 6-month MMR achievement is the percent of patients with baseline BCR-ABL1> 0.1% who achieve < 0.1% by 6 months • Achieving 6-month MMR is more challenging with increasing baseline transcript categories from 0.1-1% to >10% • Seeing shifts to MMR within all baseline categories >0.1% indicates robust efficacyBest BCR-ABL1 (IS) response by 6 months Post-treatment BCR-ABL1 Baseline BCR-ABL1 Response Category MR5 (DMR) ≤0.001 MR4.5 (DMR) >0.001 to 0.0032 MR4 (DMR) >0.0032 to 0.01% MR3 (MMR) >0.01 to 0.1% MR2 >0.1 to 1% MR1 >1 to 10% >10% MR5 (DMR) ≤0.001 MR4.5 (DMR) >0.001 to 0.0032 MR4 (DMR) >0.0032 to 0.01% MR3 (MMR) >0.01 to 0.1% MR2 >0.1 to 1% MR1 >1 to 10% >10% Not in MMR at baseline> MMR at baseline > MMR Achieved (%)> MMR maintained (%) 3-logs to MMR 2-logs to MMR 1-log to MMR 22
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Upcoming Data for TERN-701 will Build on 4Q24 Interim Data and Provide Benchmarkable Ph1 Efficacy and Safety Data Q4 2024: Proof of Clinical Activity and Safety (n=15) ✓ No DLTs in dose escalation; no MTD ✓ Linear PK with target coverage > asciminib 80mg ✓ Compelling molecular responses in heavily pre-treated patients with high baseline transcripts ✓ Rescue of response in asciminib treatment failure ✓ Rapid DMR achievement in 2G TKI failure Q4 2025: Benchmarkable Efficacy and Safety (n=50+) • 6-month molecular response: MMR achievement, cumulative MMR • Molecular responses across baseline transcript levels • Population subset analysis, including MMR achievement in: ‒ post-asciminib ‒ post-ponatinib ‒ failure to last TKI • Longer term safety data with larger number of patients and longer follow up 23
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Future of CML and Development Path Ahead Scott Harris Chief Development Officer
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TERN-701 has Potential to Further Improve Efficacy and/or Safety of the Allosteric Class in CML Adapted from Novartis ASCO Investor Event | June 2, 2024 imatinib Asciminib Superior SuperiorEfficacy Profile Safety/Tolerability Profile 2G/3G active- site TKIs Opportunities for TERN-701 25
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In a Multi-Allosteric Treatment Paradigm, TERN-701 has Ample Opportunity to Capture Market Share in 1L and 2L Note: Patient figures represent new starts by line of therapy in G7 nations (Canada, France, Germany, Italy, Japan, the United Kingdom and the United States) 1. Clearview Market Sizing 2025 and Terns market research; 2. Novartis ASCO Investor Event | June 2, 2024; 3. Average Duration of Treatment from CancerMPact® Treatment Architecture 1L 3L+ Anticipated Patient Flow and Market Share with Multiple Approved Allosteric TKIs1 2L 17K2 patients 7.4K2 patients switching to 2L 5.5K2 patients switching to 3L+ ~60% ~70% ~30% Majority of newly diagnosed patients will start on the best available therapy (i.e., allosteric)… … asciminib failures in 1L → switch to more effective allosteric … generic active-site failures in 1L → switch to allosteric (lower barrier to access) … patients who progress beyond two allosteric TKIs will likely receive an active-site Allosteric Active-site Compete for significant 1L share with potential best- in-class profile Initial target segments (2L+) as potential best option for rescue TERN-701 Potential Position 26 Generic active-sites 31 months avg DoT3 26 months avg DoT3 22 months avg DoT3
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Anticipated TERN-701 Registration Path in Early Line CML Patients • Potential for initial approval as 2L+ therapy in patients failing frontline treatment with asciminib or active-site TKI • Clinical development in newly diagnosed CML patients expected to run in parallel TERN-701 Phase 1 Phase 3 Monotherapy 2L+ CML patients Phase 3 Monotherapy Frontline CML patients Second approval Initial approval Staggered start 27
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Summarizing a Compelling Potential Opportunity for TERN-701 in CML Superior MoA with potential best-in-class allosteric profile Broad opportunity across 1L and 2L+ Accelerated development and clear regulatory pathway Limited competition in allosteric class 28
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Mission. Vision. Identity. our name tells our story 29
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Appendix
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Asciminib Showed Dose Related Increases in Pancreatic Adverse Events and Hypertension Hughes TP, et al. N Engl J Med 2019;381:2315-2326; Rea D et al. Blood 2021; 138 (21): 2031–2041; Asciminib USPI; Pamuk et al. Clin Cancer Res 2024 • TERN-701 early Ph1 data showed trend towards lower rates of pancreatic toxicity and hypertension compared to asciminib • Additional safety data (more patients, longer follow up) would further support a differentiated safety profile if trends hold ASCEMBL (N=233) Dose: 40mg BID X2101 (N=150) Cumulative dose range: 80mg - 400mg 31 0% 5% 10% 15% 20% 25% 30% 35% 40% 45% 50% Elevated pancreatic enzymes Clinical pancreatitis Hypertension Elevated pancreatic enzymes Clinical pancreatitis Hypertension All grades Grades ≥ 3