UNITED STATES
SECURITIES AND EXCHANGE COMMISSION
Washington, D.C. 20549
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FORM 8-K
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CURRENT REPORT
Pursuant to Section 13 or 15(d)
of the Securities Exchange Act of 1934
Date of Report (date of earliest event reported): December 10, 2024
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Item 7.01 Regulation FD Disclosure.
On December 10, 2024, Tourmaline Bio, Inc. (the “Company”) made available an updated corporate presentation that may be used in connection with presentations at conferences and investor meetings, which can be found on the Company’s website (the “Corporate Presentation”). The Corporate Presentation is furnished as Exhibit 99.1 to this Current Report on Form 8-K and incorporated by reference in this Item 7.01.
The information furnished under this Item 7.01, including Exhibit 99.1, shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the “Exchange Act”), or subject to the liabilities of that section, nor shall it be deemed to be incorporated by reference into any of the Company’s filings with the Securities and Exchange Commission under the Exchange Act or the Securities Act of 1933, as amended, whether made before or after the date hereof, regardless of any general incorporation language in such a filing, except as otherwise expressly stated in such filing.
Item 9.01 Financial Statements and Exhibits.
(d) Exhibits.
| Exhibit No. | Description | |||||||
| 99.1 | ||||||||
| 104 | Cover Page Interactive Data File (embedded within the Inline XBRL document) | |||||||
SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, as amended, the Registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.
| TOURMALINE BIO, INC. | ||||||||
| Date: December 10, 2024 | By: | /s/ Ryan Robinson | ||||||
Name: | Ryan Robinson | |||||||
Title: | Chief Financial Officer and Treasurer | |||||||
Corporate Overview December 2024 Exhibit 99.1
The material in this presentation regarding Tourmaline Bio, Inc. (“we,” “us” or the “Company”) is for informational purposes only. This presentation contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 that involve substantial risks and uncertainties. All statements, other than statements of historical facts, contained in this presentation, including statements regarding the timing of initiation, progress and results of the Company’s current and future preclinical and clinical trials for its product candidates, including pacibekitug (also referred to as TOUR006); the therapeutic potential of pacibekitug; the timing and likelihood of seeking regulatory approval for the Company’s product candidates, including pacibekitug; the timing of submitting investigational new drug applications and other regulatory documents; the Company’s ability to achieve planned milestones; the competitive landscape for the Company’s product candidates; and the Company’s estimates regarding expenses, future revenue, capital requirements, cash runway and needs for additional financing. The words “may,” “will,” “should,” “expects,” “intends,” “plans,” “anticipates,” “believes,” “estimates,” “predicts,” “potential,” “continue,” and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. The Company may not actually achieve the plans, intentions, or expectations disclosed in these forward-looking statements, and you should not place undue reliance on these forward-looking statements. Actual results or events could differ materially from the plans, intentions and expectations disclosed in these forward-looking statements. Many factors may cause differences between current expectations and actual results, including, but not limited to, unexpected safety or efficacy data observed during preclinical or clinical studies, clinical site activation rates or clinical trial enrollment rates that are lower than expected, changes in the regulatory environment, changes in expected or existing competition, unexpected litigation or other disputes, and other risks and uncertainties, including those described in the section titled “Risk Factors” in the Company’s most recent filings with the Securities and Exchange Commission. The forward-looking statements included in this presentation represent the Company’s views as of the date of this presentation. The Company undertakes no obligation to update the information contained in this presentation to reflect new events or circumstances, except as required by law. In addition, certain information contained in this presentation relates to or is based on studies, publications, surveys and other data obtained from third-party sources and the Company’s own internal estimates and research. While the Company believes these third-party sources to be reliable as of the date of this presentation, it has not independently verified, and makes no representation as to the adequacy, fairness, accuracy or completeness of any information obtained from third-party sources. In addition, all of the market data included in this presentation involves a number of assumptions and limitations, and there can be no guarantee as to the accuracy or reliability of such assumptions. Finally, while we believe our own internal research is reliable, such research has not been verified by any independent source. This presentation contains trademarks, services marks, trade names and copyrights of the Company and other companies, which are the property of their respective owners. The use or display of third parties’ trademarks, service marks, trade name or products in this presentation is not intended to, and does not, imply a relationship with the Company, or an endorsement of sponsorship by the Company. Solely for convenience, the trademarks, service marks and trade names referred to in this presentation may appear without the ®, TM or SM symbols, but such references are not intended to indicate, in any way, that the Company will not assert, to the fullest extent under applicable law, their rights or the right of the applicable licensor to these trademarks, service marks and trade name. Disclaimer 2
Our mission 3 We are driven by our mission to develop transformative medicines that dramatically improve the lives of patients with life-altering immune and inflammatory diseases
Emil deGoma, MD Senior Vice President, Medical Research Gerhard Hagn Senior Vice President, Head of Commercial & BD Kevin Johnson, PhD Chief Regulatory Officer Experienced leadership team 4 Ryan Robinson, CPA Chief Financial Officer Sandeep Kulkarni, MD Co-Founder and Chief Executive Officer Brad Middlekauff, JD Chief Business Officer and General Counsel Susan Dana Jones, PhD Chief Technology Officer Dora Rau Senior Vice President, Head of Quality Management Team Board of Directors Clay Siegall, PhD Chairman Caley Castelein, MD Aaron Kantoff Mark McDade Sapna Srivastava, PhD Parvinder Thiara Sandeep Kulkarni, MD Don Fitch Senior Vice President, Product Development
Pacibekitug (also referred to as TOUR006) has demonstrated best-in class potential: long-acting, low immunogenicity, and low-volume subcutaneous administration observed in clinical trials to date Two paths to significant value creation: (1) cardiovascular inflammation and (2) thyroid eye disease Key highlights 5 An IL-6 renaissance is underway: new insights emerging about a broad range of indications where IL-6 may be clinically validated A late-stage clinical company: Phase 2 TRANQUILITY trial in CV and pivotal Phase 2b spiriTED trial in TED ongoing Two potentially transformative data readouts expected in 2025: Topline data from TRANQUILITY trial expected in Q2 2025 and topline data from spiriTED trial expected in H2 2025 Well-financed: cash expected to fund operations into 2027, enabling the delivery of key anticipated milestones for both paths
1Across six clinical trials in healthy volunteers and RA, SLE, and CD patients. 2Data on file; single intravenous 10mg dose in Ph1 MAD study in RA patients; as measured by C-reactive protein (CRP), a pharmacodynamic marker of IL-6 signaling. 3Generated from Medarex transgenic mouse platform; across approximately 450 subjects dosed with pacibekitug, only 2 subjects generated anti-drug antibodies (ADAs) following treatment. 4Data on file. 5To be evaluated in CV Phase 2 trial. 6To be evaluated in TED Phase 2 trial. Every 8-week dosing was achieved in prior Phase 2 trials. CD: Crohn’s Disease. CV: cardiovascular. SC: subcutaneous. RA: rheumatoid arthritis. SLE: systemic lupus erythematosus. TED: thyroid eye disease. Pacibekitug: a long-acting anti-IL-6 monoclonal antibody with best-in-class potential 6 Potential value to patientsAttributes observed to date Existing data from approximately 450 study participants1 Fully human with ADAs in only 0.5% of patients³ >90% pathway inhibition after single 10mg dose² Long-acting with terminal half-life of ~7 weeks¹ High affinity to IL-6⁴ • Dosing quarterly5 (CV) or every 8 weeks6 (TED) • Rapid and robust impact across diseases • Generally well-tolerated safety profile observed to date • Volume of ≤1ml for SC injection5,6 • Durable benefit without need to increase dose
The timing of regulatory and clinical trial milestones are subject to change and additional discussion with the FDA AMI: acute myocardial infarction. ASCVD: atherosclerotic cardiovascular disease. CKD: chronic kidney disease. Satra: satralizumab. TED: thyroid eye disease. Zilti: ziltivekimab Two paths to unlock major value creation 7 IL-6 Renaissance Emerging insights implicating IL-6 in a wide range of rare & large diseases Pacibekitug Long-acting Low immunogenicity Low volume, SC Cardiovascular Inflammation Thyroid Eye Disease + Q2 2025: TRANQUILITY Phase 2 topline data 2025 / 2026: Zilti ASCVD in CKD Phase 3 (ZEUS) topline data H2 2025: spiriTED Phase 2b topline data 2026: Satra TED Phase 3 (Satra- GO) topline data 2026: Zilti AMI Phase 3 (ARTEMIS) topline data Key expected readouts Milestones key: Internal External
Disease Focus Indication Preclinical Phase 1 Phase 2 Phase 3 Expected key milestones Cardiovascular inflammation Atherosclerotic Cardiovascular Disease (ASCVD) Phase 2 topline x data expected in Q2 2025 Abdominal aortic aneurysm (AAA) Phase 2 PoC trial initiation expected after TRANQUILITY topline data Autoimmune disease Thyroid Eye Disease (TED) Phase 2b topline data expected in H2 2025 Clinical development plan for pacibekitug 8 Note: Hatched bars represent trials that have not yet commenced The timing of regulatory submissions and clinical trial milestones are subject to change and additional discussion with the FDA
Cardiovascular Inflammation
Reducing inflammation: the next frontier in CV diseases 10 Increasing validation for IL-6 driven inflammation as a critical and modifiable risk factor driving residual cardiovascular risk Potential of IL-6 inhibition spans a broad range of cardiovascular indications, affecting tens of millions of patients globally Pacibekitug’s potentially best-in-class profile, including quarterly SC administration, is being evaluated in the Phase 2 TRANQUILITY trial – over-enrollment completed, topline data expected in Q2 2025 Converging lines of human evidence across multiple settings support the transformative potential of IL-6 inhibition IL-6 inhibition is being evaluated in multiple cardiovascular outcomes trials with external readouts expected over the next 12 to 24 months
World-class Cardiovascular Scientific Advisory Board providing insight on our development strategy for pacibekitug 11 James Min, MD Cleerly, Inc. Pradeep Natarajan, MD, MMSC Massachusetts General Hospital Harvard Medical School Michael D. Shapiro, DO, MCR Wake Forest University Michael Szarek, PhD University of Colorado CPC Clinical Research Marc P. Bonaca, MD, MPH University of Colorado CPC Clinical Research Douglas L. Mann, MD Washington University School of Medicine Joshua A. Beckman, MD, MSc University of Texas Southwestern Robin Choudhury, MA, DM University of Oxford Dipender Gill, MD, PhD Sequoia Genetics Deepak L. Bhatt, MD, MPH, MBA SAB Chair Mount Sinai Fuster Heart Hospital
1Adapted from Ridker, Eur Heart J (2016). Many CV disease patients have residual inflammatory risk 12 Differential secondary prevention treatment options for statin-treated patients1 Known cardiovascular disease LDL 3.8 mmol/L (150 mg/dL) hs-CRP 4.5 mg/L High-intensity statin “Residual cholesterol risk” LDL 2.8 mmol/L (110 mg/dL) hs-CRP 1.8 mg/L Additional LDL reduction “Residual inflammatory risk” LDL 1.15 mmol/L (45 mg/dL) hs-CRP 3.8 mg/L Additional inflammation reduction “Lower is better” Our focus
Research increasingly highlights inflammation as a driver of CV risk and supports therapeutic potential of IL-6 inhibition 13
List of therapies not exhaustive. ACEI: angiotensin-converting enzyme inhibitor. ACL: adenosine triphosphate-citrate lyase. ANGPTL3: angiopoietin-like protein 3. ApoB: apolipoprotein B. ApoC3: apolipoprotein C3. ARB: angiotensin receptor blocker. CETP: Cholesteryl ester transfer protein. CRISPR: clustered regularly interspaced short palindromic repeats. GIP: gastric inhibitory polypeptide. GLP-1: glucagon-like peptide-1. IL-6: Interleukin-6. MTP: microsomal triglyceride transfer protein. NLRP3: nucleotide-binding domain, leucine-rich–containing family, pyrin domain–containing-3. NPC1L1: Niemann-Pick C1-Like 1. PAR: protease-activated receptors. PCSK9: proprotein convertase subtilisin/ kexin type 9. P2Y12R: purinergic 2Y type 12 receptor. SGLT2: sodium-glucose cotransporter 2. Cardiovascular inflammation largely unaddressed by existing treatments 14 Thrombosis Hypertension Atherogenic lipoproteins Diabetes, Insulin resistance, Obesity Inflammation None readily available Blood pressure ApoB, Non-HDL-C, LDL-C, Triglycerides, Lipoprotein(a) HbA1c, Fasting glucose, Weight C-reactive protein Aspirin P2Y12R inhibitors Factor Xa inhibitors PAR-1 antagonists ACEI/ARB Calcium channel blockers Thiazide diuretics Renin inhibitors Beta-blockers Mineralocorticoid antagonists Statins PCSK9 inhibitors Icosapent ethyl NPC1L1 inhibitors ACL inhibitors Bile acid sequestrants MTP inhibitors ANGPTL3 inhibitors Apheresis SGLT2 inhibitors GLP-1 agonists GIP/GLP-1 agonists Colchicine Atherothrombotic Pathways Biomarkers Approved Therapies Factor XI inhibitors Factor XIa inhibitors Angiotensinogen inhibitors Aldosterone synthase inhibitors Endothelin antagonists Renal denervation Baroreceptor activation CETP inhibitors Lipoprotein(a) inhibitors ApoC3 inhibitors Fibrates CRISPR PCSK9 base editing GIP/GLP-1/glucagon agonists Amylin agonists GIP-1/amylin agonists IL-6 inhibitors NLRP3 inhibitors Therapies in Late-Stage Development
1RESCUE: Ridker et al., Lancet (2021). Ziltivekimab 15mg q4w arm. 2Chertow et al., Nat Med (2024). Clazakizumab 5mg q4w arm. 3CANTOS: Ridker et al., N Eng J Med (2017). 150mg q3m arm. 4Fiolet et al., PLOS ONE (2020). Colchicine 0.5mg QD. 5SELECT: Plutzky et al., EAS Congress (2024). Semaglutide 2.4mg QW maintenance. 6Borlaug et al., Nat Med (2024). Tirzepatide up to 15mg QW. 7Ridker et. al., Lancet (2017). Time course values obtained by webplotdigitizer. Values are not placebo adjusted. CVD: cardiovascular disease. GIP: gastric inhibitory polypeptide. GLP-1: glucagon-like peptide-1. hs-CRP: high sensitivity C-reactive protein. Certain data in this presentation are based on a cross-trial comparison and are not based on head-to-head clinical trials. Cross trial comparisons are inherently limited and may suggest misleading similarities or differences in outcomes. Results of head-to-head comparisons may differ significantly from those set forth herein. IL-6 inhibition has produced rapid and robust hs-CRP reductions in patients with established or at high-risk of CVD 15 -100% -90% -80% -70% -60% -50% -40% -30% -20% -10% 0% 0 13 26 39 52 % h s- C R P r ed uc tio n fr om b as el in e (% ) Ziltivekimab (IL-6)1 Clazakizumab (IL-6)2 Canakinumab (IL-1β)3 Colchicine4 Tirzepatide (GLP-1/GIP)6 Semaglutide (GLP-1)5 Week 82% 82% 55% 36% 40% 0% 20% 40% 60% 80% 100% IL-6 (week 12)IL-6 (week 12) IL-1b (month 3) Colchicine (day 30) GLP-1/GIP (week 52) Therapy (target, time) Ziltiv kimab (IL-6, wk 12)1 Clazakizumab (IL-6, wk 12)2 Canakinumab (IL-1β, mo. 3)7 Colchicine (NA, day 30)4 Tirzepatide (GLP-1/GIP, wk. 52)6 Baseline hs-CRP (mg/L), median 5.70 7.2 4.25 4.40 3.1 Percent reduction in hs-CRP % of patients with hs-CRP <2 mg/L
~55% ~55% ~60% ~55% ~55% 100% ~55% ~75% ~60% ~60% ~60% ~60% ~75% 25M 18M 8.5M 5.5M 3.7M 900K 800K 2.3M 7.0M 3.2M 3.2M 600K 1.3M ASCVD – Total CAD Ischemic stroke ASCVD + CKD 3/4 PAD Acute MI* Acute ischemic stroke* AAA - Total HF - Total HFpEF HFrEF HFmrEF Acute HF* ASCVD – Total CAD Ischemic stroke ASCVD + CKD 3-4 PAD Acute MI* Acute ischemic stroke* A - Total HF - Total HFpEF HFrEF HFmrEF Acute HF* 1Publications available upon request. *Annual incidence AAA: abdominal aortic aneurysm. ASCVD: atherosclerotic cardiovascular disease. CAD: coronary artery disease. CKD: chronic kidney disease. HF: heart failure. HFmrEF: Heart Failure with Mid-Range Ejection Fraction. HFpEF: heart failure with preserved ejection fraction. HFrEF: heart failure with reduced ejection fraction. MI: myocardial infarction. PAD: peripheral artery disease. IL-6 inhibition has the potential to address millions of patients across a wide range of inflammation mediated CV conditions 16 Estimated US prevalence (2024)1 Populations are not mutually exclusive Key Elevated hs-CRP Normal hs-CRP Our current focus
ASCVD: atherosclerotic cardiovascular disease Convergence of human evidence supports therapeutic potential of IL-6 inhibition for ASCVD 17 Evidence suggests IL-6 may drive ASCVD risk Human genetic evidence Epidemiological evidence Clinical trial evidence
1Ference et al., J. Am. Coll. Cardiol. (2012). 2Casula et al., Pharm. Res. (2019). 7 13Levin et al, Circulation Research (2021). 14Georgakis et al., Circulation (2021). 15Swerdlow et al., Lancet (2012). 16Georgakis et al., Circ Genom Precis Med. (2020). 17Georgakis et al., BCM Med. (2022).18Minikel et al., Nature (2024). 3Zhao et al., Ann Rheum Dis (2022). 4Spiera eta al. N Engl Med (2023). 5Wan et al., Hypertension (2021). 6The Blood Pressure Lowering Treatment Trialists’ Collaboration, Lancet (2021). Voight et al., Lancet (2012). 8Keene et al., BMJ (2014). 9Gregson et al., Eur J Prev Cardiol. (2017). 10Fras et al., Arch Med Sci. (2021). 11Kang et al., Neurology (2021). 12Lenercept Multiple Sclerosis Study Group, Neurology (1999). Human genetic studies provide initial support for IL-6 pathway inhibition to lower ASCVD risk 18 Concordance between results of human genetic studies and randomized clinical trials Therapeutic target Genetic Result RCT Result Lowering LDL-C to lower ASCVD risk1,2 Positive Positive Inhibiting IL-6 to treat polymyalgia rheumatica3,4 Positive Positive Lowering blood pressure to lower ASCVD risk5,6 Positive Positive Raising HDL-C to lower ASCVD risk7,8 Negative Negative Inhibiting LpPLA2 to lower ASCVD risk9,10 Negative Negative Inhibiting TNFα to treat multiple sclerosis11,12 Negative (harm) Negative (harm) Inhibiting IL-6 to lower ASCVD risk13-17 Positive Trials Ongoing “Probability of success for drug mechanisms with genetic support is 2.6 times greater than those without.”18
1Women’s Health Study. MACE: CV death, MI, stroke, coronary revascularization. Increased risk defined as 1-relative risk, compared to lowest quintile of Lp(a) and hs-CRP population, adjusted for age, initial randomization treatment group, smoking (current, past, never), presence of diabetes, and Framingham blood pressure categories. Table 2. Ridker et al, NEJM (2024). Emerging evidence suggests that hs-CRP is more strongly associated with MACE than both LDL and Lp(a) 19 1.00 1.01 0.94 1.04 1.33 1.00 1.00 1.07 1.23 1.36 1.00 1.11 1.19 1.38 1.70 0.8 1.0 1.2 1.4 1.6 1.8 Quintile 1 (reference) Quintile 2 Quintile 3 Quintile 4 Quintile 5 Risk of MACE 30-year longitudinal data from the Women’s Health Study1 (n=27,929) Late breaking data presented at European Society of Cardiology 2024 Congress and simultaneously published in the New England Journal of Medicine Quintile (r f r ) i til i til i til i til hs-CRP mg/L baseline <0.65 0.65 to <1.47 1.47 to <2.75 2.75 to <5.18 ≥5.18 LDL-C mg/dL baseline <96.1 96.1 to <113.5 113.5 to <129.7 129.7 to <150.7 ≥150.7 Lp(a) mg/dL baseline <3.6 3.6 to <7.6 7.6 to <15.5 15.5 to <44.1 ≥44.1
1 2Adapted from Ridker et al., Circ. Res. (2016), Ridker et al., N. Engl. J. Med. (2017). Arnold et al., Eur. J. Cardiol. (2021) and Muller et al., J Lipid Res (2015) Landmark CANTOS study validated therapeutic potential of addressing inflammation in ASCVD 20 10,061 patients • Stable CAD (post MI) • On Statin, ACE/ARB, BB, ASA • hs-CRP ≥2 mg/L Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS) Trial Design1 Primary endpoint: Time to the first occurrence of MACE (CV death, non-fatal MI, or non-fatal stroke) Canakinumab 50 mg Q3M n = 2,170 Placebo Q3M n = 3,344 Canakinumab 150 mg Q3M n = 2,284 Canakinumab 300 mg Q3M n = 2,263 IL-1β is upstream of IL-62 NLRP3 Inflammasome IL-6 IL-1β canakinumab pacibekitug ziltivekimab clazakizumab C-reactive protein (marker of inflammation) PAI-1 Anti- fibrinolytic Pro- clotting Fibrinogen + - NLRP inflammasome inhibitors colchicine Lipoprotein(a)
Reduction in MACE shown as 1-Hazard Ratio. ITT: intent to treat. MACE: major adverse cardiovascular events including CV death, myocardial infarction (MI), stroke. n.s.: not statistically significant. ITT CANTOS analysis presents data for 150mg dose group; values for CANTOS subanalyses combine all doses (50, 150, 300 mg). Ridker et al., NEJM (2017). Ridker et al., Lancet (2018). Adjusted for age, gender, smoking, hypertension, diabetes, BMI, baseline hs-CRP, baseline LDL-C. Ridker et al., Eur Heart J (2018). Adjusted for age, gender, smoking, hypertension, diabetes, BMI, baseline IL-6, baseline LDL-C. Ridker et al., JACC (2018). Lessons from canakinumab (anti-IL-1β mAb): “Lower is better” for downstream biomarkers of IL-6 activity 21 On-treatment On-treatment -15% -25% -30% -35% -60% -50% -40% -30% -20% -10% 0% R ed u ct io n in M A C E IL-6 low tertile hs-CRP <2 mg/L CKD ITT hs-CRP <2 mg/L R ed u ct io n in C V D ea th IL-6 low tertile hs-CRP <2 mg/L hs-CRP <2 mg/L -12% -31% -34% -59% -60% -50% -40% -30% -20% -10% 0% ITT CKD n.s.
Reduction in MACE shown as 1-Hazard Ratio. MACE: major adverse cardiovascular events including CV death, myocardial infarction (MI), stroke except for: ODYSSEY OUTCOMES (all death, MI, ischemic stroke); COLCOT (CV death, MI, stroke, resuscitated cardiac arrest); LoDoCo2 (CV death, MI, ischemic stroke); main CANTOS analysis presents data for 150mg dose group; values for CANTOS subanalyses combine all doses (50, 150, 300mg); control arms were placebo + background SoC. Certain data in this slide are based on a cross-trial comparison and are not based on head-to-head clinical trials. Cross-trial comparisons are inherently limited and may suggest misleading similarities or differences in outcomes. Results of head-to-head comparisons may differ significantly from those set forth herein. NNT (number needed to treat) values obtained from absolute risk extracted from Kaplan-Meier figures via webplotdigitizer, unless directly reported. NNT for IL-6 < median shown; not reported for IL-6 low tertile. The information on this slide is based on Tourmaline-generated analysis of third-party data and is being presented for hypothesis generating purposes only. As a result, the actual MACE risk reduction hypothesized may be more or less than the data presented in this slide. Publications available upon request. Lessons from canakinumab (anti-IL-1β mAb): Robust inhibition of IL-6 pathway has transformative potential in ASCVD 22 -30% -35% -14% -15% -15% -20% -20% -26% -28% -50% -40% -30% -20% -10% 0% R ed u ct io n in M A C E IL-6 low tertile hs-CRP <2 mg/L CKD Alirocumab ODYSSEY Bempedoic acid CLEAR Colchicine COLCOT Evolocumab FOURIER Semaglutide SELECT Icosapent ethyl REDUCE-IT Colchicine LoDoCo2 3-year estimates for NNT (number needed to treat) support transformative potential and efficient Phase 3 study designs 14 20 63 CANTOS: On-treatment 57368350nr85
-17% -47% -59% -68% -4% -77% -88% -92% 19% -86% -90% -92%-100% -80% -60% -40% -20% 0% 20% PBO 50 mg 150 mg 300 mg PBO 7.5 mg 15 mg 30 mg PBO 2.5 mg 5 mg 10 mg 1Ridker et al., NEJM (2017). 2Ridker et al., Lancet (2021). 3Chertow, Nature (2024). Certain data in this presentation are based on a cross-trial comparison and are not based on head-to-head clinical trials. Cross trial comparisons are inherently limited and may suggest misleading similarities or differences in outcomes. Results of head-to-head comparisons may differ significantly from those set forth herein. In independent studies, direct IL-6 inhibition lowered hs-CRP more than upstream IL-1β blockade 23 M ed ia n % r ed u ct io n in h s- C R P (W ee k 12 ) Ziltivekimab Monthly (Phase 2 RESCUE)2 Canakinumab Quarterly (Phase 3 CANTOS)1 Direct IL-6 inhibition achieved ~2x placebo-adjusted reductions in hs-CRP compared to upstream IL-1β Clazakizumab Monthly (Phase 2b)3
The timing of clinical trial milestones are subject to change. ASCVD: atherosclerotic cardiovascular disease. CKD: chronic kidney disease. CVOT: cardiovascular outcome trial. ESKD: End Stage Kidney Disease. HFpEF: heart failure with preserved ejection fraction. MACE: major adverse cardiovascular event. MI: myocardial infarction. 1Clinicaltrials.gov: NCT05021835. 2Clinicaltrials.gov: NCT06118281. 3Clinicaltrials.gov: NCT06200207 4Clinicaltrials.gov: NCT05636176 5Clinicaltrials.gov: NCT05485961 (Phase 3 portion only) Five Phase 3 CVOTs enrolling >24,000 patients 24 Ziltivekimab 15 mg QM + Standard of Care Placebo QM + Standard of Care 6,200 patients • ASCVD • CKD stage 3-4 • hs-CRP ≥2 mg/L 1:1 ZEUS: ASCVD w/CKD1 Primary endpoint: Time to the first occurrence of MACE (CV death, non-fatal MI, or non-fatal stroke) ATHENA: HFpEF3 Primary endpoint: Change in KCCQ-CSS at 1 year ARTEMIS: acute MI2 Ziltivekimab loading 30mg followed by 15mg QM + Standard of Care Placebo QM + Standard of Care 10,000 patients • Acute MI • First dose within 36 or 48 hrs 1:1 Primary endpoint: Time to the first occurrence of MACE (CV death, non-fatal MI, or non-fatal stroke) Ziltivekimab QM + Standard of Care Placebo QM + Standard of Care 680 patients • HF Class II-III • hs-CRP ≥2 mg/L 1:1 Topline data readouts expected 2025 / 2026 2026 2026 HERMES: HFpEF4 Primary endpoint: Time to first occurrence of a composite HF endpoint (CV death, HF hospitalization, or urgent HF visit) Ziltivekimab 15 mg QM + Standard of Care Placebo QM + Standard of Care 5,600 patients • HF Class II-IV • hs-CRP ≥2 mg/L 1:1 2027 POSIBIL6: ESKD5 Primary endpoint: Time to first occurrence of CV death or MI Clazakizumab 5 mg Q4W + Standard of Care Placebo Q4W + Standard of Care 2,310 patients • ESKD • Diabetes or ASCVD • hs-CRP ≥2 mg/L 1:1 2028
CD: Crohn’s disease, CKD: chronic kidney disease, HD: hemodialysis, NDD: non-dialysis dependent, SLE: systemic lupus erythematosus. 1Incidence of ADAs in repeat-dose studies calculated as reported per dosing arm. 2Route of administration in planned or ongoing studies in patients with or at high-risk of ASCVD. 3Clinicaltrials.gov NCT03926117. 4Pergola et al., JASN (2021). 5Ridker et al., Lancet (2021). 6Wada et al., J Cardiol (2023). 7Clinicaltrials.gov NCT01490450. 8Clinicaltrials.gov NCT01545050. 9Weinblatt et al., Arthritis Rheum (2015). 10Clinicaltrials.gov NCT05485961. Data reported in publications or on clinicaltrials.gov as detailed above. No head-to-head studies have been conducted between the mabs shown here, which have each been evaluated in different populations. Pacibekitug designed to offer best-in-class potential profile in cardiovascular diseases 25 Pacibekitug Ziltivekimab Clazakizumab Company Monoclonal antibody fully human (IgG2) fully human (IgG1k, YTE mutation) humanized rabbit (IgG1k) Anti-drug antibodies1 0-1% 6-13%3,4 0-10%7-9 Route of administration2 SC 0.6 mL SC5,6 1.0 mL IV10 Longest dosing intervals in completed studies Q8W (SLE, CD) Q4W (NDD-CKD)5,6 Q4W10 (HD-CKD) Targeted dosing intervals Quarterly Monthly Monthly
CD: Crohn’s disease, OLE: open-label extension, RA: rheumatoid arthritis, SLE: systemic lupus erythematosus. Rheumatoid arthritis: B0151002 study report. Table 14.4.7.1.1. Median baseline CRP 9.0 mg/L. Key eligibility: active disease, background methotrexate. Crohn’s disease: B0151003 study report. Table 14.2.4.1.3. Median baseline hs-CRP 21.1 mg/L. Key eligibility: active disease, failed/intolerant to anti-TNF . CD OLE B0151005 study report. Table 14.2.4.1. Systemic lupus erythematosus: B0151006 study report. Table 14.3.4.1.5. Median baseline hs-CRP 2.2 mg/L. α Median pre- baseline hs-CRP 16.4 mg/L, baseline hs-CRP 4.0 mg/L. Pacibekitug achieved robust and durable suppression of CRP in patients with high-grade inflammatory autoimmune disorders 26 Dosing: 0 2 4 6 8 10 0 4 8 12 16 20 0 5 10 15 20 0 4 8 12 Phase 1 RA IV 10 mg (n=6) Phase 2 CD SC 50 mg (n=71) M ed ia n h s- C R P (m g /L ) Weeks Weeks 0 5 10 15 20 -8 -4 0 4 8 12 16 20 24 28 32 36 40 44 48 52 Phase 2 CD OLE SC 50 mg or 50100 mg (n=91; n=100) Pre Weeks 0 2 4 6 8 10 0 4 8 12 16 20 24 Phase 2 SLE SC 50 mg (n=47) Weeks
ASCVD: atherosclerotic cardiovascular disease, RA: rheumatoid arthritis, SLE: systemic lupus erythematosus, CD: Crohn’s disease. The PK and PK/PD models for pacibekitug were developed based on the data from 5 clinical studies (two phase 1 studies in healthy volunteers, one phase 1 study in RA, one phase 2 study in SLE, and one phase 2 study in CD). A two-compartment model with first-order absorption and linear elimination and a mechanism-based indirect response model (in a relationship on CRP) adequately described the PK and PK/PD relationships, respectively. Simulations were performed assuming an RA-like population with baseline CRP >2 mg/L to 10 mg/L. Results at Day 90 are shown. 1Ridker et al., Lancet (2021). Results after 12 weeks of treatment are shown. Certain data in this slide are based on a cross-trial comparison and are not based on head-to-head clinical trials. Cross-trial comparisons are inherently limited and may suggest misleading similarities or differences in outcomes. Results of head-to-head comparisons may differ significantly from those set forth herein. PK/PD modeling supports potential for quarterly dosing of pacibekitug SC in ASCVD 27 % achieving hs-CRP <2 mg/L Results of PK/PD model developed from five studies in patients with RA, SLE, CD and healthy volunteers Ziltivekimab 15 mg monthly1 15 mg50 mg 25 mg Quarterly Monthly >85% >80% >90%-100% 0%>90% >85% >90% 0% 100% Median % reduction in hs-CRP 15 mg50 mg 25 mg Quarterly Monthly % achieving hs-CRP<2 mg/L: 82% median % reduction: 88%
6 months Safety follow-up period 6 months Treatment period n = 143 ASCVD: atherosclerotic cardiovascular disease. CKD: chronic kidney disease. eGFR: estimated glomerular filtration rate. hs-CRP: high-sensitivity C-reactive protein. UPCR: urine protein-creatinine ratio. Phase 2 trial supporting development in ASCVD Pacibekitug 50 mg SC quarterly Pacibekitug 25 mg SC quarterly Pacibekitug 15 mg SC monthly Study population: • CKD stage 3-4 (eGFR 15-59 ml/min/1.73m2) or UPCR>200 mg/g • hs-CRP ≥2 mg/L and <15 mg/L • Exclude patients at higher risk for safety complications (e.g., immunocompromised patients) Primary pharmacodynamic endpoint: • Change from baseline in hs-CRP through Day 90 Additional endpoints: • Percent of participants who achieve hs-CRP <2 mg/L • Other pharmacodynamic markers, including lipoprotein (a) • Safety and tolerability R Placebo Double-blinded, placebo-controlled Phase 2 trial (NCT06362759) | Status: over-enrollment completed Follow-up 28
1Stuntz, Cardiology (2016). 2Golledge et al., Eur Heart J (2023). 3UKSAT, NEJM (2002). 4Lederle et al., NEJM (2002). 5Chaikof et al., J Vasc Surg (2018). 6Isselbacher et al., Circulation (2022). 7Schermerhorn et al., NEJM (2008). 8Yei et al., JAMA Netw Open (2022). 9Gilmore et al., Circ Cardiovasc Qual Outcomes (2024). Figure from https://medlineplus.gov/ency/article/000162.htm. AAA: abdominal aortic aneurysm. ASCVD: atherosclerotic cardiovascular disease. HCP: healthcare professional. Abdominal aortic aneurysm: a high-mortality, first-in-disease opportunity for pacibekitug 29 • High-risk vascular disease with significant unmet need in approximately 2M people in US1 • Strong strategic fit with ASCVD due to overlapping prescribers • Progressive disease with increasing risk of rupture, usually a fatal event2 • In less than 5 years, majority of medium-sized AAA grow to threshold for surgical repair3,4 • Surgical repair, recommended for large AAA to prevent rupture, is associated with complications5-9 No FDA approved treatment
Human genetic evidence 1Burgess et al., ATVB 2024. 2 3Kokje et al., Atherosclerosis (2016). Results at day 14. 4Nishihara et al., PLoS One (2017). Results at day 42. 5Patel et al., Vasc Endovascular Surg (2023). Results at day 21. AAA: abdominal aortic aneurysm. Thanigaimani et al., Biomedicine (2022). Compelling evidence supports IL-6 inhibition to slow AAA growth Genetic variant associated with reduction in risk of AAA1 Epidemiological evidence Higher IL-6 levels associated with AAA2 Experimental evidence 0% 25% 50% 75% 100% Inhibition of IL-6 pathway signaling decreased AAA expansion in multiple preclinical models3 Increase in maximum AAA diameter Elastase model3 CaCl2 model4 CaCl2+ IL-6 model5 Control IL-6 pathway inhibition 30
1Chaikof et al., J Vasc Surg (2018). Isselbacher et al., Circulation (2022). Figure adapted from Perry et al., Ann Vasc Surg (2022). AAA: abdominal aortic aneurysm. PoC: proof of concept. Phase 2 PoC study expected to use imaging to evaluate the ability of pacibekitug to inhibit AAA growth 31 • Serial imaging is the foundation of clinical care1 • Phase 2 PoC expected to use multimodality imaging to efficiently characterize pacibekitug 3D reconstruction CT Maximum aneurysm diameter Centerline analysis Next steps: – TRANQUILITY topline data in Q2 2025 – Alignment with FDA on Phase 2 PoC design – Details to be shared prior to study start
Thyroid Eye Disease
1Lazarus, Best Pract. Res. Clin. Endocrinol. Metab. (2012). 2Bartalena et al., Front. Endocrinol. (2020). . 4Tourmaline market research.3Horizon Q3 2022 earnings call TED: our beachhead indication designed to validate pacibekitug’s potential in autoantibody-driven diseases 33 High unmet medical need with significant market opportunity • TED patients experience significant disease burden driven by inflammation, proptosis, double-vision, and pain • ~30k new patients each year in the U.S. (average age at diagnosis is ~45)1,2 • ~80%3 of moderate-to-severe TED patients not receiving an FDA-approved treatment, which we believe may be related to significant limitations such as risk of permanent hearing impairment / loss: • Vast majority of US treaters report unmet need across all aspects of treatment (efficacy, safety, administration)4 Extensive third-party clinical support that IL-6 inhibition may address key unmet needs • 50+ publications with 350+ patients demonstrate the therapeutic potential of IL-6 pathway inhibition in TED • IL-6 may play a more central and upstream role in TED pathogenesis than IGF-1R or FcRn • Many TED treaters already routinely utilize IL-6 inhibition in their practice4 Pacibekitug has best-in-disease potential in TED • Deep inhibition of IL-6 pathway observed to date offers potential for durable efficacy across many endpoints • Existing clinical database supports the potential for a well-tolerated profile at selected doses • Q8W dosing would allow for a patient-friendly, low burden treatment course 1 2 3
$24 $166 $287 $344 $2 $453 $616 $590 $502 $480 $491 $494 $405 $446 $453 $467 $424 $479 $488 -- $100 $200 $300 $400 $500 $600 $700 Q1 2020 Q2 2020 Q3 2020 Q4 2020 Q1 2021 Q2 2021 Q3 2021 Q4 2021 Q1 2022 Q2 2022 Q3 2022 Q4 2022 Q1 2023 Q2 2023 Q3 2023 Q4 2023 Q1 2024 Q2 2024 Q3 2024 1. Safety issues: Risk of potentially permanent hearing loss2 2. Limited durability: Growing real-world effectiveness data reveals larger than anticipated number of non-responders / high relapse rate3,4 3. High level of inconvenience & complexity: – IV Q3W (n=8)2 but limited access to infusion centers5 – Numerous visits and high time commitment (HCPs and patients)5 – Need for serial audiograms, as per label2,6 – Burdensome reimbursement approval process7 1Horizon and Amgen company reports and filings. 2TEPEZZA FDA label. 3Kahaly et al., Thyroid (2021) (ATA 2021 presentation). 4Rosenblatt et al., Ophthalmic Plast Reconstr Surg (2023). 5Tourmaline market research. 6Chow and Silkiss, BMJ Case Rep (2022). 7Horizon Therapeutics Public Ltd. Co. Q2 2023 Form 10-Q. IGF-1R class limitations present a significant opportunity for novel therapeutic approaches in TED 34 Sales ($M)1 TEPEZZA U.S. revenues have been stagnating since 2021… …believed to be due to real-world experience
1Horizon Q3 2022 earnings call; LTM = last twelve months. 2Tourmaline market research; endo = endocrinologist; ophth = ophthalmologist. 3AAMC 2022 Physician Specialty Data Report. 4Hussey and Tao, Orbit (2022). Despite an FDA-approved medicine, the vast majority of moderate-to-severe TED patients remain untreated Most TED patients are not receiving TEPEZZA… …or only get it relatively late in the treatment journey2 Endo (~8.2k3) monitors thyroid levels, treats mainly mild TED Ophth (~18.9k3) manages moderate-severe ocular symptoms Oculoplastic Surgeons (~1.2k4) manages severe disease and/or inadequate response to steroids Mild Moderate Severe / Sight-Threatening TEPEZZA 35 Surgery 0% 20% 40% 60% 80% 100% High Proptosis, High CAS TED Patients % o f P at ie nt s Untreated 16,000 80% Treated with Tepezza 4,000 20% Simplified Treatment Journey2TEPEZZA US LTM penetration1 Most refer out to other specialists today but many indicate interest in treating as new advanced therapies become available
Adapted from Huang et al., Eye (2018); Hodgson and Rajaii, Ophthalmol Ther (2020); Fang et al, Front Endocrinol (2021); Smith et al., Eye (2019); and Cabezas et al., Front. Immunol. (2022) IL-6 inhibition has the potential to address a central and upstream driver of TED Adipocytes MyofibroblastsHyaluronan 3) Inhibits orbital fibroblast signaling and differentiation Inflammation: • Pain • Redness • Swelling Orbital tissue expansion: • Proptosis • Diplopia • Eyelid retraction • Optic nerve compression Anti-TSHR/IGF-1R autoantibodies IL-6 Orbital fibroblasts 2) Inhibits T-cell driven inflammation1) Inhibits formation of autoantibodies CD4 T-cell TFhMemory B-cell B-cell IL-6 + IL-6 + IL-6 + Survival Plasma cell IL-21 Th17 CD4 T-cell TGF-β IL-6 + IL-17A IL-22 TNFα IL-1β Anti-FcRn Anti-IGF-1R Anti-IL-6 1 3 2 36
Over 50 publications support the therapeutic potential of IL-6 pathway inhibition in TED • 350+ mostly steroid- refractory patients • Late IL-6 inhibition (>9 months post symptom onset) when disease may have exited active phase • Exposure to IL-6 inhibition may have been suboptimal (<6 months) • Tourmaline market research with over 100 TED treaters suggests many HCPs already routinely utilize IL-6 inhibition in their practice We believe many of these reports may underestimate the true efficacy of IL-6 inhibition Proptosis response rate is generally defined in the data outlined here as a ≥2 mm proptosis improvement in the worse eye at baseline without any worsening in the other eye. CAS response rate is generally defined in the data outlined here as a CAS of 0 or 1. Studies referenced in this table represent investigator-led studies and were not designed with the intent of generating evidence for an approval of tocilizumab or sarilumab in TED. The majority of these studies were not designed with power to detect statistical significance. Retro: retrospective. Obs: observational. Prosp: prospective. RCT: randomized controlled trial. CS: case series. CR: case report. NR: not reported. NS: not significant. CI: clear improvement. Tepro: teprotumumab. Publications available upon request 37 Study Details Key Endpoints First author Year Study type N treated Proptosis response rate CAS response rate % autoantibody reduction Pérez-Moreiras 2021 Retro 54 78 89 75 Sánchez-Bilbao 2020 Obs 48 NR NR NR Atienza-Mateo 2018 Retro 29 NR NR NR Lee 2024 Prosp 19 11 47 56 Pérez-Moreiras 2014 Prosp 18 72 100 76 Pérez-Moreiras 2018 RCT 15 93 60 NS de la Fuente Bursón 2020 Retro 15 NR NR NR Pereira 2023 Retro 14 NR NR NR Habroosh 2024 Prosp 13 100 31 68 Boutzios 2023 Obs 12 NR NR 84 Pampín-Sánchez 2022 Retro 11 75 73 NR Moi 2022 Retro 10 CI 80 75 Cortez 2022 Prosp 10 10 100 81 Silkiss 2020 CS 9 CI 56 74 Smith 2021 Retro 9 78 100 54 Bielefeld 2019 Obs 8 NR NR NR Ceballos-Marcias Jose 2020 CS 8 NR 75 41 Bennedjai 2020 Retro 7 NR NR 73 Moás 2022 Obs 7 NR NR 92 Toro-Tobon 2023 Retro 6 50 NR NR de Pablo Gomez 2018 CS 5 NR 60 NR Navarrete 2022 Retro 5 NR NR NR Ribi 2017 CS 3 33 67 NR Maldiney 2020 CS 3 67 NR NR Stevens 2022 Retro 3 100 67 NR Russell 2017 CS 2 NR 0 NR Sy 2017 CS 2 CI 50 69 Study Details Key Endpoints First author Year Study type N treated Proptosis response rate CAS response rate % autoantibody reduction Copperman 2019 CS 2 100 0 NR Coy 2019 CS 2 NR 50 NR Sierra Osorio 2020 CS 2 100 100 NR Park 2021 CS 2 100 100 NR Abeillon-du Payrat 2022 CS 2 100 50 NR Butnaru 2013 CR 1 NR 100 NR Gómez Rodríguez 2014 CR 1 NR 100 NR Bielefeld 2017 CR 1 CI NR NR Canas 2018 CR 1 100 NR NR Pascual-Camps 2018 CR 1 NR NR NR Garreta Fontelles 2019 CR 1 NR NR 93 Mehmet 2020 CR 1 0 NR NR Kaplan 2020 CR 1 NR 0 85 Cayon-Blanco 2020 CR 1 NR 100 NR Tran 2020 CS 1 NR NR NR Ruiz 2021 CR 1 NR NR NR Albrashdi 2022 CR 1 100 NR NR Cezara 2022 CR 1 NR 0 NR Mohamed 2022 CS 1 0 0 NR Moleiro 2022 CR 1 100 NR 86 Almazrouei 2023 CR 1 NR NR NR Cuculescu 2023 CR 1 CI 0 NR Nirmalan 2023 CS 1 NR NR NR Pramono 2023 CR 1 NR NR NR Rymuza 2024 CR 1 100 0 8 Weighted Mean 68% 72% 71% Smith 2017 (tepro Phase 2) 71% 69% N/A Douglas 2020 (tepro Phase 3) 83% 59% N/A
*This target product profile outlines the desired characteristics of pacibekitug in TED. It will be informed by clinical data from Phase 2b and Phase 3 and additional evidence generated from other programs including from the real world. MOA: mechanism of action. QoL: quality of life. TED: thyroid eye disease. SC: subcutaneous The characteristics presented reflect outcomes that may not be representative of pacibekitug. The results of past clinical trials may not be indicative of future results, and the results of future or ongoing clinical trials may not demonstrate some or any of the characteristics presented. Pacibekitug’s target product profile is expected to be well- differentiated in TED… 38 Target product profile in TED* Targeted points of differentiation Study population • Moderate-to-severe active TED patients MOA • IL-6 inhibition E ffi ca cy Primary endpoint • Proptosis Secondary endpoints • Diplopia, clinical activity score (CAS), inflammation, and lid retraction Additional measures • Lower rate of relapse and retreatment • Rapid time to response • Lower rate of surgical intervention S af et y Warnings & precautions • No anticipated risk of permanent hearing loss or warnings beyond typical IL-6 safety considerations Dosing & administration • Every 8-week, low volume subcutaneous injection through pre-filled syringe • Finite dosing Targeting inflammation which is at core of disease Holistic impact on many QoL-impacting symptoms Emphasis on response durability Well-tolerated without the risk of hearing loss Least frequent and most patient-friendly SC dosing
1In a masked survey of future potential product entrants - HCP Quant Research with N = 60 General Ophthos, N = 40 Endos and N = 40 Oculoplastic Surgeons (February 2024). FcRn: neonatal fragment crystallizable receptor. Rx: prescriptions. SC: subcutaneous. TED: thyroid eye disease. IGF-1R: insulin- like growth factor 1 receptor. IL-6: interleukin-6. …resulting in leading market share, capitalizing on increasing Rx from endocrinologists and ophthalmologists 39 36% 26% 12% 5% 21% 28% 47% 73% 48% 63% 66% 0% 10% 20% 30% 40% 50% 60% 70% 80% Endos General ophthos Oculoplastic surgeons I treat and manage moderate to severe active TED patients rather than referring out to another physician today As additional treatments become available for TED, including SC therapies, I will treat and manage moderate to severe active TED patients rather than referring out to another physician 50% 39% 11% IL-6 class Pacibekitug Satralizumab Off-label IL-6(R) Other biologic IGF-1R class Not treated with biologic FcRn Pacibekitug ranked highest in future market share among 140 TED treaters in US1 Impact on Rx if SC therapies are available1
24 weeks24 weeks24 weeks pivotal trial in first-line TED n = 81 (27 / arm) Pacibekitug 50 mg SC Q8W x 3 Pacibekitug 20 mg SC Q8W x 3 Period A: Primary efficacy Study population: • Moderate-to-severe TED, with proptosis ≥ 3mm above normal (based on race and gender) • Active phase, with symptom onset ≤ 15 months, CAS ≥ 4 and positive TSI • First-line setting, with cap on prior corticosteroid use (< 1g methylprednisolone or equivalent) Primary efficacy endpoint: • Proptosis response rate at week 20 Additional endpoints: • CAS • Diplopia • QoL, safety, PK/PD/ADA Double-masked, placebo-controlled Phase 2b trial (NCT06088979) Placebo R 40 Any patient who receives rescue therapy/intervention in Period A will not receive pacibekitug in Period B and will instead undergo follow-up only* Pacibekitug 50 mg SC Q8W x 3 Follow-up Period B: Extension Proptosis non- responders* Proptosis responders Open label Study drug dosed at Day 1, Week 8, & Week 16; primary efficacy assessed at Week 20 Follow-up
Key upcoming milestones 41 Disease focus Indication Milestone Expected timing Cardiovascular inflammation ASCVD Phase 2 topline data Q2 2025 AAA Phase 2 trial start Post-TRANQUILITY topline data Autoimmune disease TED Phase 2b topline data H2 2025 AAA: abdominal aortic aneurysm. ASCVD: atherosclerotic cardiovascular disease. TED: thyroid eye disease.
