Kalaris Therapeutics, Inc. · NASDAQ:KLRS

Kalaris Therapeutics — Investor Presentation (July 2026)

57 slides from Kalaris Therapeutics's investor presentation, Jul 17, 2026

  1. Slide 1: Kalaris Company Overview

    July 2026 Kalaris Company Overview Exhibit 99.2

  2. Slide 2: Forward-Looking Statements & Disclaimer

    Forward-Looking Statements & Disclaimer This presentation contains “forward-looking statements” within the meaning of the U.S. Private Securities Litigation Reform Act of 1995 and Section 21E of the Securities Exchange Act of 1934, as amended, that involve substantial risk and uncertainties. All sta

  3. Slide 3: Kalaris vision and mission

    Your Vision Our Mission Kalaris is a clinical stage biopharmaceutical company dedicated to the development and commercialization of treatments for prevalent retinal diseases Our lead asset, TH103, was invented by Dr. Napoleone Ferrara, whose pioneering research established the anti-VEGF class of the

  4. Slide 4: TH103 investment highlights

    Invented by VEGF pioneer and scientific co-founder Dr. Napoleone Ferrara, TH103 is a dual-action biologic targeting VEGF, the primary mediator of disease activity in the retina, and HSPG, abundant in retinal layers Phase 1b/2 clinical trial currently enrolling nAMD patients with data expected in 1H

  5. Slide 5: Engineered to improve upon a drug class

    Engineered to improve upon a drug class that has helped millions of patients, with optimization built directly into the molecule itself. Fully humanized, recombinant fusion protein designed for intravitreal delivery, with potential to be best-in-class for neovascular and exudative retinal diseases.

  6. Slide 6: Anti-VEGF Therapeutics Background

    Anti-VEGF Therapeutics Background

  7. Slide 7: Anti-VEGF therapy market growth

    Anti-VEGF therapy has revolutionized treatment for major retinal diseases, a global market projected to grow to over $18B by 2029 Sources: 2025 Retinal Pharmaceuticals Market Report, Market Scope October 2025; FDA Approvals TH103 Kalaris is focused on driving the next wave of innovation for retinal

  8. Slide 8: Unmet need remains high

    Unmet need remains high, with suboptimal real-world outcomes Sources: 1) Mulligan, K., Seabury, S. A., Dugel, P. U., Blim, J. F., Goldman, D. P., & Humayun, M. S. (2020). Economic value of anti–vascular endothelial growth factor treatment for patients with wet age-related macular degeneration in the

  9. Slide 9: Lead asset developed by Napoleone Ferrara

    Recognizing persistent unmet need, our lead asset was developed by VEGF pioneering scientist, Napoleone Ferrara Co-discoverer of VEGF and VEGF isoforms while at Genentech Scientist behind Anti-VEGF Agents: Winner of Major Awards including Lasker Award, Champalimaud Vision Award and Breakthrough Priz

  10. Slide 10: Our Solution: TH103

    SKalaris ora ‘Therapeutics Our Solution: TH103

  11. Slide 11: TH103: Dual-targeting next generation drug

    TH103: Dual-targeting, next generation drug engineered to address major unmet needs in retina disease Optimized VEGF Binding: Leverages higher-affinity VEGFR11, potentially leading to enhanced VEGF inhibition Extended Ocular Retention: Leverages high-affinity binding to HSPG2, potentially providing

  12. Slide 12: VEGF-A primary mediator of neovascularization

    R# = Receptor 1, 2, and 3 Source: Karkkainen, M. J., & Petrova, T. V. (2000). Vascular endothelial growth factor receptors in the regulation of angiogenesis and lymphangiogenesis. Oncogene, 19(49), 5598-5605. VEGFR1 VEGFR2 VEGFR3 VEGF-B PlGF VEGF-A VEGF-D VEGF-C VASCULAR ENDOTHELIAL CELL LYMPHATIC E

  13. Slide 13: VEGF binds Receptor 1 with greater affinity

    VEGF binds to Receptor 1 with ≥10-fold greater affinity than Receptor 2 Sources: Karkkainen, M. J., & Petrova, T. V. (2000). Vascular endothelial growth factor receptors in the regulation of angiogenesis and lymphangiogenesis. Oncogene, 19(49), 5598-5605; Cudmore et al., Scientific Reports (2020); W

  14. Slide 14: TH103 leverages VEGFR1 binding domains

    TH103 leverages the key binding domains from VEGFR1 IgG= Immunoglobulin G; Fc =Fragment Crystallizable Region Source: Xin, H., Biswas, N., Li, P., Zhong, C., Chan, T. C., Nudleman, E., & Ferrara, N. (2021). Heparin-binding VEGFR1 variants as long-acting VEGF inhibitors for treatment of intraocular n

  15. Slide 15: Higher affinity VEGFR1 may enhance VEGF inhibition

    Using higher affinity VEGFR1 may confer enhanced VEGF inhibition Source: Xin, H., Biswas, N., Li, P., Zhong, C., Chan, T. C., Nudleman, E., & Ferrara, N. (2021). Heparin-binding VEGFR1 variants as long-acting VEGF inhibitors for treatment of intraocular neovascular disorders. Proceedings of the Nati

  16. Slide 16: VEGFR1 domain enables binding to retina

    VEGFR1 domain 3 enables potential TH103 binding to retina Source: 1) Xin H, Biswas N, Li P, et al. 2021. 'Heparin-binding VEGFR1 variants as long-acting VEGF inhibitors for treatment of intraocular neovascular disorders', Proc Natl Acad Sci U S A, 118.; 2) Holash, J., Davis, S., Papadopoulos, N., Cr

  17. Slide 17: HSPG present throughout retinal layers

    Sources: 1) Clark SJ, Keenan TD, Fielder HL, et al. 2011. 'Mapping the differential distribution of glycosaminoglycans in the adult human retina, choroid, and sclera', Invest Ophthalmol Vis Sci, 52: 6511-21; 2) Regatieri, C. V., Dreyfuss, J. L., Melo, G. B., Lavinsky, D., Hossaka, S. K., Rodrigues,

  18. Slide 18: Preclinical Data Review & Phase 1a Clinical Data

    Preclinical Data Review & Phase 1a Clinical Data

  19. Slide 19: Increased VEGF-inhibitory activity vs. aflibercept preclinically

    Notes: 1) human choroidal endothelial cells proliferate in nAMD pathologic angiogenesis; 2) The rodent laser-induced CNV model is the most widely used animal model to study the effects of anti-VEGFs in inhibiting CNV; Data are based on three independent experiments with at least five mice per group;

  20. Slide 20: Prolonged retinal retention vs. aflibercept

    Note: 1) Serum levels of aflibercept and TH103 in mice at different time points after intravitreal injection. Each molecule was injected in both eyes in equimolar amounts (2.4 μg). After 1, 3, 7, 14, and 21 d, peripheral blood was collected from the tail vein. Human Fc levels were measured by ELISA.

  21. Slide 21: Prolonged bioactivity in animal model

    Note: TH103 and aflibercept administered 14 days prior to laser injury; CNV measurement at Day 7 post-laser; Symbols denote significant differences (Student’s t test) between TH103 and control (***P < 0.001) and between TH103 and aflibercept (^^^P < 0.001). Source: Adapted from Xin H, Biswas N, Li P

  22. Slide 22: Phase 1a SAD data summary

    Phase 1a SAD data summary BCVA = Best Corrected Visual Acuity; CST = Central Subfield Thickness; PK = Pharmacokinetics Durability: PK analysis consistent with greater TH103 intraocular retention vs. other leading agents Single-dose durability signal suggests potential for stronger durability outcome

  23. Slide 23: Phase 1a Single Ascending Dose Study design

    Phase 1a Single Ascending Dose (SAD) Study in Treatment-Naïve nAMD Multi-center U.S. study to evaluate safety, tolerability, pharmacokinetics, and anti-VEGF activity following a single injection of TH103 Study Details Primary timepoint for analysis at Month 1 Frequent follow-up visits within the fir

  24. Slide 24: Baseline characteristics of Phase 1a patients

    Key baseline characteristics of patients in Phase 1a SAD trial of TH103 No study dropouts and 100% protocol adherence Tx.-Naïve (efficacy analysis population) Including Tx-Experienced Dec. 2025 Data Release (n=13) Additional Tx-Naïve Patients (n=4)4 All Tx.-Naïve Patients (n=17) Tx.-Experienced2 (n=

  25. Slide 25: Phase 1a SAD data summary: efficacy

    Phase 1a SAD data summary ✓ Efficacy: rapid, robust response on BCVA and OCT parameters observed across dose levels at one month

  26. Slide 26: Mean 9.2 letter gain in BCVA

    ETDRS = Early Treatment Diabetic Retinopathy Study Note: n = 17 at all timepoints except Month 1, where n =16; one patient in the 0.5 mg cohort was treated with aflibercept at Week 2 and therefore the Month 1 data point is censored. Brackets indicate standard error Mean 9.2 letter gain in BCVA lette

  27. Slide 27: BCVA change vs. market-leading agents

    Eylea (VIEW 1&2) BCVA Baseline Mean: ~54, n= 607 Eylea (PULSAR) BCVA Baseline Mean: ~59, n=336 Eylea (T&L) BCVA Baseline Mean: ~60, n = 664 Eylea HD BCVA Baseline Mean: ~60, n=673 Vabysmo BCVA Baseline Mean: ~60, n=665 Change in mean visual acuity in treatment-naïve nAMD patients for current market-

  28. Slide 28: Improvement in CST and retinal fluid volume

    Rapid, robust improvement in CST and total retinal fluid (TRF) volume at Week 1 and Month 1 Case Example (1.5 mg) Mean ~89% resolution of TRF by Week 1 maintained at Month 12 Month 1 Note: n = 17 at all timepoints except Month 1, where n =16; one patient in the 0.5 mg cohort was treated with afliber

  29. Slide 29: CST change vs. market-leading agents

    Eylea (VIEW 1&2) CST Baseline Mean: ~324, n=607 Eylea (PULSAR) CST Baseline Mean: ~367, n=336 Eylea (T&L) CST Baseline Mean: ~358, n = 664 Eylea HD CST Baseline Mean: ~370, n=673 Vabysmo CST Baseline Mean: ~357, n=665 Change in mean CST in treatment-naïve nAMD patients for current market-leading age

  30. Slide 30: Resolution of intraretinal fluid volume

    Note: Measurement of intraretinal fluid volume (nL) in the central subfield, depicting individual patients (n = 16; one patient in the 0.5 mg cohort was treated with aflibercept 2mg at Week 2 and excluded from the analysis); patients with zero measured IRF throughout depicted timeframe appear as ove

  31. Slide 31: Phase 1a SAD data summary: safety

    Phase 1a SAD data summary Efficacy: rapid, robust response on BCVA and OCT parameters observed across dose levels at one month Safety: TH103 generally well tolerated, supporting exploration of multi-dose regimen ✓ ✓

  32. Slide 32: Safety Summary from Phase 1a SAD Trial

    Safety Summary from Phase 1a SAD Trial No dose limiting toxicity (DLT) or treatment-emergent serious adverse events (SAEs) observed Transient, mild-moderate intraocular inflammation (IOI) presented at Day 4 in 2 patients dosed at 2.5mg with TH103 manufacturing batch #11 No cases of IOI in 6 patients

  33. Slide 33: Phase 1a SAD data summary: durability

    Phase 1a SAD data summary Efficacy: rapid, robust response on BCVA and OCT parameters observed across dose levels at one month Safety: TH103 generally well tolerated, supporting exploration of multi-dose regimen Durability: PK analysis consistent with greater TH103 intraocular retention vs. other le

  34. Slide 34: PK data consistent with greater intraocular retention

    PK data consistent with greater TH103 intraocular retention *Mean, except for Vabysmo which is median Sources: 1) Data from BLA761355 and published studies; 2) Data from BLA761355 ; 3) Data from BLA761235; 4) Data from KLRS-100 Clinical Trial Notes: Dose normalization of a parameter involves convert

  35. Slide 35: Single-dose durability signal

    Single-dose durability signal suggests potential for stronger durability outcomes after standard four-dose loading regimen, currently being evaluated in ongoing Ph 1b/2 study M2 M3 M5 M6 M4 M1 Single TH103 Phase 1a Single-Dose Time to Retreatment (n = 17, Tx-naïve) 41% ≥ 4M Time to first retreatment

  36. Slide 36: Case Example: durable response past Month 6

    Case Example: TH103 single-injection durable response past Month 6 Single Dose TH103 (0.5mg) 234 ��m improvement at Month 6 Week 1 Month 1 Month 6 Source: As measured by independent reading center

  37. Slide 37: Phase 1a data support best-in-class potential

    New Phase 1a SAD data continue to support TH103’s potential as best-in-class, first-line treatment for retinal vascular diseases CSF = Central Subfield Efficacy: rapid, robust response on BCVA and OCT parameters observed across dose levels at one month Mean 9.2-letter BCVA improvement at Month 1 aft

  38. Slide 38: TH103 Ongoing Development Program

    TH103 Ongoing Development Program

  39. Slide 39: Ongoing Phase 1b/2 Trial in nAMD

    *Confirmed by independent reading center Ongoing Phase 1b/2 Trial in nAMD; preliminary endpoint data expected 1H 2027 Open label, multiple ascending dose design followed by randomized, masked, multi-dose cohort-expansion phase M1 M2 M3 M9 Study Phase Extension Phase Monthly disease activity assessme

  40. Slide 40: Clinical development program and anticipated milestones

    Cash runway expected to fund company into Q4 2027 TH103 Clinical Development Program & Anticipated Milestones Enrollment continues in Phase 1b/2 MAD study – preliminary data expected in 1H 2027 Pending the results from the Phase 1b/2 trial, potential Phase 3 trial initiation in nAMD planned by year-

  41. Slide 41: Product candidate pipeline

    Product Candidate Indication Discovery IND Enabling Phase 1 Phase 2 Phase 3 TH103 nAMD* TH103 DME / DR** TH103 RVO** *Two ongoing nAMD studies – Phase 1a and Phase 1b/2 **Subject to IND submission and clearance Planned expansions beyond nAMD into other prevalent VEGF-mediated diseases such as DME, D

  42. Slide 42: Corporate

    jerapeutics Corporate oom

  43. Slide 43: TH103 manufacturing batch process improvements

    TH103 Manufacturing Batch #1 Fusion protein produced through CHO cell culture, with process impurities (HCP) removed through downstream steps to levels acceptable to FDA TH103 Manufacturing Batch #2 Added reagents to manufacturing process to dissociate and separate HCPs from TH103 Overall HCP apprec

  44. Slide 44: Intellectual Property

    Intellectual Property TH103 Compositions of Matter Issued/allowed in United States, Japan, China, Australia, Colombia, and Eurasia Pending in Europe, China, Korea, India, Brazil, Mexico, Singapore, New Zealand, Hong Kong, and Israel 1 TH103 Methods of Use Issued/allowed in United States, Europe, Jap

  45. Slide 45: Board of Directors and Management Team

    David Hallal Board Chairman Anthony Adamis, MD Director Srinivas Akkaraju, MD, PhD Director & Co-founder Mike Dybbs, PhD Director & Co-founder Napoleone Ferrara, MD Director & Co-Founder Leone Patterson Director Board of Directors Andrew Oxtoby CEO Matthew Feinsod, MD CMO Kristine Curtiss SVP Clinic

  46. Slide 46: TH103 Advantage: Established yet Differentiated

    TH103 Advantage: Established yet Differentiated ESTABLISHED Part of a Proven Class1 Targets VEGF-A, primary mediator of disease activity in the retina Soluble decoy receptor MoA2 Biologic (recombinant fusion protein); simple protein structure Drug class with well-established path to approval Drug ad

  47. Slide 47: TH103 investment highlights

    Invented by VEGF pioneer and scientific co-founder Dr. Napoleone Ferrara, TH103 is a dual-action biologic targeting VEGF, the primary mediator of disease activity in the retina, and HSPG, abundant in retinal layers Phase 1b/2 clinical trial currently enrolling nAMD patients with data expected in 1H

  48. Slide 48: Kalaris Therapeutics

    i>) Kalaris Therapeutics

  49. Slide 49: Glossary

    ‘Therapeutics Glossary

  50. Slide 50: Glossary

    Glossary BCVA: Best Corrected Visual Acuity Cmax: Maximum Plasma Concentration CNV: choroidal Neovascularization CST: Central Subfield Thickness DLT: Dose Limiting Toxicity DME: Diabetic Macular Edema DR: Diabetic Retinopathy ETDRS: Early Treatment Diabetic Retinopathy Study HSPG: Heparan Sulfate Pr

  51. Slide 51: Anti-VEGF Therapeutics Background

    Anti-VEGF Therapeutics Background

  52. Slide 52: Anti-VEGF market and sources

    Sources: 1) Witmer, A. N., Vrensen, G. F. J. M., Van Noorden, C. J. F., & Schlingemann, R. O. (2003). Vascular endothelial growth factors and angiogenesis in eye disease. Progress in retinal and eye research, 22(1), 1-29.2) Solomon, Sharon D., Kristina Lindsley, Satyanarayana S. Vedula, Magdalena G.

  53. Slide 53: VEGF is the primary mediator of pathologic angiogenesis

    VEGF is the primary mediator and the key target for pathologic angiogenesis and exudation (permeability) in retinal disease Growth and leakage from abnormal vessels leads to visual impairment in diseases such as nAMD, DME, and RVO. VEGF is a primary mediator of this pathology. Source: Apte, R. S., C

  54. Slide 54: Anti-VEGF therapy has revolutionized treatment

    Anti-VEGF therapy has revolutionized treatment for major retinal diseases Source: Solomon, S. D., Lindsley, K., Vedula, S. S., Krzystolik, M. G., & Hawkins, B. S. (2014). Anti‐vascular endothelial growth factor for neovascular age‐related macular degeneration. Cochrane Database of Systematic Reviews

  55. Slide 55: VEGF primary target for over 20 years

    *According to the VABYSMO Prescribing Information, “The contribution of Ang-2 inhibition to the treatment effect and clinical response for nAMD, DME, and RVO has yet to be established.”1 Source: 1) VABYSMO Prescribing Information accessed via AccessData.FDA.gov July 8, 2025 Additional Sources: Tatsu

  56. Slide 56: >$15B global branded anti-VEGF market

    >$15B global branded anti-VEGF market in 2024, projected to grow to approximately $18B by 20291,2 Sources: 1) 2025 Retinal Pharmaceuticals Market Report, Market Scope October 2025; 2) Based on publicly available sales data 2024 Global Anti-VEGF Units in Retinal Disease (2024)1 Compounded bevacizumab

  57. Slide 57: Unmet need for a long-acting agent

    A major unmet need remains for a long-acting agent that preserves patient vision and reduces patient visit burden Real World Study7 Registrational Clinical Trial6 Days Mean Visual Activity Difference from Baseline (LOCF) (letters) Mean Change in Visual Acuity (no. of letters) Day 7 Month 3 Month 6 M

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