Kalaris Therapeutics, Inc. · NASDAQ:KLRS
Kalaris Therapeutics — Investor Presentation (March 2026)
58 slides from Kalaris Therapeutics's investor presentation, Mar 9, 2026
Slide 1: Kalaris Company Overview
March 2026 Kalaris Company Overview Exhibit 99.1
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
Slide 3: Your Vision, Our 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
Slide 4: Potential best in class, dual-action, anti-VEGF therapeutic
Potential best in class, dual-action, anti-VEGF therapeutic TH103 was engineered by Dr. Napoleone Ferrara for extended intraocular retention with enhanced VEGF inhibition Early clinical data from Phase 1a SAD study validates molecular design Ongoing Phase 1b/2 multi-dose trial Preliminary Phase 1b/2
Slide 5: Engineered to improve upon a drug class that has helped millions
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.
Slide 6: Anti-VEGF Therapeutics Background
Anti-VEGF Therapeutics Background
Slide 7: Anti-VEGF therapy has revolutionized treatment; market projected to exceed $18B by 2029
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
Slide 8: Unmet need remains high, with suboptimal real-world outcomes
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
Slide 9: Lead asset developed by VEGF pioneer 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
Slide 10: Our Solution: TH103
SKalaris ora ‘Therapeutics Our Solution: TH103
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
Slide 12: VEGF receptors and VEGF-A as primary mediator
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
Slide 13: VEGF binds Receptor 1 with ≥10-fold 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
Slide 14: TH103 leverages key binding domains from VEGFR1
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
Slide 15: Higher affinity VEGFR1 may confer enhanced 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
Slide 16: VEGFR1 domain enables potential TH103 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
Slide 17: HSPG is present throughout the 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,
Slide 18: Preclinical Data Review & Initial Phase 1a Clinical Data
Preclinical Data Review & Initial Phase 1a Clinical Data
Slide 19: Increased VEGF-inhibitory activity vs. aflibercept in preclinical studies
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;
Slide 20: Prolonged retinal retention vs. aflibercept in preclinical studies
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.
Slide 21: Prolonged bioactivity vs. aflibercept in an 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
Slide 22: Phase 1a initial data summary
Phase 1a initial 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 out
Slide 23: Phase 1a Single Ascending Dose Study in Treatment-Naïve nAMD
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
Slide 24: Key baseline characteristics of Phase 1a patients
Key baseline characteristics of patients in Phase 1a trial of TH103 who have reached study completion No study dropouts and 100% protocol adherence Study Cohort 0.5 mg (n=3) 1.5 mg (n=7) 2.5 mg (n=3) All Patients (n=13) 1 Age (mean) 78 77 82 79 Sex (female / male) 3 / 0 5 / 2 1 / 2 9 / 4 BCVA (ETDRS
Slide 25: Phase 1a initial data summary: Efficacy
Phase 1a initial data summary ✓ Efficacy: rapid, robust response on BCVA and OCT parameters observed across dose levels at one month
Slide 26: Mean 10 letter BCVA gain at Month 1
ETDRS = Early Treatment Diabetic Retinopathy Study Note: n = 13 at all timepoints except Month 1, where n =12; one patient in the 0.5 mg cohort was treated with aflibercept at Week 2 and therefore the Month 1 data point is censored. Patients dosed at 2.5 mg with additionally purified material (n=6)
Slide 27: Change in mean visual acuity vs. market-leading agents at Month 1
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-
Slide 28: Rapid, robust improvement in CST and total retinal fluid
-129��m mean CST change Rapid, robust improvement in CST and total retinal fluid (TRF) volume at Week 1 and Month 1 Case Example (1.5 mg) Mean ~87% resolution of TRF by Week 12 Mean ~90% resolution of TRF at Month 12 Month 1 Note: n = 13 at all timepoints except Month 1, where n =12; one patient in
Slide 29: Change in mean CST vs. market-leading agents at Month 1
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
Slide 30: Rapid and consistent resolution of intraretinal fluid
Note: Measurement of intraretinal fluid volume (nL) in the central subfield, depicting individual patients (n = 12; one patient in the 0.5 mg cohort was treated with aflibercept 2mg at Week 2 and excluded from the analysis); 3 patients had zero measured IRF throughout depicted timeframe and appear a
Slide 31: Phase 1a initial data summary: Efficacy and Safety
Phase 1a initial 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 further dose-escalation ✓ ✓
Slide 32: Safety Summary from Phase 1a Trial
Safety Summary from Phase 1a Trial No dose limiting toxicity (DLT) or serious adverse events (SAEs) observed Transient, mild-moderate intraocular inflammation (IOI) presented at Day 4 in 2 patients dosed at 2.5mg, attributed to product host cell protein (HCP) levels Further processing steps added to
Slide 33: Phase 1a initial data summary: Durability
Phase 1a initial 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 further dose-escalation Durability: PK analysis consistent with greater TH103 intraocular retention vs.
Slide 34: Initial SAD plasma PK data consistent with greater intraocular retention
Initial SAD plasma PK data is 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 para
Slide 35: Single-dose durability signal suggests stronger durability potential
Single-dose durability signal suggests potential for stronger durability outcomes after standard four-dose loading regimen Ongoing Phase 1b/2 study designed to further explore durability signal following a standard four-dose loading regimen M2 M3 M5 M6 M4 M1 Single TH103 Without any retreatment Phas
Slide 36: Case Example: single-injection 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
Slide 37: First-in-Human data support TH103's best-in-class potential
First-in-Human data support TH103’s potential to be best-in-class, first-line treatment for prevalent retinal diseases Data as of safety cut-off date Dec 15, 2025 Update after Dec 17, 2025, data release; patients are not included in efficacy analyses CSF = Central Subfield Efficacy: rapid, robust re
Slide 38: TH103 Ongoing Development Program
TH103 Ongoing Development Program
Slide 39: Ongoing Phase 1b/2 Trial in nAMD
*Confirmed by independent reading center Ongoing Phase 1b/2 Trial in nAMD; preliminary 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 assessment Patien
Slide 40: Manufacturing process: clinical batches and HCP reduction
Original Clinical Batch Fusion protein produced through CHO cell culture, with process impurities (HCP) removed through downstream steps to levels acceptable to FDA Batch used for original 13 patients in Phase 1a trial Current Clinical Batch Added reagents to manufacturing process to dissociate and
Slide 41: Reduced HCP levels consistent with clinical findings
IOI = Intraocular inflammation *Goal for future clinical batches Notes: a) Mild-moderate, resolved; b) Moderate, resolved; c) Moderate anterior vitreous cell and mild arteriolar abnormalities without leak or occlusion; asymptomatic; improved BCVA/CST from baseline; resolving Original Clinical Batch:
Slide 42: Cash runway extended into Q4 27; anticipated milestones
Cash runway extended and expected to fund company into Q4 2027 TH103 Clinical Development Program & Anticipated Milestones Preliminary data from ongoing Phase 1b/2 MAD study expected in 1H 2027 Pending the results from the Phase 1b/2 trial, potential Phase 3 trial initiation in nAMD planned by year-
Slide 43: 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
Slide 44: Corporate Overview
jerapeutics Corporate oom
Slide 45: 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
Slide 46: Experienced Board & 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 Morana Jovan-Embiricos, PhD Director Leone Patterson Director Board of Directors Andrew Oxtoby CEO & Director Mat
Slide 47: 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
Slide 48: Potential best in class, dual-action, anti-VEGF therapeutic
Potential best in class, dual-action, anti-VEGF therapeutic TH103 was engineered by Dr. Napoleone Ferrara for extended intraocular retention with enhanced VEGF inhibition Early clinical data from Phase 1a SAD study validates molecular design Ongoing Phase 1b/2 multi-dose trial Preliminary Phase 1b/2
Slide 49: Kalaris Therapeutics
i>) Kalaris Therapeutics
Slide 50: Glossary
‘Therapeutics Glossary
Slide 51: 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
Slide 52: Anti-VEGF Therapeutics Background
Anti-VEGF Therapeutics Background
Slide 53: Sources: 1) Witmer, A. N., Vrensen, G. F. J. M., Van Noorden, C. J.
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.
Slide 54: VEGF is the primary mediator and key target for 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
Slide 55: Anti-VEGF therapy has revolutionized treatment for major retinal diseases
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
Slide 56: VEGF has been the primary target for retinal diseases 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
Slide 57: >$15B global branded anti-VEGF market in 2024
>$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
Slide 58: Major unmet need remains 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
Kalaris Therapeutics — Investor Presentation (March 2026) on 6ix