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 A

March 2026 Kalaris Company Overview

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 statements, other than statements of historical fact, contained in this presentation, including statements regarding the strategy, future operations, future financial position, projected costs, prospects,

plans and objectives of management of Kalaris, the therapeutic potential of TH103 for neovascular Age-related Macular Degeneration and other exudative and neovascular retinal diseases, the anticipated timeline for reporting data from the ongoing

Phase 1a clinical trial of TH103 and the ongoing Phase 1b/2 clinical trial of TH103, plans to advance TH103 into Phase 3 clinical trials and to develop TH103 for additional indications, plans to improve the manufacturing process for TH103 and the

sufficiency of Kalaris' cash resources for the period anticipated, are forward-looking statements. The words "anticipate," "believe," "continue," "could," "estimate,"

"expect," "intend," "may," "might," "plan," "potential," "predict," "project," "should," "target," "would" and

similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. These statements are based on current expectations and beliefs of the management of Kalaris as well

as assumptions made by, and information currently available to, the management of Kalaris and are subject to risks and uncertainties. There can be no assurance that future developments affecting Kalaris will be those that it has anticipated. Actual

results or events could differ materially from the plans, intentions and expectations disclosed in these forward-looking statements as a result of various important factors, including: risks associated with the clinical development and regulatory

approval of its product candidate, including potential delays in the completion of clinical trials; expectations regarding the therapeutic benefits, clinical potential and clinical development of TH103; the timing of and Kalaris' ability to

enroll patients in clinical trials; whether results from preclinical studies and initial data from early clinical trials will be predictive of the final results of the clinical trials or future trials; dependence on third parties for the development

and manufacture of TH103; risks related to the inability of Kalaris to obtain sufficient additional capital to continue to advance its product candidate; uncertainties in obtaining successful clinical results for product candidates and unexpected

costs that may result therefrom; risks related to the failure to realize any value from any product candidates being developed and anticipated to be developed in light of inherent risks and difficulties involved in successfully bringing product

candidates to market; the ability to obtain, maintain, and protect intellectual property rights related to product candidates; changes in regulatory requirements and government incentives; Kalaris' competitive position and expectations

regarding developments and projections relating to its competitors and any competing therapies that are or become available; the risk of involvement in current and future litigation; and such other factors as are set forth in Kalaris' public

filings with the U.S. Securities and Exchange Commission, including, but not limited to, those described under the heading "Risk Factors". Kalaris may not actually achieve the plans, intentions or expectations disclosed in its

forward-looking statements, and you should not place undue reliance on its forward-looking statements. Actual results or events could differ materially from the plans, intentions and expectations disclosed in the forward-looking statements Kalaris

makes. The forward-looking statements contained in this presentation are made as of the date of this presentation, and Kalaris does not assume any obligation to update any forward-looking statements, whether as a result of new information, future

events or otherwise, except as required by applicable law. This presentation also contains estimates, projections and other statistical data made by independent parties and by Kalaris relating to market size and growth and other data about

Kalaris' industry and business. This data involves a number of assumptions and limitations, and you are cautioned not to give undue weight to such estimates. Kalaris has not independently verified the accuracy and completeness of the

information obtained by third parties included in this presentation. In addition, projections, assumptions and estimates of Kalaris' future performance and the future performance of the market in which Kalaris operates are necessarily subject

to high degree of uncertainty and risk.

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 therapies for retinal and oncology diseases, to address major remaining unmet needs TH103 is an anti-VEGF therapeutic specifically engineered to achieve extended intraocular retention with enhanced VEGF inhibition VEGF = Vascular

Endothelial Growth Factor

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 data expected in 1H 2027 $50MM oversubscribed private placement1 in December 2025 fortified balance sheet Sufficient cash runway to fund company into Q4 2027 1) Private placement included participation from both new and

existing investors, including ADAR1 Capital Management, Coastlands Capital, Invus, RTW Investments, Samsara BioCapital, Woodline Partners LP and others.

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. Targets VEGF as a soluble decoy receptor with high affinity for both VEGF and HSPG, engineered for increased and longer-acting activity. HSPG = Heparan Sulfate Proteoglycans TH103

Anti-VEGF Therapeutics

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 neovascular / exudative disease Dawn of anti-VEGF era Expansion of anti-VEGF therapeutics market NEXT-GEN ANTI-VEGF 2004 2006 2005 (off-label use) 2011 2019 2023 2022

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 United States. JAMA ophthalmology, 138(1), 40-47. Best outcomes may require clinic visits as frequently as every 1-2 months for monitoring and injections. Onerous visit frequency Physicians attempt to extend

the time between patient visits, reducing injection frequency. Current Solution Reduced injection frequency can lead to undertreatment and reduced efficacy. Suboptimal Outcomes "Although multiple anti-VEGF therapies exist, unmet need remains

high owing to treatment underutilization "1 regular treatment and monitoring requires substantial time commitment and may contribute to poor compliance. This treatment burden has been recognized by ophthalmologists; consequently,

personalized treatment strategies attempt to balance the treatment burden against potentially reduced efficacy"1

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 Prize in Life Sciences Napoleone Ferrara, MD Kalaris Co-Founder Genentech Fellow | Professor, UCSD TH103

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 prolonged retinal retention and driving enhanced efficacy and/or durability Source: 1) Holash, J., Davis, S., Papadopoulos, N., Croll, S. D., Ho, L., Russell, M., ... & Rudge, J. S. (2002). VEGF-Trap: a VEGF blocker with

potent antitumor effects. Proceedings of the National Academy of Sciences, 99(17), 11393-11398. 2) 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.

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 ENDOTHELIAL CELL VEGF-A is the primary mediator of neovascularization and exudation

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); Wiesmann et al., Cell (1997); Ferrara et al., Nature Medicine (2003) VEGFR1 VEGFR2 VASCULAR ENDOTHELIAL CELL 10x binding VEGF-A

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 neovascular disorders. Proceedings of the National Academy of Sciences, 118(21), e1921252118. Domain 2 Domain 3 Fc

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 National Academy of Sciences, 118(21), e1921252118.

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., Croll, S. D., Ho, L., Russell, M., ... & Rudge, J. S. (2002). VEGF-Trap: a VEGF blocker with potent antitumor effects. Proceedings of the National Academy of Sciences, 99(17), 11393-11398. In contrast, domain 3 from VEGFR2:

Binds less strongly to HSPG, leading to reduced tissue sequestration (preferred for systemic circulation, e.g., ZALTRAP , but suboptimal for ocular retention)2 aflibercept Domain 3 from VEGFR1: Binds strongly to HSPG which

are present in all retinal layers, thereby sequesteringTH103 in the eye TH103

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, E. B., & Nader, H. B. (2010). Quantitative evaluation of experimental choroidal neovascularization by confocal scanning laser ophthalmoscopy: fluorescein angiogram parallels heparan sulfate proteoglycan

expression. Brazilian Journal of Medical and Biological Research, 43, 627-633. Adult human retina cross section HSPG has been shown to be highly concentrated near CNV lesions2, potentially prolonging ocular retention precisely at the

site of disease activity Blue: DAPI staining of cell nuclei Green: Heparan sulfate antibody HSPG is present throughout the retinal layers1

Preclinical Data Review &

Initial Phase 1a Clinical Data

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; Asterisks denote significant differences (Student's t test) compared to the appropriate IgG control groups (**P < 0.01, *P < 0.05); Source: Adapted from 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. TH103: Increased VEGF-inhibitory activity vs. aflibercept in preclinical studies TH103 achieved 100% inhibition vs.

aflibercept 80% inhibition of VEGF-induced endothelial cell proliferation (in vitro, bovine choroidal endothelial cell proliferation assay1) aflibercept TH103 Concentration Dependent VEGF Inhibition Mean CNV Area Mean CNV Area (ratio to IgG control)

Standard error = TH103 increased reduction in mean choroidal neovascularization (CNV) area after administration at Day -12 (in vivo, murine model)

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 g). After 1, 3, 7, 14, and 21 d, peripheral blood was collected from the tail vein. Human Fc

levels were measured by ELISA. Values shown are means SEM. n = 8 per point; Source: Adapted from 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. TH103: Demonstrated prolonged retinal retention vs. aflibercept in preclinical studies Serum Levels of TH103 Compared to Aflibercept After Bilateral Intravitreal Injection aflibercept TH103 Rabbit Retina

Cross-Sections at Day 14 Equimolar dose administrated; Darker immuno-histochemistry staining indicates higher drug levels present TH103 demonstrated increased retention in the retina as compared to aflibercept at two weeks post-injection (in vivo,

rabbit model) TH103 demonstrated reduced systemic exposure after intravitreal administration1 (in vivo, murine model) Serum huFc levels (ng/mL) 0 50 100 150 1 d 3 d 7 d 14 d 21 d 3 d 7 d 14 d 21 d 1 d aflibercept TH103 50 100 150

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, 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. TH103: Demonstrated prolonged bioactivity vs.

aflibercept in an animal model Mean CNV Area Mean CNV Area (ratio to IgG control) Standard error = In a second murine experiment, rather than at Day -1, TH103 and aflibercept were administered at Day -14 prior to laser injury to assess durability of

treatment effect. In this model, TH103 showed smaller mean CNV area compared to equimolar aflibercept 21 days after injection.

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 outcomes after standard four-dose loading regimen 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

Phase 1a Single Ascending Dose

(SAD) Study in Treatment-Na ve 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