CABA Cabaletta Bio Inc

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CABA-201 Initial Clinical Data from the RESET-Myositis™ & RESET-SLE™ Phase 1/2 Trials JUNE 2024 Exhibit 99.1

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Disclaimer The following presentation, including any printed or electronic copy of these slides, the talks given by the presenters, the information communicated during any delivery of the presentation and any question and answer session and any document or material distributed at or in connection with the presentation (collectively, the “Presentation”) has been prepared by Cabaletta Bio, Inc. (“we,” “us,” “our,” “Cabaletta” or the “Company”) and is made for informational purposes only. This Presentation does not purport to be a prospectus, to be complete or to contain all of the information you may desire. Statements contained herein are made as of the date of this Presentation unless stated otherwise, and this Presentation shall not under any circumstances create an implication that the information contained herein is correct as of any time after such date or that information will be updated or revised to reflect information that subsequently becomes available or changes occurring after the date hereof. This Presentation may contain “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995 relating to our business, operations, and financial conditions, and include, but are not limited to, express or implied statements regarding our current beliefs, expectations and assumptions regarding: our business, future plans and strategies for our CAAR T and CARTA technologies; our ability to grow our autoimmune-focused pipeline; the ability to capitalize on and potential benefits resulting from our research and translational insights; including those related to any similarly-designed constructs or dosing regimens; the anticipated market opportunities for CABA-201 in patients with autoimmune diseases; the Company’s business plans and objectives; our expectations around the potential success and therapeutic benefits of CABA-201, including our belief that CABA-201 may enable an “immune system reset”; Cabaletta's belief of the potential for CAR T to enable a paradigm shift in autoimmunity, including its potential achieve durable remissions without chronic therapy;; our plans for Phase 1/2 clinical trials of CABA-201 in patients with systemic lupus erythematosus (SLE), myositis, SSc, and generalized myasthenia gravis (gMG), and for advancement of a RESET-PV sub-study within the ongoing DesCAARTes trial in PV, including the timing thereof, including our anticipated progress, timing of enrollment, expectations for the efficiency of the clinical trial designs, updates related to status, safety data, or otherwise and the expected timing of the related data read-outs, and ability to leverage our experience in autoimmune cell therapy; our initial clinical data read-out in the first half of 2024 at the EULAR 2024 symposium for patients with myositis and SLE treated with CABA-201; our planned initial clinical data read-out in the second half of 2024 for patients with SSc and gMG treated with CABA-201 and additional data; our ability to enroll the requisite number of patients, dose each dosing cohort in the intended manner, and advance the trial as planned in our Phase 1/2 clinical trials of CABA-201; the timing any planned regulatory filings for our development programs, including IND applications; the progress and results of our DesCAARTes™ Phase 1 trial, including the significance and impact around reported safety and clinical and translational data of cohorts from our DesCAARTes™ and MusCAARTes™ Phase 1 trials; Cabaletta's potential to eliminate the need for apheresis by using a simpler collection process to obtain the starting material for the CABA-201 manufacturing process the therapeutic potential and clinical benefits of our product candidates; the expectation that Cabaletta may improve outcomes for patients suffering from SLE, SSc, myositis, gMG, mucosal pemphigus vulgaris, MuSK myasthenia gravis, or other autoimmune diseases; the ability of our clinical strategy to reduce risk, maximize reach and accelerate timelines of our Phase 1/2 clinical trials of CABA-201; our ability to successfully complete our preclinical and clinical studies for our product candidates, including our ability to enroll the requisite number of patients, dose each dosing cohort in the intended manner, and progress the trial; our ability to obtain and maintain regulatory approval of our product candidates, including our expectations regarding the intended incentives conferred by and ability to retain Orphan Drug Designation and Fast Track Designations for our product candidates, as applicable; our ability to accelerate our pipeline and to develop meaningful therapies for patients, including in collaboration with academic and industry partners and the ability to optimize such collaborations on our development programs; our ability to contract with third-party suppliers and manufacturers and retain such manufacturers, whether due to legislative action or otherwise; to implement an enhanced manufacturing process and further develop our internal manufacturing strategy, capabilities and facilities; our potential commercial opportunities, including value and addressable market, for our product candidates; and our expectations regarding our use of capital and other financial results, including our ability to fund operations into the first half of 2026. Words such as, but not limited to, “look forward to,” “believe,” “expect,” “anticipate,” “estimate,” “intend,” “plan,” “would,” “should” and “could,” and similar expressions or words, identify forward-looking statements. Various risks, uncertainties and assumptions could cause actual results to differ materially from those anticipated or implied in our forward-looking statements. Such risks and uncertainties include, but are not limited to, risks related to the success, cost, and timing of our product candidate development activities and preclinical studies and clinical trials, risks related to our ability to demonstrate sufficient evidence of safety, efficacy and tolerability in our preclinical studies and clinical trials of CABA-201, DSG3-CAART and MuSK-CAART, the risk that the results observed with the similarly-designed construct, including, but not limited to, due to dosing regimen, are not indicative of the results we seek to achieve with CABA-201, our plans to evaluate additional cohorts in the DesCAARTes™ trial, including a cohort implementing a pre-treatment regimen, the risk that signs of biologic activity or persistence may not inform long-term results, the risk that persistence observed with effective CD19-CAR T oncology studies in combination with lymphodepletion is not indicative of, or applicable to, clinical responses in patients with mPV, risks related to clinical trial site activation or enrollment rates that are lower than expected, our ability to protect and maintain our intellectual property position, risks related to our relationships with third parties, uncertainties related to regulatory agencies’ evaluation of regulatory filings and other information related to our product candidates, our ability to retain and recognize the intended incentives conferred by any Orphan Drug Designations and Fast Track Designations, risks related to regulatory filings and potential clearance, the risk that any one or more of our product candidates will not be successfully developed and commercialized, the risk that the results of preclinical studies or clinical studies will not be predictive of future results in connection with future studies, and risks related to volatile market and economic conditions and public health crises. New risks and uncertainties may emerge from time to time, and it is not possible to predict all risks and uncertainties. Except as required by applicable law, we do not plan to publicly update or revise any forward-looking statements contained herein, whether as a result of any new information, future events, changed circumstances or otherwise. Although we believe the expectations reflected in such forward-looking statements are reasonable, we can give no assurance that such expectations will prove to be correct. Accordingly, you are cautioned not to place undue reliance on these forward-looking statements. No representations or warranties (expressed or implied) are made about the accuracy of any such forward-looking statements. For a discussion of these and other risks and uncertainties, and other important factors, any of which could cause our actual results to differ materially from those contained in the forward-looking statements, see the section entitled "Risk Factors" in our most recent annual report on Form 10-K, as well as discussions of potential risks, uncertainties, and other important factors in our other and subsequent filings with the Securities and Exchange Commission. 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. The Company is the owner of various trademarks, trade names and service marks. Certain other trademarks, trade names and service marks appearing in this Presentation are the property of third parties. Solely for convenience, the trademarks and trade names in this Presentation are referred to without the ® and TM symbols, but such references should not be construed as any indicator that their respective owners will not assert, to the fullest extent under applicable law, their rights thereto.

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Today’s Agenda AGENDA TOPIC SPEAKER CABA-201 Overview Steven Nichtberger, MD Chief Executive Officer Current & Investigational Treatments for Patients with Autoimmune Disease Iain McInnes, MD, FRCP, PhD, FRSE, FMedSci Vice Principal and Head of the College of Medical, Veterinary and Life Sciences, Muirhead Chair of Medicine and Versus Arthritis Professor of Rheumatology at the University of Glasgow Initial CABA-201 Data in Myositis & Lupus David Chang, MD, MPH, FACR Chief Medical Officer Conclusions Steven Nichtberger, MD Chief Executive Officer Q&A

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4 Designed to replicate and expand on the academic clinical data that generated interest in the field CABA-201: CD19-CAR T specifically designed for autoimmunity​ PK, pharmacokinetics; PD, pharmacodynamics, SAEs: serious adverse events Peng, BinghaoJ, et al. Presented at: American Society Gene and Cell Therapy 26th Annual Meeting; 2023 May 19; Los Angeles, CA. Dai, Zhenyu, et al. Journal of Cellular Physiology. 2021;236(8): 5832-5847. Evaluated as part of CT120, a dual-CD19xCD22 CAR T product candidate under development by Nanjing IASO Biotherapeutics, Co., Ltd. (IASO Bio). Fully human anti-CD19 binder Similar binding affinity and biologic activity to FMC63, with binding to the same epitopes1,2 Safety data in ~20 oncology patients evaluated and reported by IASO as part of a dual-CAR3 4-1BB costimulatory domain Same domain as used in academic studies CD3-zeta signaling domain CABA-201 CABA-201 designed to optimize the potential safety and efficacy of CD19-CAR T for patients with autoimmune disease Key Questions for RESET™ Phase 1/2 Studies Safety of CABA-201 CABA-201 AE profile CRS, ICANS, SAEs   Dose selection 1 x 106 cells/kg PK – CAR T persistence PD – B cell depletion Autoantibody reduction Clinical outcomes

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Innovative and scalable clinical strategy with potential for accelerated development path CABA-201 pipeline targeting a broad range of autoimmune diseases RESET™ – REstoring SElf-Tolerance; IMNM – Immune-mediated necrotizing myopathy; SLE – Systemic lupus erythematosus; Ab – Antibody; AChR – Acetylcholine receptor; gMG – Generalized myasthenia gravis, PV – Pemphigus vulgaris FDA Fast Track Designation received in dermatomyositis, SLE and lupus nephritis, systemic sclerosis, mucosal pemphigus vulgaris, and MuSK-Ab positive MG. 1. Sub-study incorporated into DesCAARTes™ study. 2. Data cut-off as of 28 May 2024. Program Trial Preclinical Phase 1/2 Pivotal CABA-201 4-1BB CD19-CAR T RESET-Myositis™ CARTA Chimeric Antigen Receptor T cells for Autoimmunity RESET-SLE™ RESET-SSc™ RESET-MG™ RESET-PV™ Sub-study1 Dermatomyositis Anti-synthetase syndrome IMNM Lupus Nephritis Non-Renal SLE Skin + Organ Cohort AChR-Ab neg. gMG AChR-Ab pos. gMG Skin Cohort FTD Mucocutaneous & mucosal pemphigus vulgaris Juvenile Myositis Clinical & translational data2 support the selected single dose of CABA-201 at 1 x 106 cells/kg Rheumatology Neurology Dermatology Contains cohort(s) without preconditioning Pediatric Indication

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Acceleration in enrollment anticipated in 2H24 with initial CABA-201 data & engaged clinical investigators Sites actively recruiting patients in the RESETTM clinical program1 5 patients enrolled across RESET-SLETM & RESET-MyositisTM, with 3 patients enrolled over the last 2 months 18 actively recruiting clinical sites in the U.S. across the RESETTM studies RESET-SScTM and RESET-MGTM trials now open for enrollment 1. As of June 12, 2024. SLE sites Myositis sites SSc sites MG sites

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Current & Investigational Treatments for Patients with Autoimmune Diseases

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Broad immunosuppression and chronic administration often required to achieve partial, transient responses Current therapies for autoimmunity do not achieve drug-free remission (Hematopoietic stem cell transplant has been shown to be curative in systemic sclerosis but has increased mortality in the first year6) There is a need for durable, effective and safe therapies that reestablish immune tolerance to eliminate the need for long-term therapy5,6 Khoo T, et al. Nat Rev Rheumatol. 2023;19(11):695-712. Octapharma. Accessed June 10, 2024. Hoover PJ, Costenbader KH. Kidney Int. 2016;90(3):487-92. High Unmet Clinical Need in SLE & Myositis Potential for life-threatening complications ~40% of patients with SLE develop LN3,4 ~25% risk of death or ESRD within 10y Incomplete responses despite chronic therapy High mortality due to lung & cardiac involvement1 Only FDA & EMA-approved therapy is IVIg in DM2 Many patients remain refractory to standard of care therapies – particularly high unmet need in IMNM1 Lupus Current Therapies in Autoimmunity Broad immunosuppression Modest & inconsistent clinical responses Chronic therapy requirements Hahn BH, et al. Arthritis Care Res (Hoboken). 2012; 64(6): 797–808. Rosenblum MD, et al. Sci Transl Med. 2012;4(125):125sr1. Swart J, et al. Nat Rev Rheumatol. 2017;13:244-256. Myositis

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Potential for treatment paradigm to evolve in autoimmunity CAR T therapy has the potential to provide drug-free, durable & reliable responses Promising clinical responses reported in 15 patients with an academic 4-1BB CD19-CAR T1-3 100% Clinical responses in SLE, myositis, SSc off immunosuppressive therapies 2+ years SLE drug-free remission with single infusion of CD19-CAR T3 Within 7 months Repopulation of naïve B cells post-infusion <7% Rate of CRS more severe than fever (1/15) Rate of ICANS (1/15) What are the clinical outcomes with autologous 4-1BB CD19-CAR T cell therapy? CRS – Cytokine release syndrome; ICANS – Immune effector cell-associated neurotoxicity syndrome Müller, Fabian, et al. "CD19 CAR T-Cell Therapy in Autoimmune Disease—A Case Series with Follow-up." New England Journal of Medicine 390.8 (2024): 687-700. The construct utilized in these studies has a similar design to CABA-201, sharing the 4-1BB costimulatory domain, but is a different construct. It has been publicly reported that one idiopathic inflammatory myopathy subject in this academic study had a reoccurrence of disease following ~18 months of clinical remission.​ How is CAR T cell therapy designed to reset the immune system? A ‘living drug’ potentially enabling complete B cell depletion in the blood, tissues, lymph nodes & secondary lymphoid organs While autologous CD19-CAR T has potential to deliver drug-free, durable & reliable responses, multiple other therapeutic modalities may find a role within the future treatment paradigm

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Initial CABA-201 Data in Myositis & Lupus

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Phase 1/2 Myositis Study for CABA-201 CY, cyclophosphamide; EULAR/ACR, European Alliance of Associations for Rheumatology/America College of Rheumatology; FLU, fludarabine; HSCT, hematopoietic stem cell transplantation. TIS, Total Improvement Score. Juvenile idiopathic inflammatory myopathy (JIIM, juvenile myositis) cohort recently incorporated into trial Key inclusion criteria Age ≥18 and ≤75 with a definite or probable clinical diagnosis of IIM (2017 EULAR/ACR classification criteria) Diagnosis of antisynthetase syndrome (ASyS), dermatomyositis (DM), or immune-mediated necrotizing myopathy (IMNM) based on presence of serum myositis-specific antibodies Evidence of active disease despite prior or current treatment with standard of care Key exclusion criteria Cancer-associated myositis Significant lung or cardiac impairment B cell-depleting agent within prior ~6 months Previous CAR T cell therapy and/or HSCT Screening ASyS n ≥6 IMNM cohort n ≥6 DM cohort n ≥6 Day 1 Day 29 Follow-up through year 3 Leukapheresis and CABA-201 production Preconditioning with FLU and CY Single infusion of CABA-201 (1 × 106 cells/kg) Primary endpoint: Incidence and severity of adverse events Secondary endpoints: TIS CK / muscle enzymes Myositis-specific autoantibody levels Adverse events PK / PD analysis

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Phase 1/2 Lupus Study for CABA-201 ANA, antinuclear antibody; SLEDAI-2K, Safety of Estrogens in Lupus Erythematosus National Assessment Systemic Lupus Erythematosus Disease Activity Index-2K. Key inclusion criteria Age ≥18 to ≤65 with an SLE diagnosis (2019 EULAR/ACR classification criteria) ANA+ or anti-dsDNA+ at screening For SLE (non-renal) cohort: active, moderate to severe SLE, SLEDAI 2K ≥8 despite standard therapy For Lupus Nephritis cohort: active, biopsy-proven LN class III or IV, ± class V Key exclusion criteria B cell-depleting agent within prior ~6 months Previous CAR T cell therapy and/or HSCT Presence of kidney disease other than LN Screening LN cohort n ≥6 Day 1 Day 29 Follow-up through year 3 Leukapheresis and CABA-201 production Preconditioning with FLU and CY Single infusion of CABA-201 (1 × 106 cells/kg) Primary endpoint: Incidence and severity of adverse events SLE non-renal cohort n ≥6 Secondary endpoints: SLE disease activity (e.g., SLEDAI-2K) Complete renal response Adverse events PK / PD analysis Biomarker analyses

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Time to B cell repopulation B cell phenotype3 Autoantibody changes Durability of clinical activity Rate & severity of infection Chronic maintenance / concomitant medications, if any Up to 12+ months Translational & clinical parameters inform framework to evaluate advanced modalities in autoimmunity Metrics to assess outcomes of B cell depletion in autoimmunity Indicates data being presented for either or both of the first two patients in the RESET clinical program. Illustrative graphic, adapted from Taubmann, J., et al. "OP0141 Long Term Safety and Efficacy Of CAR-T Cell Treatment in Refractory SLE-Data from the First Seven Patients." (2023): 93-94. Müller, Fabian, et al. "CD19 CAR T-Cell Therapy in Autoimmune Disease—A Case Series with Follow-up." New England Journal of Medicine 390.8 (2024): 687-700. Flow phenotyping data; confirmatory analyses ongoing. Following treatment with autologous CD19-CAR T, 6 pts with 12+ mo. of drug-free remission, as reported by Erlangen group2 Infusion 1 mo. 3 mo. 12+ mo. 6 mo. CD19-CAR T Cells Naïve B cells Healthy B cells Autoreactive B cells CAR T & B cell levels1 Translational measures Clinical data Patient experience B cell depletion: Timing & depth CAR T expansion: Magnitude & timing Rate of CRS more severe than fever Rate & grade of ICANS Rate & severity of infection Hospitalization requirements Apheresis & preconditioning Single vs. multiple infusions Autoantibody changes Vaccine titer changes Inflammatory marker changes Early efficacy signals Rate & severity of infection Chronic maintenance therapy / concomitant medications, if any Within 1 month ~3 months Metrics of evaluation

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Both patients with refractory disease, including to B cell-targeting antibodies & other agents Baseline characteristics of first two patients in RESET™ trials dsDNA, double-stranded DNA; IMNM, immune-mediated necrotizing myopathy; MMF, mycophenolate mofetil; MMT-8, manual muscle testing of 8 muscles; MTX, methotrexate; Ro-52, ribonucleoprotein 52; SRP, signal recognition particle. Baseline=pre-preconditioning visit. Disease manifestations were assessed according to Myositis Disease Activity Assessment Tool (MDAAT) and SLEDAI-2K for myositis and SLE, respectively. RESET-Myositis Patient #1 RESET-SLE Patient #1 Age (years), sex 33, male 26, male Cohort IMNM Non-renal SLE Disease duration ~2 years ~6 years Prior disease-specific therapy IVIG, rituximab, MTX, glucocorticoids Cyclophosphamide, voclosporin, belimumab, tacrolimus Disease-specific therapy at screening MTX, glucocorticoids MMF, hydroxychloroquine, glucocorticoids Autoantibodies SRP, Ro-52 ANA, dsDNA Disease activity1 MMT-8: 130, CK: 617 SLEDAI-2K: 26 Disease manifestations1,2 Muscle weakness, dysphagia Vasculitis, arthritis, alopecia, hematuria, proteinuria (isolated class V LN), low complement Expanding CD19-CAR T experience in IMNM & SLE IMNM #1 SLE #1

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No CRS, ICANS or infections of any grade reported through follow-up period1 CABA-201 was well-tolerated in initial patients Data cut-off as of 28 May 2024. Protocol requires a minimum of 4-day hospitalization for monitoring. PI-directed taper from 10mg daily prednisone. Grade 4 leukopenia, neutropenia and lymphopenia reported for SLE Patient #1, the Grade 4 cytopenias resolved and were attributed to the preconditioning regimen (fludarabine and cyclophosphamide). RESET-Myositis Patient #1 RESET-SLE Patient #1 Dose of CABA-201 83 million (1 x 106/kg) CAR+ cells 63 million (1 x 106/kg) CAR+ cells Duration of inpatient monitoring2 4 days 4 days CRS None None ICANS None None Infections None None Hypogammaglobulinemia None None Serious adverse events None None Concomitant disease-specific therapy Discontinued MTX prior to infusion; Prednisone discontinued day 3 post-infusion Discontinued MMF and HCQ prior to infusion; Ongoing taper from prednisone 10mg daily by 8 weeks3 Duration of follow-up1 84 days 28 days Both patients discharged after 4 days of monitoring post-infusion & neither received tocilizumab Vaccination titers preserved post-infusion, with no reported infections in the duration of follow-up period1 IMNM #1 SLE #1 Adverse events4

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CABA-201 exhibited anticipated profile of expansion and contraction1 CABA-201 demonstrated expansion & targeted B cell depletion Response appears to be consistent with published data of cryopreserved CAR T products as well as the expansion profile of BCMA-CAR T products in patients with multiple myeloma, in which the number of target cells is more similar to autoimmune disease than to B cell leukemias and lymphomas.2-6 Shah BD, et al. Lancet. 2021;398(10299):491-502. Awasthi R, et al. Blood Adv. 2020;4(3):560-572. IMNM #1 SLE #1 Expansion of CAR T cells to anticipated range suggests target engagement Complete B cell depletion achieved by day 15 on flow cytometry Peripheral peak CAR T expansion occurred at approximately 2 weeks & rapid contraction suggests systemic B cell aplasia was achieved 4.98% of T cells 3.32% of T cells CABA-201 cells/µL Blood 102 101 100 0 −5 0 5 10 15 20 25 30 Days post infusion SLE #1 IMNM #1 Preconditioning CABA-201 infusion CD19+ CD20+ B cells/µL 60 80 60 20 0 −5 0 5 10 15 20 25 30 Days post infusion Munshi NC, et al. N Engl J Med. 2021;384(8):705-716. Cohen AD, et al. Blood Cancer J. 2022;12(2):32. Müller F, et al. N Engl J Med. 2024;390(8):687-700.

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Complete B cell depletion achieved by day 15 on flow cytometry & maintained in context of WBC recovery Systemic B cell depletion with CABA-201 WBC, white blood cell. 1. Nadir of lymphocyte count following fludarabine and cyclophosphamide administration estimated based on respective product labels.2,3 2. Fludarabine phosphate injection. Prescribing information. 2010. https://www.accessdata.fda.gov/drugsatfda_docs/label/2011/022137s003lbl.pdf. 3. Cyclophosphamide. Prescribing information. 2013. https://www.accessdata.fda.gov/drugsatfda_docs/label/2013/012141s090,012142s112lbl.pdf. B cell depletion was achieved & maintained in follow up or until naïve B cell recovery; early, transient leukopenia observed in both patients, as expected with preconditioning1 CD19+ CD20+ B cells/µL SLE #1 IMNM #1 Preconditioning CABA-201 infusion 0.0 −5 0 5 10 15 20 25 30 Days post infusion 2.5 5.0 7.5 10.0 103 cells/µL WBC Counts 0 −5 0 5 10 15 20 25 30 Days post infusion 2 4 6 8 103 cells/µL Neutrophil Counts 0.0 −5 0 5 10 15 20 25 30 Days post infusion 0.5 1.0 1.5 103 cells/µL Lymphocyte Counts 0.0 −5 0 5 10 15 20 25 30 Days post infusion 0.5 1.0 1.5 103 cells/µL Monocyte Counts 60 80 60 20 0 −5 0 5 10 15 20 25 30 Days post infusion CD19+ CD20+ B cell count Leukocyte counts IMNM #1 SLE #1

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Antibody reduction & clinical improvement in disease activity as anticipated with follow-up of 12 weeks1 CK reduction & clinical improvement observed in SRP IMNM Data cut-off as of May 28, 2024. Luminex assay developed and performed by Cabaletta Labs. Qualitative commercial assay (Myositis Antigen Panel, performed at National Jewish Health Advanced Diagnostic Laboratories) suggests SRP54 antibody remains strongly positive at Week 12; Ro-52 normalizes by week 8. Based on patient’s moderate level of muscle disease at baseline, mild-moderate disability and limited extramuscular manifestations, the maximum achievable score is 70 points on the 100-point TIS scale. Patient treated in third-party CASTLE Phase I/II basket study, TIS data at Week 12 and 24 provided via personal communication with and as presented by Dr. Georg Schett at the EULAR 2024 symposium. Müller F, et al. N Engl J Med. 2024;390(8):687-700. IMNM #1 Discontinued all disease-specific therapies Disease markers continuing to trend positively Patient reported symptoms as much improved Disease activity & improvement measures Quantitative translational assay shows ongoing reduction in SRP & Ro-52 antibodies2,3 12-week TIS consistent with IMNM case report5 Baseline Week 4 ULN U/L 600 400 200 0 Week 8 Week 12 Creatine Kinase Normal strength MMT-8 150 140 130 120 Baseline Week 4 Week 8 Week 12 Score Major Score (points) 100 80 Minor Moderate 60 40 20 Week 24 Baseline Week 12 None TIS RESET-Myositis IMNM #1 patient treated with CABA-201 IMNM patient in CASTLE basket study5 ASyS patients treated at Univ. Hospital Erlangen via German expanded access program6 Academic published data overlaid for illustrative purposes SRP9 SRP54 SS-A/Ro-52 Week 8 Week 4 Baseline 10000 5000 0 Week 8 Week 4 Baseline 1500 500 2000 Week 12 1000 0 Net MFI Net MFI SRP

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0 0 Month 3 Month 6 SLEDAI-2K Score 25 20 30 10 5 15 Academic published data for illustrative purposes 19 Trend toward improvement in disease manifestations with follow up of 4 weeks2 Early efficacy signals in first patient in non-renal SLE cohort1 Patient in non-renal SLE cohort due to isolated Class V LN. Data cut-off as of 28 May 2024. Baseline and Day 29 SLEDAI-2K score are reflective of disease activity at study visit day. SLE #1 Vasculitis, arthritis and hematuria resolved within 4 weeks despite discontinuation of all therapies at infusion other than ongoing taper from prednisone 10mg per day Alopecia Low complement Increased DNA binding4 Proteinuria5 Hematuria Arthritis Vasculitis 26 10 20 SLEDAI-2K3 10 0 Baseline Week 4 30 SLE patient #1 Academic SLE data6 4. Anti-dsDNA antibody titer decreased from 1:40 to 1:10 from Baseline to Week 4. 5. Urine Protein Creatinine Ratio decreased from 1.08 to 0.80 from Baseline to Week 4. 6. SLE patients treated at Univ. Hospital Erlangen via German expanded access program; Müller F, et al. N Engl J Med. 2024;390(8):687-700.

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BAFF B cells Preconditioning CABA-201 infusion IMNM patient data provides insights supporting tissue-level effects of CAR T B cell repopulation occurred at 2 months in first IMNM patient Data cut-off as of May 28, 2024. IFNγ peak prior to peripheral CABA-201 peak suggests tissue-resident B cell cytotoxicity Systemic B cell depletion triggers BAFF to encourage bone marrow B cell repopulation IFN�� T cells Preconditioning CABA-201 infusion CABA-201 cells/µL Blood 102 101 100 0 −5 0 5 10 15 20 25 30 Days post infusion IFN�� (pg/mL) 150 100 50 0 IMNM #1 15000 10000 5000 0 0 25 50 Days post infusion CD19+ CD20+ B cells/µL BAFF (pg/mL) 80 60 40 20 0

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Initial patient phenotyping data consistent with potential immune system reset; confirmatory analyses ongoing B cell repopulation with naïve B cells BCR, B cell receptor; Note: Flow plot gating reflects CD19+ CD20+ live lymphocytes. 1. Patient received multiple courses of rituximab, with most recent dose approximately 9 months prior to CABA-201 infusion. 2. Cambier JC, et al. Nat Rev Immunol. 2007;7(8):633-643. Pre-B cell Early Naïve (Transitional) B cell (CD38Hi CD24Hi) Naïve B cell (CD38Med CD24Med) Mature BCR Igα Igβ Bone marrow Periphery B cell precursors Image adapted from Cambier JC, et al. 2007.2 Pre-plasma/ plasma cell B Cell, % CD20 Baseline CD19 107 106 105 104 0 0 104 106 105 B cells (CD19+, CD20+) 5.08 Week 12 107 106 105 104 0 0 104 106 105 B cells (CD19+, CD20+) 6.56 107 Day 15 107 106 105 104 0 0 104 106 105 B cells (CD19+, CD20+) 0 Week 8 107 106 105 104 0 0 104 106 105 B cells (CD19+, CD20+) 7.02 CD38 CD24 106 105 104 0 0 104 106 105 106 105 104 0 0 104 106 105 106 105 104 0 0 104 106 105 B cell phenotyping data 1 Early Naïve (Transitional) B cell Naïve B cell Remaining CD19+ CD20+ B cells B cell maturation process1 Memory B cell

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Conclusions

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Key takeaways from initial CABA-201 data in first two patients1 Data cut-off as of 28 May 2024. Müller F, et al. N Engl J Med. 2024;390(8):687-700. Third-party CASTLE Phase I/II basket study. As of June 12, 2024. 18 clinical sites now enrolling patients in the CABA-201 RESET™ program across four trials – myositis, SLE/LN, systemic sclerosis and myasthenia gravis4 CABA-201: Engineered specifically for autoimmune patients at the selected dose based on a construct design and function that is similar to the academic CD19-CAR T construct2 Safety of CABA-201 Dose selection 1 x 106 cells/kg Clinical & translational data support the selected dose of CABA-201 PK: IFNγ peak prior to peak of CABA-201 suggests tissue-level B cell cytotoxicity PD: Systemic B cell depletion followed by repopulation with naïve B cells Autoantibody levels: Decline generally consistent with Univ. Hospital Erlangen data2 Clinical & translational data: Improvement consistent with reported CD19-CAR T data2,3 In the first 2 patients (IMNM & SLE), CABA-201 was well-tolerated No CRS, ICANS or infections reported through follow-up period

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24 Realizing the vision to transform autoimmune disease treatment 1H24: No reported CRS or ICANS in first myositis or SLE patients2 Clinical update on each patient at EULAR symposium2 Evaluating CABA-201 without preconditioning in PV study Advancing program to potentially eliminate apheresis Securing scalable commercial manufacturing Cash runway into 1H26 Engineered CABA-201 specifically for use in autoimmune patients Leveraging data from an academic 4-1BB CD19-CAR T construct with favorable safety data & durable, drug free remissions1 Designed & implemented novel Phase 1/2 clinical program to accelerate path to approval No requirement for dose escalation Independent, parallel 6-patient cohorts Broad portfolio of trials in autoimmunity 2H24: Additional data from myositis & SLE trials Initial clinical data in SSc & gMG trials Initiated CABA-201 dosing in two company-sponsored studies SLE – Systemic lupus erythematosus; SSc – Systemic sclerosis; gMG – Generalized myasthenia gravis; PV – Pemphigus vulgaris Müller, Fabian, et al. "CD19 CAR T-Cell Therapy in Autoimmune Disease—A Case Series with Follow-up." New England Journal of Medicine 390.8 (2024): 687-700. The construct utilized in these studies has a similar design to CABA-201, sharing the 4-1BB costimulatory domain, but is a different construct. Data cut-off as of 28 May 2024.

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Q&A

Exhibit 99.2

 

Cabaletta Bio Reports Positive Initial Clinical Data from Phase 1/2 RESET-Myositis^™ and RESET-SLE^™ Trials of CABA-201

– No CRS, ICANS, infections or serious adverse events observed in either of the first two

patients through data cut-off of May 28, 2024 –

– CABA-201 exhibited anticipated profile of CAR T cell expansion and contraction with complete

B cell depletion observed in both patients by day 15 post-infusion –

– Improvements in both patients’ specific disease measures, consistent with academic

experience of a similar 4-1BB CD19-CAR T, suggest emerging clinical benefit with CABA-

201 while discontinuing all disease-specific therapies other than a planned steroid taper in

one patient –

– Immature, naïve B cell repopulation in first IMNM patient observed at week 8 consistent with a

potential immune system reset –

– 18 sites open and recruiting across four Phase 1/2 RESET^™ trials with 5 patients enrolled as of

June 12, 2024; initial clinical and translational data support continued development of

CABA-201 at the current dose –

– Company to host live investor conference call and webcast today at 8:00 a.m. ET –

PHILADELPHIA, June 14, 2024 – Cabaletta Bio, Inc. (Nasdaq: CABA), a clinical-stage biotechnology company focused on developing and launching the first curative targeted cell therapies designed specifically for patients with autoimmune diseases, today reported positive initial clinical data from each of the first two patients dosed with CABA-201 in the Phase 1/2 RESET-Myositis and RESET-SLE trials. These data will be presented today at 8:15 a.m. CEST (2:15 a.m. ET) at a EULAR European Congress of Rheumatology 2024 Industry Symposia session titled “Immune Reset: The Potential of CAR T Cell Therapy to Transform the Treatment of Patients with Autoimmune Disease” in Vienna, Austria. Slides from the presentation can be found on the company’s website here.

“We are encouraged by the initial safety, clinical and translational data from the RESET-Myositis and RESET-SLE trials which we believe provide important early validation regarding the potential of the selected clinical dose of CABA-201 to enable an immune system reset for patients with autoimmune diseases. By demonstrating a potentially well-tolerated safety profile along with initial clinical and translational data consistent with the academic experience of a similar 4-1BB CD19-CAR T construct, we believe CABA-201 may be uniquely positioned to fulfill unmet patient needs across a broad range of autoimmune diseases,” said David J. Chang, M.D., Chief Medical Officer of Cabaletta. “With the RESET-SSc^™ and RESET-MG^™ trials recently opening for enrollment, an additional cohort evaluating patients with juvenile myositis incorporated into the RESET-Myositis trial and the momentum provided by the promising early clinical data, we are looking forward to accelerating clinical trial enrollment in the RESET clinical program. We continue to expect to report initial clinical data from the Phase 1/2 RESET-SSc and RESET-MG trials as well as additional data from the RESET-Myositis and RESET-SLE trials in the second half of this year.”

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Cabaletta designed CABA-201, a 4-1BB-containing fully human CD19-CAR T cell investigational therapy, to deeply and transiently deplete CD19-positive B cells following a one-time infusion that may enable a reset of the immune system with the potential for durable remission without chronic therapy in patients with autoimmune diseases. Cabaletta is advancing four Phase 1/2 RESET trials evaluating CABA-201 within a total of ten cohorts with six patients in each cohort. All cohorts are evaluating the same single, weight-based dose of 1 x 10⁶ cells/kg, following a preconditioning regimen of fludarabine and cyclophosphamide consistent with the dosing regimen used in the academic experience, without a dose escalation requirement.

As of May 28, 2024, the data cut-off date, one patient treated in the immune-mediated necrotizing myopathy (IMNM) cohort in the RESET-Myositis trial had completed three months of follow-up and one patient enrolled in the systemic lupus erythematosus (SLE) non-renal cohort in the RESET-SLE trial had completed one month of follow-up. The patient with IMNM is a 33-year-old male with a two-year history of disease, positive for anti-SRP antibody and who had prior disease-specific therapy that included IVIg, rituximab, methotrexate and glucocorticoids. The patient with SLE is a 26-year-old male with a six-year history of disease, positive for anti-dsDNA antibody and who had prior disease specific therapy that included cyclophosphamide, voclosporin, belimumab, tacrolimus, mycophenolate mofetil, hydroxychloroquine and glucocorticoids. Both patients were administered a one-time infusion of CABA-201 at 1 x 10⁶ cells/kg, following a preconditioning regimen of fludarabine and cyclophosphamide. The primary endpoint of each trial is safety and tolerability within 28 days of infusion. Secondary endpoints include translational assessments and clinical outcomes.

Initial Clinical Data Summary

Safety and Tolerability

 

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CABA-201 was administered during a four-day hospital stay, as currently required by the protocol, and was generally well-tolerated with no serious adverse events reported for either patient through the follow-up period.

 

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No evidence of cytokine release syndrome (CRS) or immune effector cell-associated neurotoxicity syndrome (ICANS) of any grade was observed for either patient through the follow-up period. Tocilizumab was not administered for either patient.

 

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No infections were observed for either patient through the follow-up period.

 

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All chronic maintenance therapy or concomitant medications were discontinued for both patients through the follow-up period, other than a planned prednisone taper for the SLE patient.

Clinical and Translational Profile

 

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Complete B cell depletion was observed within 15 days post-infusion with CABA-201 in both patients. Both patients had early, transient leukopenia, as expected with the preconditioning regimen.

 

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CAR T cell expansion associated with CABA-201 reached its peak magnitude at day 15 post-infusion in both patients and the magnitude of expansion was consistent with the academic experience with a similar 4-1BB CD19-CAR T construct.

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At week 12 of follow-up for the IMNM patient, the data show a decline in creatinine kinase from 617 at infusion to 308 and a total improvement score (TIS) of 30, which is consistent with the clinically meaningful improvement seen in the academic experience of a similar 4-1BB CD19-CAR T construct that also recently reported data from an IMNM patient.

 

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At week 4 of follow-up for the SLE patient, the data demonstrated an improvement in the SLEDAI-2K (systemic lupus erythematosus disease activity index) score from 26 at baseline to 10.

 

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B cell repopulation was observed in the IMNM patient at week 8 with immature naïve B cell phenotypes as demonstrated by flow cytometry, suggesting potential immune system reset with confirmatory analyses ongoing.

Investor Conference Call and Webcast Information

Cabaletta will host a conference call and webcast today, June 14, 2024, at 8:00 a.m. ET to review the initial clinical data presented at the satellite symposium at the EULAR 2024 Congress and provide an update on the RESET clinical development program. A webcast of the live call can be accessed on the News and Events section of the Company’s website at www.cabalettabio.com. An archived replay will be available on the Company’s website.

About the RESET-Myositis^™ Trial

The RESET-Myositis^™ trial is a Phase 1/2 open-label study of CABA-201 in subjects with active idiopathic inflammatory myopathy (IIM, or myositis), including the subtypes of dermatomyositis (DM), anti-synthetase syndrome (ASyS), immune-mediated necrotizing myopathy (IMNM) and juvenile myositis (JM), each evaluated in individual cohorts. Subjects will receive a one-time infusion of CABA-201 at a dose of 1 x 10⁶ cells/kg, following a preconditioning regimen of fludarabine and cyclophosphamide. Key inclusion criteria for the DM, ASyS and IMNM cohorts include patients between ages 18 to 75 (inclusive), evidence of active disease and disease activity despite prior or current treatment with standard of care treatments. Key exclusion criteria for the DM, ASyS and IMNM cohorts include cancer-associated myositis, significant lung or cardiac impairment, treatment with a B cell depleting agent within the prior approximately six months or treatment with a biologic agent within the prior approximately three months.

About the RESET-SLE^™ Trial

The RESET-SLE^™ trial is a Phase 1/2 open-label study of CABA-201 in subjects with systemic lupus erythematosus (SLE) and lupus nephritis (LN), each evaluated in individual cohorts. Subjects will receive a one-time infusion of CABA-201 at a dose of 1 x 10⁶ cells/kg, following a preconditioning regimen of fludarabine and cyclophosphamide. Key inclusion criteria include patients between ages 18 to 65 (inclusive), evidence of active disease and disease activity despite prior or current treatment with standard of care treatments. Key exclusion criteria include treatment with a B cell depleting agent within the prior approximately six months or treatment with a biologic agent within the prior approximately three months.

About CABA-201

CABA-201 is designed to deeply and transiently deplete CD19-positive cells following a one-time infusion, which may enable an “immune system reset” with the potential for durable remission without chronic therapy in patients with autoimmune diseases. Cabaletta is evaluating CABA-201 in multiple autoimmune conditions within five disease-specific company sponsored INDs including myositis (idiopathic inflammatory myopathy, or IIM), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), generalized myasthenia gravis (gMG) and pemphigus vulgaris (PV; a sub-study to evaluate CABA-201 without preconditioning).

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About Cabaletta Bio

Cabaletta Bio (Nasdaq: CABA) is a clinical-stage biotechnology company focused on the discovery and development of engineered T cell therapies that have the potential to provide a deep and durable, perhaps curative, treatment for patients with autoimmune diseases. The CABA^™ platform encompasses two strategies: the CARTA (chimeric antigen receptor T cells for autoimmunity) strategy, with CABA-201, a 4-1BB-containing fully human CD19-CAR T, as the lead product candidate being evaluated in the RESET^™ (REstoring SElf-Tolerance) clinical trials in systemic lupus erythematosus, myositis, systemic sclerosis and generalized myasthenia gravis and in the RESET-PV^™ sub-study within the DesCAARTes^™ clinical trial in pemphigus vulgaris, along with the CAART (chimeric autoantibody receptor T cells) strategy, with multiple clinical-stage candidates, including DSG3-CAART for mucosal pemphigus vulgaris and MuSK-CAART for MuSK-associated myasthenia gravis. The expanding CABA^™ platform is designed to develop potentially curative therapies that offer deep and durable responses for patients with a broad range of autoimmune diseases. Cabaletta Bio’s headquarters and labs are located in Philadelphia, PA.

Forward-Looking Statements

This press release contains “forward-looking statements” of Cabaletta Bio within the meaning of the Private Securities Litigation Reform Act of 1995, as amended, including without limitation, express or implied statements regarding: Cabaletta’s ability to grow its autoimmune pipeline; Cabaletta’s future plans and strategies for its CAAR T and CARTA technologies and the company’s business plans and objectives as a whole; Cabaletta’s expectations around the potential safety and therapeutic benefits of CABA-201, including its belief that CABA-201 may enable an “immune system reset” with the potential for durable remission without chronic therapy in patients with autoimmune diseases; the Company’s advancement of separate Phase 1/2 clinical trials of CABA-201 in patients with SLE, myositis, SSc and gMG and advancement of a RESET-PV sub-study within the ongoing DesCAARTes trial in PV, including the Company’s expectations for the efficiency of the trial designs and updates related to status, safety data, or otherwise and the expected timing of the related data read-outs; Cabaletta’s ability to accelerate its pipeline, develop meaningful therapies for patients and leverage its research and translational insights; the clinical significance of the initial clinical data read-out at the EULAR 2024 Congress in June 2024 for patients with myositis and SLE treated with CABA-201; Cabaletta’s additional planned initial clinical data read-outs for patients with SSc and gMG treated with CABA-201 or otherwise; Cabaletta’s advancement of the process to activate clinical trial sites and pursue patient enrollment; and Cabaletta’s planned assessment of its DesCAARTes^™ and MusCAARTes^™ trials.

Any forward-looking statements in this press release are based on management’s current expectations and beliefs of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements. These risks and uncertainties include, but are not limited to: risks related to regulatory filings and potential clearance; the risk that signs of biologic activity or persistence may not inform long-term results; Cabaletta’s ability to demonstrate sufficient evidence of safety, efficacy and tolerability in its preclinical studies and clinical trials of CABA-201; the risk that the results observed with the similarly-designed construct employed in academic publications, including due to the dosing regimen, are not indicative of the results we seek to achieve with CABA-201; risks related to clinical trial site activation, delays in enrollment

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generally or enrollment rates that are lower than expected; delays related to assessment of clinical trial results; risks related to unexpected safety or efficacy data observed during clinical studies; risks related to volatile market and economic conditions and public health crises; Cabaletta’s ability to retain and recognize the intended incentives conferred by Orphan Drug Designation and Fast Track Designation or other designations for its product candidates, as applicable; risks related to Cabaletta’s ability to protect and maintain its intellectual property position; risks related to fostering and maintaining successful relationships with Cabaletta’s collaboration and manufacturing partners, including in light of recent legislation; uncertainties related to the initiation and conduct of studies and other development requirements for its product candidates; the risk that any one or more of Cabaletta’s product candidates will not be successfully developed and/or commercialized; and the risk that the initial or interim results of preclinical studies or clinical studies will not be predictive of future results in connection with future studies. For a discussion of these and other risks and uncertainties, and other important factors, any of which could cause Cabaletta’s actual results to differ from those contained in the forward-looking statements, see the section entitled “Risk Factors” in Cabaletta’s most recent annual report on Form 10-K as well as discussions of potential risks, uncertainties, and other important factors in Cabaletta’s other filings with the Securities and Exchange Commission. All information in this press release is as of the date of the release, and Cabaletta undertakes no duty to update this information unless required by law.

Contacts:

Anup Marda

Chief Financial Officer

investors@cabalettabio.com

William Gramig

Precision AQ

william.gramig@precisionaq.com

IMMUNE Reset: The potential of car t cell therapy to transform the treatment of patients with autoimmune disease Exhibit 99.3

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Symposium Speakers Drs Georg Schett and Carl June are members of Cabaletta Bio’s Scientific Advisory Board. David J. Chang, MD, MPH, FACR Chief Medical Officer Cabaletta Bio Philadelphia, PA Carl H. June, MD Director of the Center for Cellular Immunotherapies Penn Medicine Philadelphia, PA Georg Schett, MD Vice President Research Friedrich-Alexander Universität [FAU] Erlangen-Nürnberg Erlangen, Germany

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8:15 am-8:20 am 8:20 am-8:35 am 8:35 am-8:50 am 8:50 am-9:15 am 9:15 am-9:30 am Welcome and introductions David J. Chang, MD, MPH, FACR Evolving the potential of chimeric antigen receptor (CAR) T cell therapies to autoimmunity Carl H. June, MD Resetting the immune system of patients with autoimmune disease Georg Schett, MD Unlocking the potential of CD19-CAR T cell therapy in myositis and lupus David J. Chang, MD, MPH, FACR Agenda Questions and answers

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Learning Objectives Learn about the history of CAR T cell therapies in oncology and their potential in autoimmunity Review the role of B cells in autoimmune disease and the potential for CD19-CAR T cell therapy to transform treatment Understand the potential of CD19-CAR T cell therapy to reset the immune system in myositis and lupus

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Evolving the Potential of Chimeric Antigen Receptor (CAR) T Cell Therapies to Autoimmunity

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Engineered T cells that combine the targeting ability of antibodies with the cell-killing machinery of T cells What Are Chimeric Antigen Receptor (CAR) T Cells? CD, cluster of differentiation; HLA, human leukocyte antigen. June CH, Sadelain M. N Engl J Med. 2018;379;64-73. T CELL RECEPTOR CHIMERIC ANTIGEN RECEPTOR Target cell T cell T cell receptor Target antigen CD3 CD3 Target antigen Chimeric antigen receptor Targeting domain (antibody fragment) 4-1BB or CD28 (costimulatory domain) Transmembrane domain CD3ζ Target cell T cell HLA Image adapted from June CH and Sadelain M. 2018. Transmembrane domain

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Personalized Manufacturing of CAR T Cells C&EN Oncology. Accessed June 10, 2024. https://cen.acs.org/pharmaceuticals/oncology/Controlling-CAR-T-scientists-plan/96/i19. Image adapted from C&EN Oncology 2018. T cell source: A patient’s own T cells 1 Leukapheresis: T cells collected from blood 2 Viral vector T cell Reprogramming: Viral vectors deliver gene encoding CAR 3 CAR T treatment: CAR T cells are infused intravenously 6 Preparation: Standard lymphodepleting preconditioning regimen 5 Preconditioning CAR T cell Proliferation: CAR T cells expanded in a bioreactor 4

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Personalized cell therapy product that behaves as a ‘living drug’ by fully eliminating target cells in the body1 Considerations and Efficacy Outcomes of CAR T in Cancer FDA, US Food and Drug Administration. 1. Holzinger A, Abken H. Pharmacology. 2022;107(9-10):446-463. 2. Pietrobon V, et al. Int J Mol Sci. 2021;22(19):10828. 3. Maude SL, et al. N Engl J Med. 2018;378(5):439-448. 4. Schuster SJ, et al. N Engl J Med. 2019;380(1):45-56. 5. Locke FL, et al. Lancet Oncol. 2019;20(1):31-42. 6. Abramson JS, et al. Lancet. 2020;396(10254):839-852. 7. Wang M, et al. N Engl J Med. 2020;382(14):1331-1342. 8. Schuster SJ, et al. Lancet Oncol. 2021;22(10):1403-1415. 9. Neelapu SS, et al. Blood. 2023;141(19):2307-2315. COMPLETE remission rate: 40%-67%3-7 2017 Kymriah (tisagenlecleucel) 4-1BB CD19-CAR T cells have been FDA approved for lasting remission of B cell cancers1 CAR T is a ‘living drug’1 Engrafts & expands in the body Penetrates across tissues Activated by target cells1 Preconditioning key in oncology2 Eliminates cytokine sinks Increases CAR T expansion, persistence & activity 2017 Yescarta (axicabtagene ciloleucel) CD28 2020 Tecartus (brexucabtagene autoleucel) CD28 2021 Breyanzi (lisocabtagene maraleucel) 4-1BB LONG-TERM remission rate: 30%-59%6-9

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Familiarity with CAR T-associated AEs has increased in oncology, enabling potential outpatient administration Common Adverse Events Associated With CAR T Cell Therapy AE, adverse event; BiPAP, bilevel positive airway pressure; CPAP, continuous positive airway pressure; CRS, cytokine release syndrome; ICANS, immune effector cell-associated neurotoxicity syndrome; ICE, immune effector cell encephalopathy; ICP, intracranial pressure. Zhang Y, et al. J Clin Med. 2023;12(19):6124. Grade 1 Grade 2 Grade 3 Grade 4 ICE SCORE 7-9 3-6 0-2 Unarousable/unable to perform ICE DEPRESSED LEVEL OF CONSCIOUSNESS Awakens spontaneously Awakens to voice Awakens only to tactile stimulus Unarousable or requires vigorous tactile stimuli to arouse or coma SEIZURE None None Any clinical seizure that resolves rapidly or nonconvulsive seizure that resolves with intervention Life-threatening prolonged seizure (>5 min) or repetitive clinical or electrical seizures with no return to baseline in between ELEVATED ICP/CEREBRAL EDEMA None None Focal/local edema on neuroimaging Diffuse cerebral edema on neuroimaging; decerebrate or decorticate posturing; or cranial nerve VI palsy; papilledema; or Cushing’s triad MOTOR FINDINGS None None None Deep focal motor weakness such as hemiparesis or paraparesis Diagram adapted from Zhang Y, et al. 2023. CRS (cytokine release syndrome) ICANS (immune effector cell-associated neurotoxicity syndrome) Examples of standard therapies for CRS and ICANS Corticosteroids Tocilizumab Supportive care Temperature ≥38°C FEVER with No vasopressors Vasopressor +/- vasopressin HYPOTENSION Multiple vasopressors and/or Low-flow nasal cannula or blow-by High-flow nasal cannula face mask, nonrebreather mask, or Venturi mask HYPOXIA Positive pressure (CPAP, BiPAP)

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Potential Adverse Events After CAR T Cell Therapy in Cancer 1. Bonifant CL, et al. Mol Ther Oncolytics. 2016;3:16011. 2. Verdun N, Marks P. N Eng J Med. 2024;390(7):584-586. 3. Adkins S. J Adv Pract Oncol. 2019;10(suppl 3):21-28. 4. FDA. Accessed June 10, 2024. https://www.fda.gov/vaccines-blood-biologics/safety-availability-biologics/fda-requires-boxed-warning-t-cell-malignancies-following-treatment-bcma-directed-or-cd19-directed. 5. Wu L. Accessed June 10, 2024. https://endpts.com/jpm24-fdas-peter-marks-says-some-secondary-cancer-cases-after-car-t-therapy-may-be-causal-but-benefits-still-outweigh-risks/. 6. Expediting the Development of Cell and Gene Therapy. Accessed June 10, 2024. https://www.youtube.com/watch?v=jt3CNgsCXAk. CBER, Center for Biologics Evaluation and Research. Immune response to recombinant (eg, murine) protein Secondary malignancies In November 2023, the FDA reported identifying 22 cases of T cell cancers that occurred among the 34,000 patients who previously received treatment with CAR T products2 In April 2024, the FDA required approved CAR T products (CD19 and BCMA targeted) to add a boxed warning for T cell malignancy when used in patients treated for hematologic malignancies4 In January 2024, the Director of FDA’s CBER suggested the risk:benefit profile of CAR T is not in question in oncology or in moving forward development programs in autoimmune diseases5,6 Image adapted from Bonifant CL, et al. 2016,1 Verdun N and Marks P. 2024,2 Adkins S, et al. 2019.3 Secondary malignancies Insertional oncogenesis Hypogamm. & cytopenias (incl. neutropenia), increasing risk of infection

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Product in lymphoma studya Costim domain CRS ICANS Requiring tocilizumab Requiring steroids All Gr Gr ≥3 All Gr Gr ≥3 Axicabtagene ciloleucel4 CD28 93% 13% 64% 28% 43% 27% Brexucabtagene autoleucel5 CD28 91% 15% 63% 31% 59% 22% Tisagenlecleucel6 4-1BB 58% 22% 21% 12% 14% 10% Lisocabtagene maraleucel7 4-1BB 42% 2% 30% 10% 18% 10% A human CD19 binder and 4-1BB costimulatory domain may be ideal for a CD19-CAR T construct Differences in CD19-CAR T Constructs aSimilar safety outcomes comparing 4-1BB and CD28 costimulatory domains were also demonstrated in patients with B-ALL.8,9 B-ALL, B cell acute lymphoblastic leukemia; Costim, costimulatory. Gr, grade. 1. June CH, Sadelain M. N Engl J Med. 2018;379;64-73. 2. Brekke OH, Sandlie I. Nat Rev Drug Discov. 2003;2(1):52-62. 3. Cappell KM, Kochenderfer JN. Nat Rev Clin Oncol. 2021;18(11):715-727. 4. Neelapu SS, et al. N Engl J Med. 2017;377(26):2531-2544. 5. Wang M, et al. N Engl J Med. 2020;382(14):1331-1342. 6. Schuster SJ, et al. N Engl J Med. 2019;380(1):45-56. 7. Abramson JS, et al. Lancet. 2020;396(10254):839-852. 8. Zhao X, et al. Mol Ther Oncolytics. 2020;18:272-281. 9. Wu L, et al. Cancers (Basel). 2023;15(10):2767. In oncology, a 4-1BB costimulatory domain is associated with a reduced incidence and severity of CRS and ICANS events6,7 Chimeric Humanized Fully human Approved products (FMC63) Candidates under development with potentially lower risk of immune responses Sources of CAR constructs IMMUNOGENICITY2 Image adapted from June CH and Sadelain M. 2018.1 Image adapted from Brekke OH and Inger Sandlie. 2003.2

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Significant experience with CAR T in B cell cancers provided the foundation for autoimmune application Success of CAR T in Oncology Established Over Decades 1. Kuwana Y, et al. Biochem Biophys Res Commun. 1987;149(3):960-968. 2. Moritz D, et al. Proc Natl Acad Sci USA. 1994;91:4318-4322. 3. Roberts MR, et al. Blood. 1994;84(9):2878-2889. 4. Krause A, et al. J Exp Med. 1998;188:619-626. 5. Brentjens RJ, et al. Nat Med. 2003;101(4):1637-1644. 6. Imai C, et al. Leukemia. 2004;18:676-684. 7. O’Leary MC, et al. Clin Cancer Res. 2019;25(4):1142-146. 8. Mougiakakos D, et al. N Engl J Med. 2021;385(6):567-569. 9. Krishnamurthy A, et al. Wells Fargo, November 2017. 10. Clinicaltrials.gov. Accessed June 10, 2024. https://clinicaltrials.gov/search?intr=chimeric%20antigen%20receptor. Multiple types of cell therapies are in phase 1/2 studies, with the majority being autologous CAR T cell therapy9 Over 800 ongoing CAR T trials, with the majority in the US and China10 2017 First CAR T cell therapy approved by FDA (tisagenlecleucel)7 1998 First CD28-costimulated CAR reported4 1994 First report of CAR T cells killing tumor cells in mice2 1994 First clinical trial of CAR T for HIV initiated3 2003 First anti-CD19 CAR reported5 2004 In an endeavor to improve safety, first 4-1BB-costimulated CAR reported6 2021 First report of CAR T cell therapy for autoimmune disease8 1987 First CAR design1 Experience in oncology has established foundation for application in autoimmune disease

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Factors that predict adverse events and relapse are minimized in autoimmune diseases1 Considerations for CAR T Therapy in Cancer and Autoimmunity TME, tumor microenvironment. 1. Baker DJ, et al. Nature. 2023;619(7971):707-715. 2. Sterner RC, Sterner RM. Blood Cancer J. 2021;11(4):69. 3. Breyanzi. Prescribing information; 2024. 4. Yescarta. Prescribing information; 2024. 5. Kymriah. Prescribing information; 2022. 6. Müller F, et al. N Engl J Med. 2024;390(8):687-700. 7. Sender, R et al. PNAS 2023 e2308511120. Diseased cell Healthy cells CAR T cell Necrotic cell TME Fibroblast Treg Cancer cells Risk of side effects related to target B cell burden1,2 Risk of treatment failure due to mutational load (antigen escape)1,2 Risk of permanent B cell aplasia due to prior bone marrow damage2 Risk of environmental barriers for CAR T cell infiltration Safety, including CRS, ICANS, and prolonged B cell aplasia3-5 High risk1-5 Anticipated risk of suboptimal outcomes Images adapted from Baker DJ, et al. 2023.1 Lower Risk1,6 Cancer Autoimmune disease Healthy B cells 300 billion cells7 Cancer (DLBCL) ~10 trillion cells

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Key Takeaways CAR T cells are engineered T cells that are designed to combine the targeting ability of antibodies with the cell-killing machinery of T cells1 Key learnings from oncology have the potential to accelerate the adoption of CAR T cell therapy for autoimmune disease2,3 Differences in CD19-CAR T costimulatory domains seem to impact safety in cancer3-5 Many factors that drive adverse events & disease relapse post-CAR T are not at play in autoimmune disease driven by B cells3,6 Potentially lower risk of CRS & ICANS due to lower B cell burden Evolving the Potential of CAR T Cell Therapies to Autoimmunity 1. Holzinger A, Abken H. Pharmacology. 2022;107(9-10):446-463. 2. Baker DJ, et al. Nature. 2023;619(7971):707-715. 3. Cappell KM, Kochenderfer JN. Nat Rev Clin Oncol. 2021;18(11):715-727. 4. Davey AS, et al. Cancers. 2021;13(38). 5. Zhao X, et al. Molecular Therapy Oncolytics. 2020;18. 6. Müller F, et al. N Engl J Med. 2024;390(8):687-700.

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Resetting the Immune System of Patients With Autoimmune Disease

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B Cells Play a Central Role in the Pathogenesis of Autoimmune Diseases B cells contribute to autoimmunity through a variety of mechanisms1,2 Autoantibody production Antigen presentation T cell co-stimulation Production of proinflammatory cytokines While circulating B cells are sensitive to depletion, tissue-resident B cells easily escape depletion2 BCR, B cell receptor; MHC, major histocompatibility complex. 1. Barnas JL, et al. Curr Opin Immunol. 2019;61:92-99. 2. Rubin SJS, et al. Nat Rev Rheumatol. 2019;15(5):303-315. Images adapted from Rubin SJS, et al. 20192 Autoantibodies BCR Autoantigen Autoreactive B cell Cytokines MHC class II TCR Autoreactive T cell Autoantibody production Cytokine production Antigen presentation CD80 or CD86 CD28 Co-stimulation

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Current Therapies for B Cell Driven Autoimmune Disease Rarely Achieve Drug-Free Remission 1. Schett G, et a. Ann Rheum Dis. 2024. PMID: 38777374. 2. Bucci, L. et al. Nat Med. 2024; PMID 38671240. Current challenges Despite good peripheral B cell depletion, bispecific and antibody-based B cell targeting therapies rarely induce stable drug-free remission in autoimmune disease Shallow B cell depletion that does not tackle resident autoimmune B cell clones may be the reason for this limitation Goals of newer therapies Deeper B cell depletion with a ‘living drug’ to allow targeting resident autoimmune B cell clones, enabling potential immune tolerance such that long-term drug therapy is not needed Reversibility of B cell depletion enabling a good safety profile B cells Autoreactive B cells CD19+ plasmablasts CD19- plasma cells CAR T cell mediated B cell depletion Monoclonal antibody Mediated B cell depletion

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Emerging Academic Evidence of CD19-CAR T in Autoimmunity CK: creatinine kinase; Flu/Cy, fludarabine/cyclophosphamide; LN, lupus nephritis; SLE, systemic lupus erythematosus; SLEDAI-2K, systemic lupus erythematosus disease activity index 2K. Müller F, et al. N Engl J Med. 2024;390(8):687-700. 15 patients with refractory systemic autoimmune disease Age range of 18 to 60 years; 60% female All patients with disease duration >12 months All patients had inadequate response to ≥2 lines of therapy ~50% of patients received B cell depletion therapy Muscle and lung involvement median CK of 4298 U/L Myositis (n=3) Median SLEDAI-2K score of 13; all had LN class III or IV All had active skin and lung involvement SSc (n=4) All patients received a single dose of 1x106/kg CD19-CAR T cells following Flu/Cy preconditioning SLE (n=8)

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Preconditioning results in transient WBC decrease, though B cell depletion is sustained CD19-CAR T Cells Can Result in Targeted B Cell Depletion WBC, white blood cell. Müller F, et al. N Engl J Med. 2024;390(8):687-700. Circulating CAR T cell numbers after CD19-CAR T treatment (N=15) CD19-CAR T cells Circulating CD19+ B cells within first 10 days after treatment (N=15) Circulating total WBCs within first 30 days after treatment (N=15) CD19+ B cells WBC WBC/µL

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Reconstitution With Naïve B Cells Within 7 Months1 BL, baseline; FU, follow-up; Ig, immunoglobulin; IIM, idiopathic inflammatory myopathy; RC, reconstitution. 1. Müller F, et al. N Engl J Med. 2024;390(8):687-700. 2. Mackensen, Andreas A, et al. Nature Medicine. 2022;28(10):1-9. B cell reconstitution Circulating B cell numbers after CD19-CAR T treatment (N=15)1 Changes in B cell subtype numbers from baseline to B cell reconstitution (n=5)2 Distribution of heavy chain in the BCRs at baseline and after B cell reconstitution by mRNA sequencing (n=5)2

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Patients maintained off immunosuppressive therapies, suggesting an ‘immune reset’ is possible Long-term Efficacy Outcomes With CD19-CAR T Cells Figures adapted from Müller F, et al. 2024. C3, complement component 3; EUSTAR-AI, European Scleroderma Trials and Research Group activity index; dsDNA, double stranded DNA; mRSS, modified Rodnan skin score; TIS, total improvement score. Müller F, et al. N Engl J Med. 2024;390(8):687-700. Myositis (n=3) SLE (n=8) Achieved initial responses by 3 months Decreased disease activity by 6 months Achieved response by 6 months Myositis (n=3, ASyS) SLE (n=8) SSc (n=4)

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Preliminary academic data suggests potential slower IMNM improvement due to muscle-predominant disease1,2 Initial HMGCR IMNM Patient Treated With CD19-CAR T1 MMT8 Units 120 100 80 60 0 50 100 150 81-year-old woman with HMGCR IMNM Myositis subtype involving primarily muscle Manifestations may affect response kinetics Treated with CD19-CAR T in CASTLE study Potential for disease-specific timing & magnitude of response to CD19-CAR T 1. Patient treated in CASTLE Phase I/II basket study. CK and MMT8 data as presented at the Global Conference on Myositis in March 2024 and TIS data at Week 12 and 24 provided via personal communication with Dr. Georg Schett. 2. Müller F, et al. N Engl J Med. 2024;390(8):687-700. Disease activity & improvement measures U/L 2,000 1,500 1,000 500 0 0 50 100 150 200 CK 200 Week 24 Baseline Week 12 Major 100 80 Minor Moderate 60 40 20 None TIS IMNM patient in CASTLE basket study1 ASyS patients treated at Univ. Hospital Erlangen via German expanded access program2 Score (points)

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AE profile consisted primarily of fever in 4-1BB costimulatory domain-containing CD19-CAR T Safety & Tolerability of CD19-CAR T in Autoimmunity1 a2 patients (1 SLE, 1 myositis) had preexisting hypogammaglobulinemia due to previous rituximab exposure b1 patient had preexisting hypogammaglobulinemia. cPneumonia occurred in an SLE patient 7 weeks after CAR T cell therapy. ILD, interstitial lung disease; IVIG, intravenous immunoglobulin; URTI, upper respiratory tract infection. 1. Müller F, et al. N Engl J Med. 2024;390(8):687-700. Hypogammaglobulinemia 5 patients developed hypogamm.a 2 patients required IVIg supplementationb Vaccine titers remained stable Cytokine release syndrome 67% (10 of 15 patients) with only grade 1 (fever) 1 patient with myositis with grade 2 Preexisting ILD with increased oxygen requirement for 1 day while febrile 6 patients received tocilizumab Infection 1 hospitalization due to pneumoniac All other infections were mild and mostly manifested as URTIs (including COVID) 2 events of herpes zoster reactivation ICANS Possible grade 1 ICANS in 1 ASyS patient Mild dizziness at 2w post-infusion Resolved following oral steroids

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Key Takeaways Academic Data Demonstrates Drug-free and Durable Responses in Patients With Myositis, SLE and SSc 1. Müller F, et al. N Engl J Med. 2024;390(8):687-700. 2. Mackensen, Andreas A, et al. Nat Med. 2022;28(10):1-9. Case series provides preliminary support for the feasibility, efficacy and safety of a 4-1BB CD19-CAR T in patients with autoimmune disease1,2 Durable disease- and drug-free remission Acute adverse events post-CAR T consisted primarily of fever Repopulation with naïve B cells within 7 months Most infections were mild in severity, with only one case of pneumonia requiring hospitalization

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Unlocking the Potential of CD19-CAR T Cell Therapy in Myositis and Lupus

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Designed to replicate and expand on the academic clinical data that generated interest in the field REstoring SElf-Tolerance (RESET™) Development Program PK, pharmacokinetics; PD, pharmacodynamics, SAEs: serious adverse events 1.Peng, BinghaoJ, et al. Presented at: American Society Gene and Cell Therapy 26th Annual Meeting; 2023 May 19; Los Angeles, CA. 2. Dai, Zhenyu, et al. Journal of Cellular Physiology. 2021;236(8): 5832-5847. 3. Evaluated as part of CT120, a dual-CD19xCD22 CAR T product candidate under development by Nanjing IASO Biotherapeutics, Co., Ltd. (IASO Bio). Fully human anti-CD19 binder Similar binding affinity and biologic activity to FMC63, with binding to the same epitopes1,2 Safety data in ~20 oncology patients evaluated and reported by IASO as part of a dual-CAR3 4-1BB costimulatory domain Same domain as used in academic studies CD3-zeta signaling domain CABA-201 CABA-201 designed to optimize the potential safety and efficacy of CD19-CAR T for patients with autoimmune disease Key Questions for RESET Phase 1/2 Studies Safety of CABA-201 CABA-201 AE profile CRS, ICANS, SAEs   Dose selection 1 x 106 cells/kg PK – CAR T persistence PD – B cell depletion Autoantibody reduction Clinical outcomes

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Phase 1/2 Myositis Study for CABA-2011 CY, cyclophosphamide; EULAR/ACR, European Alliance of Associations for Rheumatology/America College of Rheumatology; FLU, fludarabine; HSCT, hematopoietic stem cell transplantation. TIS, Total Improvement Score. 1. ClinicalTrials.gov. Accessed June 10, 2024. https://classic.clinicaltrials.gov/ct2/show/NCT06154252. Key inclusion criteria Age ≥18 and ≤75 with a definite or probable clinical diagnosis of IIM (2017 EULAR/ACR classification criteria) Diagnosis of antisynthetase syndrome (ASyS), dermatomyositis (DM), or immune-mediated necrotizing myopathy (IMNM) based on presence of serum myositis-specific antibodies Evidence of active disease despite prior or current treatment with standard of care Key exclusion criteria Cancer-associated myositis Significant lung or cardiac impairment B cell-depleting agent within prior ~6 months Previous CAR T cell therapy and/or HSCT Screening ASyS n ≥6 IMNM cohort n ≥6 DM cohort n ≥6 Day 1 Day 29 Follow-up through year 3 Leukapheresis and CABA-201 production Preconditioning with FLU and CY Single infusion of CABA-201 (1 × 106 cells/kg) Primary endpoint: Incidence and severity of adverse events Secondary endpoints: TIS CK / muscle enzymes Myositis-specific autoantibody levels Adverse events PK/PD analysis Juvenile IIM cohort recently incorporated into trial

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Phase 1/2 Lupus Study for CABA-2011 ANA, antinuclear antibody; SELENA-2K, Systemic Lupus Erythematosus Disease Activity Index-2K. 1. ClinicalTrials.gov. Accessed June 10, 2024. https://classic.clinicaltrials.gov/ct2/show/NCT06121297. Key inclusion criteria Age ≥18 to ≤65 with an SLE diagnosis (2019 EULAR/ACR classification criteria) ANA+ or anti-dsDNA+ at screening For SLE (non-renal) cohort: active, moderate to severe SLE, SLEDAI-2K ≥8 despite standard therapy For Lupus Nephritis cohort: active, biopsy-proven LN class III or IV, ± class V Key exclusion criteria B cell-depleting agent within prior ~6 months Previous CAR T cell therapy and/or HSCT Presence of kidney disease other than LN Screening LN cohort n ≥6 Day 1 Day 29 Follow-up through year 3 Leukapheresis and CABA-201 production Preconditioning with FLU and CY Single infusion of CABA-201 (1 × 106 cells/kg) Primary endpoint: Incidence and severity of adverse events SLE non-renal cohort n ≥6 Secondary endpoints: SLE disease activity (e.g., SLEDAI-2K) Complete renal response Adverse events PK/PD analysis Biomarker analyses

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Indicates data being presented for either or both of the first two patients in the RESET™ clinical program. aFlow phenotyping data; confirmatory analyses ongoing. 1. Illustrative graphic, adapted from Taubmann J, et al. OPO141. Abstract presented at: EULAR; May 31, 2023; Milan, Italy. 2. Müller F, et al. N Engl J Med. 2024;390(8):687-700. Translational & clinical parameters inform framework to evaluate advanced modalities in autoimmunity Metrics To Assess Outcomes of B Cell Depletion In Autoimmunity Time to B cell repopulation B cell phenotypea Autoantibody changes Durability of clinical activity Rate & severity of infection Chronic maintenance / concomitant medications, if any Up to 12+ months Following treatment with autologous CD19-CAR T, 6 pts with 12+ mo. of drug-free remission, as reported by Erlangen group2 Infusion 1 mo. 3 mo. 12+ mo. CD19-CAR T Cells Naïve B cells Healthy B cells Autoreactive B cells CAR T & B cell levels1 Translational measures Clinical data Patient experience B cell depletion: Timing & depth CAR T expansion: Magnitude & timing Rate of CRS more severe than fever Rate & grade of ICANS Rate & severity of infection Hospitalization requirements Apheresis & preconditioning Single vs. multiple infusions Autoantibody changes Vaccine titer changes Inflammatory marker changes Early efficacy signals Rate & severity of infection Chronic maintenance therapy / concomitant medications, if any Within 1 month ~3 months Metrics of evaluation

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IMNM: High Unmet Need & Limited Therapeutic Options1 DM, dermatomyositis; EMA, European Medicines Agency; ESRD, end-stage renal disease; IMNM, immune-mediated necrotizing myopathy; HMGCR: HMG-CoA reductase 1. Suh J, et al. Muscle Nerve. Published online May 27, 2024. doi:10.1002/mus.28114. 2. Khoo T, et al. Nat Rev Rheumatol. 2023;19(11):695-712. 3. Patient treated in third-party CASTLE Phase I/II basket study. Idiopathic inflammatory myopathy (IIM, myositis) > IMNM-associated antibodies include anti-SRP & anti-HMGCR Muscle disease (weakness, elevated CK) predominant No therapies approved by the FDA or EMA for IMNM Often refractory despite combination therapy (e.g., IVIg, rituximab) Immune-mediated necrotizing myopathy Dermatomyositis Antisynthetase syndrome Cohort for first patient treated with CABA-201 Myositis Prevalence: ~1 million globally2 HMGCR IMNM patient treated in CASTLE CD19-CAR T study with minor response by 3 months improved to major response at 6 months with no additional therapy3

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SLE: Variable Disease Course & Limited Treatments1-6 LN, lupus nephritis. 1. Tian J, et al. Ann Rheum Dis. 2023;82(3):351-356. 2. Hoover PJ, Costenbader KH. Kidney Int. 2016;90(3):487-92. 3. Benlysta. Package insert. GSK; 2018. 4. Saphnelo. Package Insert. AstraZeneca. 2021. 5. Hahn BH, et al. Arthritis Care Res (Hoboken). 2012; 64(6): 797–808. 6. Aziz F, Chaudhary, K. Curr Clin Pharmacol. 2018;13(1):4-13. 7. Mackensen, Andreas A, et al. Nature Medicine. 2022;28(10):1-9. Cohort for first patient treated with CABA-201 Highly heterogenous with potentially life-threatening complications Two biologic therapies approved with 52-week efficacy endpoint Incomplete responses & need for long-term therapy very common ~40% with LN, with Class V LN often resistant to therapy Academic CD19-CAR T data in SLE patients with predominantly renal disease suggest potential for clinical response by 3 months7 > Systemic lupus erythematosus (SLE) SLE Prevalence: >3 million globally1 Non-renal systemic lupus erythematosus Lupus nephritis

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Both patients had refractory disease, including to B cell-targeting antibodies & other agents Baseline Characteristics of First Two Patients in RESET Trials aBaseline=pre-preconditioning visit. bDisease manifestations were according to Myositis Disease Activity Assessment Tool (MDAAT) and SLEDAI-2K for myositis and SLE, respectively. dsDNA, double-stranded DNA; IMNM, immune-mediated necrotizing myopathy; MMF, mycophenolate mofetil; MMT-8, manual muscle testing of 8 muscles; MTX, methotrexate; Ro-52, ribonucleoprotein 52; SRP, signal recognition particle. RESET-Myositis Patient #1 RESET-SLE Patient #1 Age (years), sex 33, male 26, male Cohort IMNM Non-renal SLE Disease duration ~2 years ~6 years Prior disease-specific therapy IVIG, rituximab, MTX, glucocorticoids Cyclophosphamide, voclosporin, belimumab, tacrolimus Disease-specific therapy at screening MTX, glucocorticoids MMF, hydroxychloroquine, glucocorticoids Autoantibodies SRP, Ro-52 ANA, dsDNA Disease activitya MMT-8: 130, CK: 617 SLEDAI-2K: 26 Disease manifestationsa,b Muscle weakness, dysphagia Vasculitis, arthritis, alopecia, hematuria, proteinuria (isolated class V LN), low complement Expanding CD19-CAR T experience in IMNM & non-renal SLE IMNM #1 SLE #1

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No CRS, ICANS or infections reported through follow-up perioda CABA-201 was Well-tolerated in Initial Patients aData cut-off as of 28 May 2024. bProtocol requires a minimum of 4-day hospitalization for monitoring. cPI-directed taper from 10mg daily prednisone. dGrade 4 leukopenia, neutropenia and lymphopenia reported for SLE Patient #1, the Grade 4 cytopenias resolved and were attributed to the preconditioning regimen (fludarabine and cyclophosphamide). Both patients discharged after 4 days of monitoring post-infusion & neither received tocilizumab RESET-Myositis Patient #1 RESET-SLE Patient #1 Dose of CABA-201 83 million (1 x 106/kg) CAR+ cells 63 million (1 x 106/kg) CAR+ cells Duration of inpatient monitoringb 4 days 4 days CRS None None ICANS None None Infections None None Hypogammaglobulinemia None None Serious adverse events None None Concomitant disease-specific therapy Discontinued MTX prior to infusion; Prednisone discontinued day 3 post-infusion Discontinued MMF and HCQ prior to infusion; Ongoing taper from prednisone 10mg daily by 8 weeksc Duration of follow-upa 84 days 28 days Adverse eventsd IMNM #1 SLE #1

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CABA-201 exhibited anticipated profile of expansion and contraction1-5 CABA-201 Expansion in Anticipated Range aResponse appears to be consistent with published data of cryopreserved CAR T products as well as the expansion profile of BCMA-CAR T products in patients with multiple myeloma, in which the number of target cells is more similar to autoimmune disease than to B cell leukemias and lymphomas BCMA, B cell maturation antigen. 1. Shah BD, et al. Lancet. 2021;398(10299):491-502. 2. Awasthi R, et al. Blood Adv. 2020;4(3):560-572. 3. Munshi NC, et al. N Engl J Med. 2021;384(8):705-716. 4. Cohen AD, et al. Blood Cancer J. 2022;12(2):32. 5. Müller F, et al. N Engl J Med. 2024;390(8):687-700. Expansion of CAR T cells to anticipated range suggests target engagement Peripheral peak CAR T expansion occurred at approximately 2 weeksa Rapid contraction suggests systemic B cell aplasia has been achieved IMNM #1 SLE #1 4.98% of T cells 3.32% of T cells SLE #1 IMNM #1 Preconditioning CABA-201 infusion CABA-201 cells/µL Blood 102 101 100 0 −5 0 5 10 15 20 25 30 Days post infusion

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Complete B cell depletion achieved by day 15 on flow cytometry & maintained in context of WBC recovery Systemic B Cell Depletion With CABA-201 aNadir of lymphocyte count following fludarabine and cyclophosphamide administration estimated based on respective product labels.1,2 WBC, white blood cell. 1. Fludarabine phosphate injection. Prescribing information. 2010. https://www.accessdata.fda.gov/drugsatfda_docs/label/2011/022137s003lbl.pdf. 2.Cyclophosphamide. Prescribing information. 2013. https://www.accessdata.fda.gov/drugsatfda_docs/label/2013/012141s090,012142s112lbl.pdf. IMNM #1 SLE #1 CD19+ CD20+ B cell count Leukocyte counts B cell depletion was achieved & maintained in follow up or until naïve B cell recovery Early, transient leukopenia observed in both patients, as expected with preconditioninga SLE #1 IMNM #1 Preconditioning CABA-201 infusion 0.0 −5 0 5 10 15 20 25 30 Days post infusion 2.5 5.0 7.5 10.0 103 cells/µL WBC Counts 0 −5 0 5 10 15 20 25 30 Days post infusion 2 4 6 8 103 cells/µL Neutrophil Counts 0.0 −5 0 5 10 15 20 25 30 Days post infusion 0.5 1.0 1.5 103 cells/µL Lymphocyte Counts 0.0 −5 0 5 10 15 20 25 30 Days post infusion 0.5 1.0 1.5 103 cells/µL Monocyte Counts CD19+ CD20+ B cells/µL 60 80 60 20 0 −5 0 5 10 15 20 25 30 Days post infusion

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Immunologic Effects of CABA-201 IMNM #1 CABA-201 pharmacokinetics CABA-201 pharmacodynamics IFNγ peak prior to peripheral CABA-201 peak suggests tissue-resident B cell cytotoxicity Systemic B cell depletion triggers BAFF to encourage bone marrow B cell repopulation IFN�� T cells Preconditioning CABA-201 infusion BAFF B cells Preconditioning CABA-201 infusion 15000 10000 5000 0 0 Weeks post infusion CD19+ CD20+ B cells/µL BAFF (pg/mL) 80 60 40 20 0 CABA-201 cells/µL Blood 102 101 100 0 −5 0 5 10 15 20 25 30 Days post infusion IFN�� (pg/mL) 150 100 50 0 Week 8 Week 4

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Antibody reduction & clinical improvement in disease activity as anticipated with follow-up of 12 weeks CK Reduction & Clinical Improvement Observed in SRP IMNM aData cut-off as of 28 May 2024. bLuminex assay developed and performed by Cabaletta Labs. cQualitative commercial assay (Myositis Antigen Panel, performed at National Jewish Health Advanced Diagnostic Laboratories) suggests SRP54 antibody remains strongly positive at Week 12; Ro-52 normalizes by week 8. dBased on patient’s moderate level of muscle disease at baseline, mild-moderate disability and limited extramuscular manifestations, the maximum achievable score is 70 points on the 100-point TIS scale. 1. Patient treated in third-party CASTLE Phase I/II basket study, TIS data at Week 12 and 24 provided via personal communication with and as presented by Dr. Georg Schett. 2. Müller F, et al. N Engl J Med. 2024;390(8):687-700. SRP9, signal recognition particle 9; SSA, Sjögren’s syndrome–related antigen A autoantibody; TRIM21, tripartite motif 21; ULN, upper limit of normal; CK, creatine kinase. IMNM #1 Quantitative translational assay shows ongoing reduction in SRP & Ro-52 antibodiesb,c SRP9 SRP54 SS-A/Ro-52 Week 8 Week 4 Baseline 10000 5000 0 Discontinued all disease-specific therapies Disease markers continuing to trend positively Patient reported symptoms as much improved 12-week TIS consistent with IMNM case report1 Disease activity & improvement measures Baseline Week 4 ULN U/L 600 400 200 0 Week 8 Week 12 Creatine Kinase Normal strength MMT-8 150 140 130 120 Baseline Week 4 Week 8 Week 12 Score Week 8 Week 4 Baseline 1500 500 2000 Week 12 1000 0 Net MFI Net MFI SRP Score (points) Major 100 80 Minor Moderate 60 40 20 Week 24 Baseline Week 12 None TIS RESET-Myositis IMNM #1 patient treated with CABA-201 IMNM patient in CASTLE basket study1 ASyS patients treated at Univ. Hospital Erlangen via German expanded access program2 Academic published data overlaid for illustrative purposes RESET-Myositis IMNM #1 patient-specific TIS ceilingd

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Trend toward improvement in disease manifestations with follow up of 4 weeksb Early Efficacy Signals in Non-Renal SLEa Vasculitis, arthritis and hematuria resolved within 4 weeks despite discontinuation of all therapies at infusion other than ongoing taper from prednisone 10mg per day aPatient in non-renal SLE cohort due to isolated Class V LN. bData cut-off as of 28 May 2024. cBaseline and Day 29 SLEDAI-2K score are reflective of disease activity at study visit day. dUrine Protein Creatinine Ratio decreased from 1.08 to 0.80 from Baseline to Week 4. eAnti-dsDNA antibody titer decreased from 1:40 to 1:10 from Baseline to Week 4. 1. SLE patients treated at Univ. Hospital Erlangen via German expanded access program; Müller F, et al. N Engl J Med. 2024;390(8):687-700. SLE #1 Alopecia Low complement Increased DNA bindingd Proteinuriae Hematuria Arthritis Vasculitis 26 10 20 SLEDAI-2Kc Score 10 0 Baseline Week 4 30 SLE patient #1 0 0 Month 3 Month 6 SLEDAI-2K Score Academic SLE data1 25 20 30 10 5 15 Academic published data for illustrative purposes

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CABA-201 Effects on Vaccine & Infection Antibody Titers Titers preserved post-infusion, with no reported infections in the duration of follow-up perioda aData cut-off as of 28 May 2024. IMNM #1 SLE #1 Streptococcus pneumoniae HSV1 Influenza A G4 EA (H1N1) Sars-CoV-2 Epstein-Barr virus (EBV) Bordetella pertussis Cytomegalovirus (CMV) Hepatitis B Mumps virus Diphtheria Hepatitis A Rubeola virus (measles) Rubella virus Tetanus SLE patient #1 Baseline Baseline Week 8 Week 4 Week 4 IMNM patient #1 SLE patient #1 Net MFI 105 104 103 102 Net MFI 105 104 103 102

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Initial patient phenotyping data consistent with potential immune system reset; confirmatory analyses ongoing B Cell Repopulation with Naïve B Cells Note: Flow plot gating reflects CD19+ CD20+ live lymphocytes. aPatient received multiple courses of rituximab, with most recent dose approximately 9 months prior to CABA-201 infusion. BCR, B cell receptor. 1. Cambier JC, et al. Nat Rev Immunol. 2007;7(8):633-643. Pre-B cell Early Naïve (Transitional) B cell (CD38Hi CD24Hi) Naïve B cell (CD38Med CD24Med) Mature BCR Igα Igβ Bone marrow Periphery B cell precursors IMNM #1 Image adapted from Cambier JC, et al. 2007.1 Pre-plasma/ plasma cell B Cell, % CD20 Baseline CD19 107 106 105 104 0 0 104 106 105 B cells (CD19+, CD20+) 5.08 Week 12 107 106 105 104 0 0 104 106 105 B cells (CD19+, CD20+) 6.56 107 Day 15 107 106 105 104 0 0 104 106 105 B cells (CD19+, CD20+) 0 Week 8 107 106 105 104 0 0 104 106 105 B cells (CD19+, CD20+) 7.02 CD38 CD24 106 105 104 0 0 104 106 105 106 105 104 0 0 104 106 105 106 105 104 0 0 104 106 105 B cell phenotyping data a Early Naïve (Transitional) B cell Naïve B cell Remaining CD19+ CD20+ B cells B cell maturation process1 Memory B cell

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Key Takeaways 1. Müller F, et al. N Engl J Med. 2024;390(8):687-700. 2. Castle Phase 1/2 basket study. CABA-201: Designed for autoimmune patients to optimize the potential product profile of CD19-CAR T Safety: In the first 2 patients (IMNM & SLE), CABA-201 was well-tolerated No CRS, ICANS or infections reported through follow-up period Dose: Clinical & translational data support the selected dose of CABA-201 PK: IFNγ peak prior to peak of CABA-201 suggests tissue-level B cell cytotoxicity PD: Systemic B cell depletion followed by repopulation with naïve B cells Autoantibody levels: Decline generally consistent with Univ. Hospital Erlangen data1 Clinical & translational data: Improvement consistent with reported CD19-CAR T data1,2 18 clinical sites now enrolling patients in the CABA-201 RESET™ program with four trials open – myositis, SLE/LN, systemic sclerosis and myasthenia gravis

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Questions & Answers

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You are invited to stop by at Booth S18-19 for additional engagement with Cabaletta Bio! Please use the EULAR app to complete an evaluation form To learn more, please visit CabalettaBio.com & contact us at clinicaltrials@cabalettabio.com

v3.24.1.1.u2

Document and Entity Information	Jun. 14, 2024
Cover [Abstract]
Amendment Flag	false
Entity Central Index Key	0001759138
Document Type	8-K
Document Period End Date	Jun. 14, 2024
Entity Registrant Name	CABALETTA BIO, INC.
Entity Incorporation State Country Code	DE
Entity File Number	001-39103
Entity Tax Identification Number	82-1685768
Entity Address, Address Line One	2929 Arch Street
Entity Address, Address Line Two	Suite 600
Entity Address, City or Town	Philadelphia
Entity Address, State or Province	PA
Entity Address, Postal Zip Code	19104
City Area Code	(267)
Local Phone Number	759-3100
Written Communications	false
Soliciting Material	false
Pre Commencement Tender Offer	false
Pre Commencement Issuer Tender Offer	false
Security 12b Title	Common Stock, par value $0.00001 per share
Trading Symbol	CABA
Security Exchange Name	NASDAQ
Entity Emerging Growth Company	true
Entity Ex Transition Period	false

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