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 se

Selective B cell ablation for

autoimmune disease February 2020 Exhibit 99.1

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

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registration or qualification under the securities laws of any such state or jurisdiction. The 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 neither this Presentation, nor any sale of securities, shall 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" relating to our

business, operations, and financial conditions, including, but not limited to, current beliefs, expectations and assumptions regarding the future of our business, future plans and strategies, our development plans, our preclinical and clinical

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include, among others, the success, cost, and timing of our product candidate development activities and preclinical studies and clinical trials, our ability to obtain and maintain regulatory approval for our product candidates, our ability to

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Develop and launch the first curative

targeted cellular therapies for patients with autoimmune diseases Our vision

Developing CAAR T products (Chimeric

AutoAntibody Receptor T) where there is a biologic opportunity for cure (over two dozen potential targets identified) by designing CAARs to selectively eliminate ONLY pathogenic B cells displaying targeted antibody while leveraging CART19 design and

manufacturing experience from Penn DesCAARTes Phase 1 trial - DSG3-CAART in mucosal pemphigus vulgaris (PV) patients progressing to support expected timelines Orphan Drug Designation granted by the FDA in January 2020 for the treatment of PV

CABA Labs leading evaluation and development of risk mitigating approaches Expanding product pipeline with our CABA platform (Cabaletta Approach for selective B cell Ablation) preclinical data published on PV, myasthenia gravis, and hemophilia A

inhibitor robust IP portfolio emerging with first US patent issued on lead program Planned catalysts in 2020 DesCAARTes trial - Report clinical acute tolerability (8 day) data from initial cohort MuSK-CAART - Confirm in vivo target

engagement and initiate IND-enabling studies Manufacturing independence - Initiate validation of manufacturing for clinical trials with CMO1 Key messages Leveraging CAR T experience to specifically target B cell-mediated autoimmune diseases

Contract Manufacturing Organization

Diversified with long-standing history

of professional collaborations among team and with co-founders Leadership Steven Nichtberger, MD President, CEO & Chairman Scientific Advisory Board Board of Directors Michael Milone, MD PhD Co-chair, Co-founder Aimee Payne, MD PhD Co-chair,

Co-founder Jay Siegel, MD Catherine Bollard, MD PhD Mark Simon Brian Daniels, MD Richard Henriques Gwendolyn Binder, PhD EVP Science & Technology David Chang, MD Chief Medical Officer Anup Marda Chief Financial Officer Brian Stalter General

Counsel Arun Das, MD Senior Director BD Martha O'Connor Chief HR Officer

Scientific platform and strategy CAR T

CELL CD19 CANCER CELL Chimeric Antigen Receptor T cell Kymriah Targeting Domain ANTI-CD19 ANTIBODY FRAGMENTS HEALTHY B CELL CD137 Costimulatory Domain CD3-Zeta Signaling Domain CAR T Therapy No Antibody-Mediated Immunity CAAR T Therapy Normal Immune

System CAAR T CELL Chimeric AutoAntibody Receptor T cell CABA CAAR T PATHOGENIC AUTOREACTIVE B CELL AUTOANTIGEN Autoantibody Receptor HEALTHY B CELL

Our CABA (Cabaletta Approach for

Selective B cell Ablation) Platform Proven ability to identify multiple product candidates Epitope mapping to determine regions targeted by autoantibodies Optimizing CAAR construct / design with the goal of selectively ablating reactive B cells

Preclinical in vitro and in vivo testing to evaluate efficacy and safety Scientific, clinical and commercial assessment to inform product candidate development Mucosal pemphigus vulgaris (mPV) Multiple product candidates Epitope mapping CAAR

construct / design In vitro studies In vivo studies GMP manufacturing Clinical trial development Scientific, clinical and commercial assessment

Cabaletta Pipeline * In our discovery

stage, we perform epitope mapping and optimize CAAR construct and design. ** May not be required if Phase 2 is a registrational clinical trial. Multiple disease targets with preclinical evidence of selective and specific target engagement DSG3-CAART

Mucosal Pemphigus Vulgaris DSG3/1-CAART Mucocutaneous Pemphigus Vulgaris MuSK-CAART MuSK Myasthenia Gravis FVIII-CAART Hemophilia A with FVIII Alloantibodies PEMPHIGUS Phase 1 Phase 2 Phase 3** Preclinical Discovery*

CAR T therapy products are approved for

B cell cancers Cabaletta product candidates are filling an adjacent white space Clinical Pivotal Marketed Oncology B Cell-Mediated Allo/Autoimmune Diseases DSG3-CAART (mPV) MuSK-CAART (MG) FVIII-CAART (HemA inhibitor) DSG3/1-CAART (mcPV) Preclinical

/ Discovery FcRn's (argenx, Alexion, others) BTK's (Principia, others) * * * T-reg = T-regulatory, NK = Natural Killer, RBC = Red Blood Cell, Macroph = Macrophage = Cabaletta pipeline products * = non-cell therapy Cabaletta pipeline

competitors CAR T (Oncology) / CAAR T (Allo/Autoimmune) T-reg, NK, TCR, RBC, macroph1

CAR T therapy products are approved

for B cell cancers Cabaletta product candidates are filling an adjacent white space Clinical Pivotal Marketed CAR T (Oncology) / CAAR T (Allo/Autoimmune) T-reg, NK, TCR, RBC, macroph1 Oncology B Cell-Mediated Allo/Autoimmune Diseases

Preclinical / Discovery Patent Portfolio US: 1 issued / 6 filed Foreign: 13 applications T-reg = T-regulatory, NK = Natural Killer, RBC = Red Blood Cell, Macroph = Macrophage

Patent rights pursued on a target by

target basis Pursuing multiple levels of protection for CAAR constructs protein, nucleic acid, and engineered cells; and their use Expiration Dates: 2035-2039 (without patent term extensions) First issued US patent for CAAR therapy in pemphigus

Exemplary Composition of Matter Claim "A genetically modified cell comprising a CAAR comprising an extracellular domain comprising DSG1, DSG3, or a fragment thereof that binds an autoantibody expressed on a B-cell, a transmembrane domain, and

an intracellular signaling domain, wherein the cell expresses the CAAR and binds the autoantibody expressed on the B cell or induces killing of the B cell expressing the autoantibody." Patent rights owned by the University of Pennsylvania

(Penn) or co-owned by Penn and the Children's Hospital of Philadelphia and exclusively licensed globally to Cabaletta Distinct from CD19 directed CAR T patents, initial CAAR T patent covers entire human antigen Overview of Intellectual

DSG3-CAART for mucosal pemphigus

Pemphigus Vulgaris CAAR T

Preclinical Development (video) Ellebrecht Milone, Payne, Science 2016 Reengineering chimeric antigen receptor T cells for targeted therapy of autoimmune disease Christoph T. Ellebrecht,1 Vijay G. Bhoj,2 Arben Nace,1 Eun Jung Choi,1

Xuming Mao,1 Michael Jeffrey Cho,1 Giovanni Di Zenzo,3 Antonio Lanzavecchia,4 John T. Seykora,1 George Cotsarelis,1 Michael C. Milone,2* Aimee S. Payne1*

Pemphigus Vulgaris Mucosal PV: 25%

of U.S. pemphigus vulgaris Mucocutaneous PV: 75% of U.S. pemphigus vulgaris http://www.danderm-pdv.is.kkh.dk/atlas/3-157.html http://www.dermis.net/bilder/CD008/550px/img0042.jpg Associated Antibody Anti-DSG3 Clinical Signs Painful blisters of the

orifices (mouth, nose, larynx, esophagus, eyes, genitalia, rectum) Disease Incidence (US / EU) 350 / 600 Disease Prevalence (US / EU) 4,250 / 6,250 Current Treatment Broad immunosuppression with steroids, methotrexate, mycophenolate and/or

azathioprine is modestly effective and/or poorly tolerated. Similar challenges with intravenous immunoglobulin (IVIG) B cell depletion with rituximab1,2,3 offers transient remission (clinical & serologic) with up to 90% of responders relapsing

without chronic therapy Chronic B cell depletion with rituximab: 5.4% annual risk of severe infection and up to 1.9% lifetime risk of fatal infection Patients and physicians want safer and more effective treatment options Anti-DSG3 + Anti-DSG1

Blisters on orifices and skin 1,050 / 1,800 12,750 / 18,750 Epidemiology, clinical signs and treatment Image credit: D@nderm Joly, Pascal, et al. "First-line rituximab combined with short-term prednisone versus prednisone alone for the treatment of

pemphigus (Ritux 3): a prospective, multicentre, parallel-group, open-label randomised trial." The Lancet 389.10083 (2017): 2031-2040. Kushner, Carolyn J., et al. "Factors Associated With Complete Remission After Rituximab Therapy for

Pemphigus." JAMA dermatology (2019). Jancin, Bruce. "Rituximab bests mycophenolate in pemphigus vulgaris," Dermatology News, Nov 2019, Vol. 50:11, p. 2.; Press Release, Roche, 14 Oct 2019.

DSG3 antibodies are widely

considered to be necessary and sufficient to cause PV1 PV is an optimal lead indication for CAAR T therapy Serum anti-DSG3 antibodies are 98 - 100% sensitive and specific The DSG3 CAAR has published animal model proof-of-concept validation Depletion

of B cells by rituximab2 or antibody by plasmapheresis transiently improves clinical disease The B cell repertoire and antigenic epitopes on DSG1/3 are well understood, and formed the basis for DSG3 and DSG1 CAAR designs 1 2 3 4 Spindler, Volker, et

al. "Mechanisms causing loss of keratinocyte cohesion in pemphigus." Journal of Investigative Dermatology 138.1 (2018): 32-37. Joly, Pascal, et al. "First-line rituximab combined with short-term prednisone versus prednisone alone for the treatment

of pemphigus (Ritux 3): a prospective, multicentre, parallel-group, open-label randomised trial." The Lancet 389.10083 (2017): 2031-2040.

DSG3 EC1-4 CAAR is designed to

target all known pathogenic B cells in mPV DSG3-CAART encompasses all known pathogenic epitopes Ohyama, Bungo, et al. "Epitope spreading is rarely found in pemphigus vulgaris by large-scale longitudinal study using desmoglein 2-based swapped

molecules." Journal of investigative dermatology 132.4 (2012): 1158-1168. Antibodies that target the specific extracellular domain are shown below each extracellular domain. 91% 71% 51% 19% 12% % of PV sera targeting each domain1 EC5 directed

antibodies are not known to be pathogenic 2 2 2 2

No evidence of toxicity at

clinically relevant doses with selective and specific target engagement DSG3-CAART preclinical program summary of results Indicator Final Preclinical Results In vitro off-target toxicity No specific cytotoxicity observed at clinically relevant cell

numbers toward a panel of primary human & FcgR-expressing cells No confirmed interactions with human membrane proteins In vivo off-target toxicity No detected off-target effects at clinically relevant doses Anti-DSG3 autoantibody titer

Dose-dependent elimination of anti-DSG3 B cells and anti-DSG3 antibody reduction (serologic remission') CAAR T cell engraftment Dose-dependent increase in CAAR-positive cells observed via flow cytometry Tissue blistering No blistering

of oral mucosa (histologic remission') Anti-DSG3 hybridoma outgrowth Significantly delayed growth or reduction of anti-DSG3 hybridomas, even in the presence of soluble anti-DSG antibodies Tolerability Target Engagement

DSG3-CAART demonstrates target

engagement in presence of high polyclonal antibody titer Active immune model: target engagement despite soluble antibody The DSG3 protein is made of up of 5 extracellular (EC) domains, EC1-5. Antibodies against EC1-4 can be pathogenic, but

antibodies against EC5 are not. Therefore, antibodies against EC5 are not targeted by the CAAR by design. In this model, the human DSG3-CAART product is rapidly rejected. In these two animals, an incomplete response against EC1 was observed, which

correlated with loss of persistence. DSG3 Knockout Mouse DSG3 EC1-5 Immunization Generate Anti-DSG3 Antibodies Transfer Splenocytes Immunodeficient Mouse NTD DSG3- CAART DSG3- CAART 3 Weeks Target engagement and no toxicity observed 3-6 Weeks P DSG3

CAART Treatment (EC1-4 domains1) 2 2

Study Endpoint & Objectives

Primary Endpoint: Adverse Events, including Dose Limiting Toxicity Secondary Objectives: DSG3 ELISA titer changes, rate of/time to/duration of remission, manufacturing success rate, CAAR T expansion/persistence Open-label study of DSG3-CAART in

mucosal-dominant PV patients (mPV) DesCAARTes phase 1 clinical trial (IND reviewed and accepted within 30 days) Open-label study to determine the maximum tolerated dose & fractionation of DSG3-CAART in 30 (up to 48) r/r mPV patients Go:

Identification of a dosing regimen with evidence of target engagement and an acceptable safety profile Part Cohort # Subjects A - Dose Escalation Fractionated infusion at increasing dose levels A1-A4 3(+3) per cohort B - Dose

Consolidation Consolidating selected dose fractions into a single infusion B1-B2 3(+3) per cohort C - Expansion1 Expanded subject enrollment at final selected dose C ~12 Total ~30(+18) Age: 18 Inadequately managed by standard

immunosuppressive therapies Confirmed diagnosis Active disease Anti-DSG3 antibody positive Rituximab in last 6 months Prednisone > 0.25mg/kg/day Other autoimmune disorder requiring immunosuppressive therapies Recent investigational treatment ALC

< 1,000 at screening Major Inclusion Criteria Major Exclusion Criteria FDA has requested, and the Company has agreed, that we will share data from cohort A to inform a discussion on the optimal design of cohort C. According to FDA guidance, the

submission of cohort A data is not gating to planned enrollment in cohort B.

8 Days: Acute safety Up to Week -18:

Screening Day -7 to -3: Pre-infusion visit 3 Months: Primary safety endpoint 3 years: Efficacy 15 yrs: Long-term follow-up CAART infusion Week -6 to -1: Apheresis and manufacturing Clinical trial assessments and timeframes Spindler, Volker, et al.