Exhibit 99.1

2 Forward-Looking StatementThis presentation includes “forward-looking statements” within the meaning of, and made pursuant to the safe harbor provisions of, the Private Securities Litigation Reform Act of 1995, including, but not limited to: our expectation about timing and execution of anticipated milestones, including our planned progressof clinical trials and the availability of clinical data from such trials; our expectations about our collaborators’ and partners’ ability to execute key initiatives; our expectations about our manufacturing plans and strategies; estimates regarding our cash forecasts; the expected impact of the COVID-19 pandemic on our operations; and the ability of our lead product candidates to treat their respective target CNS disorders. These forward-looking statements may be accompanied by such words as “aim,” “anticipate,” “believe,” “could,” “estimate,” “expect,” “forecast,” “goal,” “intend,” “may,” “might,” “plan,” “potential,” “possible,” “will,” “would,” and other words and terms of similar meaning. These statements involve risks and uncertainties that could cause actual results to differ materially from those reflected in such statements, including: our ability to develop, obtain regulatory approval for and commercialize PBGM01, PBFT02, and future product candidates; the timing and results of preclinical studies and clinical trials; the risk that positive results in a preclinical study or clinical trial may not be replicated in subsequent trials or success in early stage clinical trials may not be predictive of results in later stage clinical trials; risks associated with clinical trials, including our ability to adequately manage clinical activities, unexpected concerns that may arise from additional data or analysis obtained during clinical trials, regulatory authorities may require additional information or further studies, or may fail to approve or may delay approval of our drug candidates; the occurrence of adverse safety events; failure to protect and enforce our intellectual property, and other proprietary rights; failure to successfully execute or realize the anticipated benefits of our strategic and growth initiatives; risks relating to technology failures or breaches; our dependence on collaborators and other third parties for the development of product candidates and other aspects of our business, which are outside of our full control; risks associated with current and potential delays, work stoppages, or supply chain disruptions caused by the coronavirus pandemic; risks associated with current and potential future healthcare reforms; risks relating to attracting andretaining key personnel; failure to comply with legal and regulatory requirements; risks relating to access to capital and credit markets; and the other risks and uncertainties that are described in the Risk Factors section of our most recent filings with the U.S. Securities and Exchange Commission. These statements are based on our current beliefs and expectations and speak only as of the date of this presentation. We do not undertake any obligation to publicly update any forward-looking statements except as required by law. By attending or receiving this presentation you acknowledge that you are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date such statements are made; you will be solely responsible for your own assessment of the market and our market position; and that you will conduct your own analysis and be solely responsible for forming your own view of the potential future performance of Passage Bio.

3 Our VisionTo fulfill the promise of genetic medicine by developing transformative therapies for people with devastating CNS diseases Two exciting lead gene therapy programsin GM1 and FTD Innovative research partnership with Penn’s Gene Therapy Program Dedicated manufacturing and process analytics capabilities Strong cash position with runway into 1H 2025

4 Global upliFT-D Dose-Escalation Study of PBFT02 Global Imagine-1 Dose-Escalation Study of PBGM01 NEXT MILESTONESInitial safety and biomarker data from Cohort 1 patients in 2H 2023 GM1 GANGLIOSIDOSISA Fatal Pediatric CNS DiseaseAdvancing Two Lead Clinical Programs in 2023 NEXT MILESTONESInitial safety and biomarker data from Cohort 4 (early infantile, high dose) by mid-2023 FRONTOTEMPORAL DEMENTIA (FTD)A Detrimental Adult CNS Disease WHERE WE ARE Strong momentum with 8 patients on study and positive interim data WHERE WE ARE First patient on study, positive momentum toward recruiting additional patients in Cohort 1

5 •Drug Candidate: PBAL05 •Gene Target: C9orf72•Approach: miRNA and cDNA combination•Hexanucleotide repeat expansion in C9orf72gene is found in 40% of familial and 8% of sporadic ALS cases1•~4,500 ALS-C9orf72 cases worldwide in 20202 AMYOTROPHIC LATERAL SCLEROSIS (ALS) •Drug Candidate: Unnamed•Gene Target: HTTand Undisclosed•Caused by an autosomal dominant trinucleotide (CAG) expansion in the huntingtin (HTT)gene•Estimated 41,000 patients in US and ~200,000 more at risk3 HUNTINGTON’S DISEASE Promising Preclinical Pipeline in Adult CNS DisordersSupported by strategic collaboration with Penn’s GTP, an unmatched leader in cutting-edge AAV gene therapy research •Drug Candidate: Unnamed•GeneTarget: Undisclosed•Common focal epilepsy affecting ~616,000 in the US4•One third are not controlled by current treatments4•No universal treatment target has been identified TEMPORAL LOBE EPILEPSY (TLE) 1. Majounieet al Lancet11:323-33, 2012; 2. Brown et al., Neuroepidemiology55: 342-353, 2021 3.HDSA; Fisher and Hayden, 2014, Mov Disord. 29:105-14. 4. Asadi-Pooyaet al., 2017 World Neurosurg. 99:662-666

6 Discovery UPenn GTPResearch Analytics and Vector Engineering Process/Analytic DevelopmentPassage CMC R&D Lab Proven Analytical CapabilitiesIntegrated Process DevelopmentGMP QC Capabilities Strong Regulatory CMC Scientific ExpertiseScale-up Capability GMP ManufacturingDedicated Suite at CatalentQualified cGMP Capacity End-to-End Clinical Supply Chain Leading CMC Capabilities Via a Hybrid Approach Dedicated Capacity and End-to-End Supply ChainKey Strategic PartnershipsInternal State-of-the-Art CMC CapabilitiesPartnershipsIn HouseEnsuring product supply while maintaining critical analytics capabilities in-house

PBGM01GM1 Gangliosidosis

8 GM1 Gangliosidosis: A Devastating Pediatric Disease FATAL, PEDIATRIC NEUROLOGICAL LYSOSOMAL STORAGE DISORDER caused by GLB1gene mutations characterized by destruction of neurons in the brain and spinal cord.Characterized by rapidly progressive neurological decline resulting in reduced muscle tone, progressive CNS dysfunction, deafness, blindness, rigidity and skeletal dysplasia. RARE AND UNDERSERVEDpopulations with incidence of up to ~1 per 100,000 live births worldwide.No disease-modifying therapies are presently approved.Source: NIH, CHOP, American Journal of Neuroradiology

9 GM1 Gangliosidosis Disease Continuum GM1 Gangliosidosis is a Continuum Disease SeverityResidual Enzyme Activity (Serum) Focus of Imagine-1 TrialNegligible to 5%~ 1–5%~ 3 –10% Type 1 (Early Infantile)•Onset <6 months•Hypotonia•Neurodegeneration•Developmental regression•Seizures•Skeletal dysplasia •Survival: <2 years without supportive careType 2a (Late Infantile)•Onset 6–24 months•Developmental plateau, followed by regression•Impaired ambulation•Impaired cognition•Seizures•Survival: 5 to 10 yearsType 2b (Juvenile)•Onset 2–5 years•Impaired ambulation•Dysarthria•Variable skeletal disease•Decreased cognition•Survival into 2nd decade Disease severity inversely related to residual β-Galenzyme activityBrunetti-PierriN., Scaglia F. Mol Genet Metab. 2008;94(4):391-396. JarnesJR, et al. Mol Genet Metab. 2017;121(2):170-179. Lang FM, et al. Mol Genet Metab. 2020;129(3):228-235. RegierDS, TifftCJ. RothermelCE. GLB1-related disorders. In: Adam MP, ArdingerHH, PagonRA, et al, eds. GeneReviews® [Internet].

10 PBGM01OUR APPROACHNext-generation, proprietary capsid delivers functional GLB1gene encoding β-gal to the brain and peripheral tissuesPRECLINICAL EVIDENCECompelling preclinical data in knock-out mouse model•Dose-related histological correction, improvements in neurological function, and survival•Meaningful transduction of both CNS and critical peripheral organsCLINICAL DEVELOPMENT•Ongoing global Phase 1/2 Imagine-1 trial focused on early and late infantile GM1•Well-tolerated, positive safety profile and dose dependent increases in transgene expression*Potential transformative therapy for rare, underserved disorder * Based on interim results from Cohorts 1-3

11 Imagine-1: Global Phase 1/2 Trial with PBGM01Completed dosing of all patients in dose-ascending portion of study Trial DesignPhase 1/2, multi-center, open-label, dose escalation and confirmatory study Route of AdministrationIntra-cisterna magna (ICM)CapsidAAVhu68DurationTwo years, with rollover into a separate long-term follow-up studyPrimary Endpoints•Safety and tolerability•Efficacy (confirmatory cohort)Regulatory Clearances and Designations•Received multiple global regulatory clearances•Received Orphan Drug, Rare Pediatric Disease and Fast Track designations by FDA and Orphan and Advanced Therapy Medicinal Product designations by EC COHORT 4Early Infantilen = 2DOSE 2 (1.1e11 GC/g)*DOSE 1 (3.3e10 GC/g)* Expansion CohortEarly Infantile Expansion CohortLate Infantile COHORT 2Late Infantilen = 2 COHORT 3Early Infantilen = 2 COHORT 1Late Infantilen = 2 IDMC review Recruiting Dosing complete* Genome copies per gram of estimated brain weight60 days between subject enrollment in Cohorts 1-4

12 * Interim data as presented on December 14, 2022. AEs=adverse events; ICM=intra-cisterna magna.Key Takeaways from Cohorts 1-3 Interim Data* SAFETYFavorable safety profile and well-tolerated•No serious AEs related to study treatment•No evidence of DRG toxicity•No evidence of cell-mediated immune response•No complications related to ICMinjection BIOMARKERS•High dose resulted in durable increases in CSF β-Gal well above NHS•High dose resulted in durable decreases in β-Gal substrate GM-1 gangliosides in CSF CLINICAL STATUS•Milderdevelopmental delay at the time of treatment is emerging as an important determinant of treatment outcomes•Pending results from high dose cohorts, we plan to incorporate degree of developmental delay into pivotal study inclusion/ exclusion criteria

13 *Based on preliminary data from University of Pennsylvania’s ODC Natural History Study (NHS) (NCT04041102); value range (0.3-1.81 nmol/mL/3hr)PBGM01 ICM Delivery Resulted in Dose Dependent Increases in Transgene Activity in CSF •PBGM01 administration resulted in dose-dependent increase in CSF β-Gal activity•High dose PBGM01 resulted in 3.6-5.2x increase in CSF β-Gal activity relative to baseline•High dose PBGM01 resulted in CSF β-Gal activity well above levels seen in Natural History Study (NHS)*•Increased CSF b-Gal activity sustained for up to 12 months in Patient 1•PBGM01 administration resulted in sustained β-Gal enzyme expression in blood Key Points 0123456060120180240300360β-Gal, nmol/mL/3hrTime (days)β-gal, CSF P1 Late Infantile P2 Late Infantile P3 Early Infantile P5 Early Infantile NHS patient value range 0 12 3 456060120180240300360β-Gal, nmol/mL/3hrTime (days)β-gal, CSF P4 Late Infantile P6 Late Infantile4.7-5.2x baseline 3.6x baseline 1.2-2.8x baseline High dose Low dose Late Infantile: CircleEarly Infantile: Square NHS patient value range

14 High Dose PBGM01 Led to Dose Dependent Decreases in CSF GM1 Gangliosides 0200400600050100150200250300350Gangliosides, apparent nMTime (days)GM1 Ganglioside, CSF P4 Late Infantile P6 Late Infantile 0200400600 8001,000050100150200250300350Gangliosides, apparent nMTime (days)GM1 Ganglioside, CSF P1 Late Infantile P2 Late Infantile P3 Early Infantile P5 Early Infantile 75% drop from baseline Late Infantile: CircleEarly Infantile: Square 1. Lang FM et al., Mol GenetMetab.2020;129:228-235; CSF= CerebrospinalFluid •PBGM01 administration resulted in dose-dependent decrease in CSF GM1 ganglioside levels•Decrease in CSF gangliosides correlated with higher levels of b-Gal activity•GM1 gangliosides hypothesized to mediate CNS manifestations of disease1 Key Points High dose Low dose

15 Patients Manifest a Wide Range of Developmental Delay at Baseline Patient 1Patient 2Patient 3Patient 4Patient 5Patient 6DiagnosisLate OnsetLate OnsetEarly OnsetLate OnsetEarly OnsetLate OnsetDosing CohortLow doseLow doseLow doseHigh doseLow doseHigh doseChronological age at baseline (months)14311518617Developmental age at baseline (Bayley; months)1270.52.50.55Developmental delay at baseline (Bayley; months)22414.515.55.512 Mild-moderate delayDevelopmental Delay at Baseline Marked delay

16 *The Vineland-II is caretaker-assessed.**The Bayley-III is based on direct observation by a neurodevelopmental specialist. Preliminary Trend: Milder Developmental Delay at Dosing Associated with Improved Treatment Response 0510 15 20 2568101214161820222426283032343638404244 Overall Developmental Age (months) Chronological Age (months)Vineland-II* P1 Late Infantile P2 Late Infantile P3 Early Infantile P5 Early Infantile P4 Late Infantile P6 Late Infantile Mild-to-moderate developmental delay Marked developmental delay 0 510 15 20 2568101214161820222426283032343638404244 Overall Developmental Age (months) Chronological Age (months)Bayley-III** P1 Late Infantile P2 Late Infantile P3 Early Infantile P5 Early Infantile P4 Late Infantile P6 Late Infantile Mild-to-moderate developmental delay Marked developmental delay Late Infantile: CircleLow Dose: Solid LineEarly Infantile: SquareHigh Dose: Dashed Line

17 Data from Cohort 4 Will Add to Understanding of Dose and Patient Selection Patient 1Patient 2Patient 3Patient 4Patient 5Patient 6Patient 7Patient 8DiagnosisLate OnsetLate OnsetEarly OnsetLate OnsetEarly OnsetLate OnsetEarly OnsetEarly OnsetDosing CohortLow doseLow doseLow doseHigh doseLow doseHigh doseHigh DoseHigh DoseChronological age at baseline (months)1431151861775.5Developmental age at baseline (Bayley; months)1270.52.50.5551.5Developmental delay at baseline (Bayley; months)22414.515.55.51224 Mild-moderate delayDevelopmental Delay at Baseline Marked delay

18 PBGM01 Program Anticipated Next Steps •Present additional data from Cohorts 1-3 at 19th Annual WORLDSymposium in February 2023•Present initial data from Cohort 4 (early infantile, high dose) by mid-2023•Analyze data from Cohort 4•Due to observed dose response and the absence of safety signals, evaluate dosing additional patients at the current high dose and/or higher dose•Continued interactions with regulatory authorities as clinical data set matures to align on design of confirmatory study and pathway to Biologics License Application Engage with regulatory authorities Determine optimal dose for confirmatory study Share additional data throughout 2023

PBFT02Frontotemporal Dementia —GRN

20 FTD-GRN: A Devastating Adult DiseaseDEVASTATING FORM OF DEMENTIA caused by a GRNgene mutation resulting in progranulin (PGRN) deficiency and haploinsufficiency. Approximately 5–10% of FTD is caused by a GRNmutation.Disease progression is rapid and degenerative including loss of speech, loss of expression, severe behavioral changes and immobility. RARE AND UNDERSERVEDpopulations with estimated U.S. prevalence of ~3,000 to 6,000 patients.No disease-modifying therapies are presently approved.

21 Maintains lysosomal activityProgranulin Deficiency Contributes to NeurodegenerationFTD BrainHealthy BrainReduced progranulin leads to neuronal dysfunction and death Progranulin is critical to maintaining CNS cell homeostasis Regulates microglial activation Regulates synapse number and structure Modulates cell signaling responses to stressors Lysosomal dysfunction Neuroinflammation Synaptic dysfunction Neurodegeneration m Source: Rhinn H et al., Trends Pharmacol Sci. 2022;43:641-652

22 PBFT02OUR APPROACHProprietary construct delivers functional GRNgene encoding progranulin (PGRN) with potential therapeutic benefit of a one-time gene therapy approachPRECLINICAL EVIDENCECompelling preclinical evidence from NHP studies•Broad transduction across the brain, including high transduction of ependymal cells•Achieved supraphysiologic CSF levels of PGRN compared to levels in healthy human volunteersCLINICAL DEVELOPMENTOngoing global Phase 1/2 upliFT-D trial focused on early symptomatic FTD-GRNPotential transformative therapy for rare, underserved disorder

23 PBFT02: NHP Preclinical Studies Utilizing ICM•AAV1 increased CSF PGRN levels ~5x more than AAV5 and AAVhu68 vectors, without further elevating peripheral levels•CSF delivery of PBFT02 to NHPs achieved supraphysiologic CSF levels of PGRN1. Hinderer et al.,Annals Clin Trans Neurology.2020Left: Two adult rhesus macaques per treatment received ICM AAV.hPGRNDose 4, (3.0 x 1013GC / 3.3 x 1011GC/g brain) on study day 01.Right: Adult rhesus macaques received ICM PBFT02 (n = 3/dose) or vehicle (n =2) on study day 0. Shading: Reference range for healthy adult controls’ PGRN levels in CSF (n = 61) (Passage Bio data) AAV1 transgene delivery led to supraphysiologic hPGRNlevels in CSF CSF PGRN (ng/mL)010203040CSF0.1110100 Day AAVhu68AAVhu68(v2)AAV5AAV1NormalLLOQ PBFT02 (AAV1) showed dose-related increases in CSF PGRN 024681012Dose 4Dose 3Dose 2VehicleHuman PGRN (ng/ml) 14 days post-ICM dose

24 PBFT02: Higher CSF PGRN May Confer Incremental Benefits Microgliosis reduction strongest at highest doses / PGRNlevels(murine FTDmodel) Lipofuscin reduced at all doses(murine FTDmodel) •Lipofuscin: increased levels with lysosomal dysfunction•Microgliosis: inflammatory response to pathogenic insults in the CNS•CD68: marker of activated microglia Thalamus data shown above. Thalamic atrophy is a key feature commonly found in FTD

25 upliFT-D: Global Phase 1/2 Trial with PBFT02 OPTIONAL DOSE 3 DOSE 2 (1.1e11 GC/g)* DOSE 1 (3.3e10 GC/g)* 60 days between subject enrollment COHORT 1n = 3 COHORT 2n = 3 OPTIONAL COHORT 3n = 3 Trial DesignPhase 1/2, multicenter, open-label, dose escalation studyRoute of AdministrationIntra-cisterna magna (ICM)VectorAAV1Duration2 years; with additional 3 years of follow-up for safety and durability of effectPrimary Endpoints•Safety and tolerabilitySecondary Endpoints•Biomarkers, functional and clinical signs of disease progressionRegulatory Clearances and Designations•Received regulatory clearances from FDA, Health Canada and ANVISA (Brazil)•Received Orphan Drug and Fast Track designations by FDA and Orphan designation by EC* Genome copies per gram of estimated brain weight IDMC review Recruiting Dosing completeInitial safety and biomarker data from Cohort 1 expected in 2H 2023

Looking Ahead

27 TIMINGMILESTONEGM1Feb 2023Additional safety and biomarker data from Cohorts 1–3 to be presented atWORLDSymposiumMid 2023Initial safety and biomarker data from Cohort 4 (early infantile, high dose)FTD-GRN2H 2023Initialsafety and biomarker data from Cohort 1patientsKey Milestones PIPELINE•Pursuing strategic alternatives to advance Krabbe and MLD clinical-stage programs•Advance preclinical programs for ALS and Huntington’s Disease•Advance target ID research program for TLE•8 additional CNS pipeline options remain through GTP partnershipBALANCE SHEET•Cash balance of $190 million as of 12/31/22*•Cash on hand to fund operations into 1H 2025* Cash, cash equivalents and marketable securities

28 Our VisionTo fulfill the promise of genetic medicine by developing transformative therapies for people with devastating CNS diseases Two exciting lead gene therapy programsin GM1 and FTD Innovative research partnership with Penn’s Gene Therapy Program Dedicated manufacturing and process analytics capabilities Strong cash position with runway into 1H 2025

Thank Youpassagebio.com|NASDAQ GS: PASG

30 Demonstrated LeadershipLEADERSHIP TEAM Deep experience in rare disease, CNS disorders and genetic medicines Simona KingChief Financial Officer Mark Forman, M.D., Ph.D.Chief Medical OfficerBOARD OF DIRECTORSMaxine Gowen, Ph.D.ChairwomanAthenaCountouriotis, M.D.AvenzoTherapeuticsDerrell Porter, M.D.CellevolveBioMichaelKamarck, Ph.D.Sanofi Biotech Advisory CouncilSandip KapadiaHarmony BiosciencesSaqib Islam, J.D.SpringWorksTom Woiwode, Ph.D.VersantWilliam Chou, M.D.Chief Executive Officer William Chou, M.D.Chief Executive Officer Chip CaleGeneral Counsel & Corporate Secretary Alex Fotopoulos Chief Technology Officer Desiree Luthman, D.D.S.SVP Global Regulatory Affairs

31 A Broad and Robust Pipeline with Global RightsTransformative therapies for CNS disorders across rare and large patient populations Program* Indication GeneDiscoveryPre-clinicalPhase 1/2Pivotal PBGM01 † GM1 gangliosidosis GLB1 PBFT02 Frontotemporal dementia GRN PBAL05 Amyotrophic lateral sclerosis C9orf72 Unnamed Huntington’s disease HTT & Undisclosed Unnamed Temporal lobe epilepsy Undisclosed PBKR03 Krabbe disease GALC PBML04 Metachromatic leukodystrophy ARSA *8 additional CNS pipeline license options remain; 3 license options were previously exercised, and rights were subsequently returned to the University of Pennsylvania.† Program includes ongoing natural history study of infantile and juvenile GM1 gangliosidosispatients Exploring strategic alternatives

32 Intra-Cisterna Magna (ICM) Administration•Directly deliver vector into the CSF via a single injection to reach both CNS and peripheral tissues*–Allows for broad CNS biodistribution–Lower doses compared to IV systemic delivery–Reduced impact of neutralizing antibodies •Administered under anesthesia using modern neuroimaging to allow for precise delivery•Currently being used in several clinical studies in both pediatric and adult populations Cisterna magna Source:Hinderer et. al,Human Gene Therapy. 2018 Jan; 29(1):15-24Utilized across three clinical-stage programs to directly target CNS