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UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

Washington, D.C. 20549

FORM 8-K

CURRENT REPORT

Pursuant to Section 13 or 15(d)

of the Securities Exchange Act of 1934

Date of Report (Date of earliest event reported): October 24, 2024

PASSAGE BIO, INC.

(Exact name of registrant as specified in its charter)

Delaware

001-39231

82-2729751

(State or other jurisdiction
of incorporation)

(Commission
File Number)

(IRS Employer
Identification No.)

One Commerce Square
2005 Market Street, 39th Floor
Philadelphia, PA

19103

(Address of principal executive offices)

(Zip Code)

(267) 866-0311

(Registrant’s telephone number, including area code)

N/A

(Former name or former address, if changed since last report)

Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:

Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)

Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)

Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))

Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Securities registered pursuant to Section 12(b) of the Act:

Title of each class

Trading symbol(s)

Name of each exchange on which registered

Common Stock, $0.0001 Par Value Per Share

PASG

The Nasdaq Stock Market LLC
(Nasdaq Global Select Market)

Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§240.12b-2 of this chapter).

Emerging growth company

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act.

Item 7.01 Regulation FD Disclosure.

On October 24, 2024, Passage Bio, Inc. (the “Company”) presented a scientific presentation at the European Society of Gene & Cell Therapy 31st Annual Congress (the “ESGCT Presentation”).

The Company also issued a press release on October 24, 2024, related to the ESGCT Presentation.

A copy of the press release and ESGCT Presentation are attached as Exhibits 99.1 and 99.2, respectively, to this Current Report on Form 8-K.

The information in this Item 7.01, including Exhibits 99.1 and 99.2 to this Current Report on Form 8-K, shall not be deemed to be “filed” for purposes of Section 18 of the Exchange Act of 1934, as amended (the “Exchange Act”), or otherwise subject to the liabilities of that section or Sections 11 and 12(a)(2) of the Securities Act of 1933, as amended (the “Securities Act”). The information contained in this Item 7.01 and in the accompanying Exhibits 99.1 and 99.2 shall not be incorporated by reference into any other filing under the Exchange Act or under the Securities Act, except as shall be expressly set forth by specific reference in such filing.

Item 9.01 Financial Statements and Exhibits.

(d)Exhibits

Exhibit No.

Description

99.1

Passage Bio, Inc. press release dated October 24, 2024

99.2

ESGCT Presentation

104

Cover Page Interactive Data File (formatted as Inline XBRL).

2

SIGNATURE

Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.

PASSAGE BIO, INC.

Date: October 24, 2024

By:

/s/ Kathleen Borthwick

Kathleen Borthwick

Chief Financial Officer

3

Ex 99.1

Passage Bio Presents Preclinical and Interim Clinical Data for PBFT02 in FTD-GRN at the European Society of Gene & Cell Therapy (ESGCT) 31st Annual Conference

Preclinical data demonstrated that an AAV1 vector achieved superior human progranulin levels in the CSF as compared to AAV5 and AAVhu68 (an AAV9 variant)

Nonclinical data showed PBFT02 improved lysosomal histopathology and reduced neuroinflammation in Grn knockout mice, and achieved widespread vector distribution throughout the nervous system in non-human primates

Company delivered data during an oral presentation on Thursday, October 24 at ESGCT

PHILADELPHIA, October 24, 2024 — Passage Bio, Inc. (Nasdaq: PASG), a clinical stage genetic medicines company focused on improving the lives of patients with neurodegenerative diseases, today announced the company delivered preclinical and interim clinical data as part of an oral presentation at the European Society of Gene & Cell Therapy (ESGCT) 31st Annual Congress being held October 22-25, 2024, in Rome, Italy.

Details of the oral presentation are below:

Abstract Title:

Non-clinical and early clinical development of PBFT02, an AAV gene therapy for frontotemporal dementia with GRN mutations (FTD-GRN)

Session:

7d: CNS gene therapy

Date & Time:

Thursday, October 24 from 9:00 a.m.-11:00 a.m. CEST (3:00 a.m.-5:00 a.m. ET)

Presenter:

Sue Browne, Ph.D., Chief Scientific Officer

Today's oral presentation at ESGCT outlined the robust preclinical data generated in the development of PBFT02, including studies that informed vector and dose selection and demonstrated the positive effects of elevating progranulin levels in vivo. Additionally, the presentation highlighted interim safety and biomarker data from the upliFT-D clinical trial, which validate the preclinical findings and position PBFT02 as a potential best-in-class progranulin-raising therapy.

“We are excited to share a detailed overview of the preclinical studies that support our PBFT02 program and informed our clinical development strategy,” said Will Chou, M.D., president and chief executive officer of Passage Bio. “These strong preclinical results gave us confidence in choosing the AAV1 vector and ICM administration as a differentiated approach to administer our gene therapy to patients in our ongoing upliFT-D clinical study. It’s also encouraging to see these preclinical findings translate into the clinic, with interim PBFT02 data demonstrating a well-tolerated safety profile and consistent, durable increases in CSF progranulin levels. We remain committed to advancing PBFT02 in FTD and look forward to exploring its therapeutic potential in additional neurodegenerative diseases that could benefit from elevated progranulin levels.”


Data Summary

Capsid comparison study in non-human primates (NHPs) showed the AAV1 vector achieved superior human PGRN levels in the CSF as compared to AAV5 and AAVhu68 (an AAV9 variant) following intra-cisterna magna (ICM) administration
Dose escalation study in Grn knockout mice showed PBFT02 improved lysosomal histopathology and reduced neuroinflammation throughout the brain following intra-CSF delivery, including evidence suggesting that higher levels of PGRN may provide additional benefits
NHP biodistribution study showed ICM administration of PBFT02 achieved high levels of gene distribution throughout the nervous system, including vector delivery to the cortical and sub-cortical brain regions affected in FTD, and to the spinal cord
PBFT02 was well tolerated in NHPs, and ICM administration resulted in dose-dependent PGRN elevations in NHP CSF
Interim safety and biomarker data from the upliFT-D clinical study demonstrated that Dose 1 of PBFT02 was generally well-tolerated after ICM administration and led to consistent, durable increases in levels of CSF progranulin in all treated Cohort 1 patients, with elevated CSF progranulin levels sustained up to 12 months post-administration

Additional details on the meeting can be found at the ESGCT 31st Annual Congress website, and a copy of the oral presentation deck will be available on the Investor Events and Presentations page of the Passage Bio corporate website.


About PBFT02

PBFT02 utilizes an AAV1 viral vector to deliver, through ICM administration, a functional GRN gene that encodes for PGRN. This vector construct and delivery approach aim to elevate PGRN levels in the central nervous system to alter the course of neurodegenerative diseases. Interim clinical data from the upliFT-D Phase 1/2 study in FTD-GRN participants shows that ICM administration of PBFT02 resulted in robust PGRN elevations in the CSF.

The potential clinical benefit of PBFT02 is supported by extensive preclinical studies. In non-human primates, a single ICM administration of PBFT02 led to broad vector distribution throughout the CNS, and robust, dose-dependent elevations in PGRN levels in CSF. An NHP study also demonstrated that AAV1 was particularly proficient at transducing ependymal cells. In a murine FTD model, PBFT02 administration improved lysosomal function and reduced neuroinflammation.

About Passage Bio

Passage Bio (Nasdaq: PASG) is a clinical stage genetic medicines company on a mission to improve the lives of patients with neurodegenerative diseases. Our primary focus is the development and advancement of cutting-edge, one-time therapies designed to target the underlying pathology of these conditions. Passage Bio’s lead product candidate, PBFT02, seeks to treat neurodegenerative conditions, including frontotemporal dementia, by elevating progranulin levels to restore lysosomal function and slow disease progression.

To learn more about Passage Bio and our steadfast commitment to protecting patients and families against loss in neurodegenerative conditions, please visit: www.passagebio.com.


Forward-Looking Statements

This press release contains “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 expectations about timing and execution of anticipated milestones, including the progress of clinical studies and the availability of clinical data from such trials; our expectations about our collaborators’ and partners’ ability to execute key initiatives; and the ability of our 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 and obtain regulatory approval for our product candidates; the timing and results of preclinical studies and 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; 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; failure to protect and enforce our intellectual property, and other proprietary rights; our dependence on collaborators and other third parties for the development and manufacture 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; and the other risks and uncertainties that are described in the Risk Factors section in documents the company files from time to time with the Securities and Exchange Commission (SEC), and other reports as filed with the SEC. Passage Bio undertakes no obligation to publicly update any forward-looking statement, whether written or oral, that may be made from time to time, whether as a result of new information, future developments or otherwise.

For further information, please contact:

Investors:

Stuart Henderson

Passage Bio

267.866.0114

shenderson@passagebio.com

Media:

Mike Beyer
Sam Brown Inc. Healthcare Communications
312.961.2502
MikeBeyer@sambrown.com  


Exhibit 99.2

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Non-clinical and early clinical development of PBFT02, an AAV gene therapy for FTD with GRN mutations (FTD-GRN) ESGCT OR070, 24 October 2024 SE Browne, YG Ni, KJ Quadrini, T Voss, MS Forman, J Chavez, N Miller, C Hinderer, JM Wilson

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2 Disclosures • Sue Browne, Ph.D, Yan Yi, Ph.D and Juan Chavez, MD, Ph.D are employees of Passage Bio, Inc. (the “Company”) and have certain equity interests in the Company • James Wilson, MD, Ph.D is a paid advisor to the Company and has certain equity interests in the Company. • James Wilson, MD, Ph.D and Christian Hinderer are inventors on patents that have been licensed to the Company and for which they may receive payments.

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3 FTD-GRN: A Devastating Adult Disease Frontotemporal Degeneration, FTD • Rapidly progressive, fatal, neurodegenerative disease affecting the frontal and temporal lobes of the brain • Common cause of early-onset dementia – Onset typically between ages of 40 and 65 years FTD-GRN • 5 to 10% of FTD is caused by mutations in the granulin (GRN) gene – Haploinsufficiency reduces brain progranulin to 30-50% of normal • Prevalence in EU + US is ~18,000 • No approved disease-modifying therapy

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4 Progranulin (PGRN) Deficiency is the Defining Characteristic of FTD-GRN, Leading to Neurodegeneration Progranulin is critical to maintaining CNS cell homeostasis Rhinn H et al. Trends Pharm Sci. 2022, 43:641-652. Our approach: AAV gene therapy to deliver functional PGRN to the brain

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5 PBFT02 Development Pathway • Transgene cassette design • Dose ranging in granulin-deficient mice • Vector selection in NHPs • Clinical lead biodistribution, safety, toxicology in NHPs • Ph 1/2 clinical study in FTD-GRN Discovery Pre-clinical Phase 1/2 Pivotal Filing/Comm IND Abbreviations: NHP, non-human primate

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6 hGRN Transgene Cassette Optimized Discovery & Lead ID • Codon-optimized sequence of the human GRN gene under the control of the ubiquitous CB7 promoter • Designed to deliver functional GRN genes encoding PGRN to brain and spinal cord • Ability to transduce multiple CNS cell types

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7 Proof of Concept: hGRN Transgene Delivery Improved Lysosomal Function in PGRN-Deficient Mice Veh 1 Veh 2 Dose 1 0 1 2 3 4 5 6 7 8 hPGRN (ng/mg) WT AAV.hGRN Grn -/- V *** hPGRN Expressed in Brain of Grn -/- mice V Veh 1 Veh 2 Dose 1 0 50 100 150 200 250 HEX Activity (nmol/mg/h) Reduced Brain Hexosaminidase Activity ### *** WT AAV.hGRN Grn -/- V Tissue collected 60 days post-ICV administration. N = 10/gp Abbreviations: CSF, cerebrospinal fluid; GRN/Grn, granulin gene; ICV, Intra-cerebroventricular; PBS, phosphate-buffered saline; V, Vehicle. Reference: Hinderer et al., Annals Clin Trans Neurology. 2020. ### p < 0.005 vs WT + V control; ***p < 0.005 vs GRN-/-+ V , one-way ANOVA + Tukey’s multiple comparisons test Efficacy in Grn knockout mice after tool AAVhu68.hGRN vector ICV administration to CSF Vehicle AAVhu68.hGRN Reduced Lipofuscin Fluorescence in Thalamus 2 mo (AAV9 variant) Grn-/-

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8 AAV1 Selected as Vector Serotype after a Capsid Comparison Study in NHPs Rhesus macaques (n=2/group) ICM-delivered AAV.hPGRN (3.3 x 1011 GC/g brain), day 0 Size and duration of elevation muted by immune response to human PGRN. Shading: Healthy adult human sample range, n = 61 (Passage Bio data) –Dose escalation in mice – Safety, tolerability, and biodistribution in NHPs BL 0 7 14 21 28 35 0 10 20 30 40 50 60 70 80 Human PGRN in NHP CSF Vector Comparison Days hPGRN (ng/mL) AAV1.CB7.hGRN AAV5.CB7.hGRN AAVhu68.CB7.hGRN AAVhu68.UbC.hGRN Healthy adult range • Superior hPGRN levels in CSF after AAV1 compared to AAV5 and AAVhu68 (AAV9 variant) ‒ Clinical delivery route, ICM • AAV1.hGRN selected as clinical candidate, PBFT02 PBFT02 taken into AAV1 IND-enabling studies Abbreviations: CSF, cerebrospinal fluid; ICM, intra-cisterna magna; hGRN, human granulin gene; NHP, non-human primate; PGRN, progranulin. Reference: Hinderer et al., Annals Clin Trans Neurology. 2020

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9 PBFT02 Dose Selection: Efficacy in Grn-/- Mice •Assayed four PBFT02 doses – Starting from 1/30 lower than dose used in prior mouse proof of concept (PoC) study Non-clinical Grn-/- mice Lipofuscinosis Lysosomal enzyme dysregulation 0 1 Microglial activation Normal lifespan Age / 7 months Focal neuronal loss Phenotype 5 Astrogliosis 2 3 4 6 8 9 10 11 12 23 Retinal degeneration Phagocytic microglia Dose-ranging in 7M old mice More progressed phenotype ICV AAV1 / PBFT02 Dose 1 Dose 2 (3x) Dose 3 (10x) PoC dose Dose 4 (30x) Abbreviations; GRN, granulin gene; ICV, Intra-cerebroventricular; M, month. Reference: Hinderer et al., Annals Clin Trans Neurology. 2020

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10 PBFT02 Improved Lysosomal Function in the Brain Lipofuscin deposition in brain was reduced by ICV PBFT02 • Partially reversed existing pathology • Also effective in cortical and sub-cortical regions after ICV administration Dose ranging in Grn-/- mice after intra-CSF delivery - - Veh Veh 1 2 3 4 -500 0 500 1000 1500 Lipofuscin Count WT Dose 1 Dose 2 Dose 3 Dose 4 Grn WT -/- V PBFT02 Baseline Grn -/- Day 90 V PBFT02 ### ### *** *** *** * Thalamus Lipofuscin ### p < 0.005 vs WT control; *p < 0.05, ***p < 0.005 vs Grn-/- + V , one-way ANOVA then Tukey’s multiple comparisons test. Abbreviations; Grn, granulin gene; ICV, Intra-cerebroventricular; V, vehicle; WT, wildtype Grn–/– and WT mice (n=14-15/gp) ICV-administered PBFT02 or vehicle (V). Baseline controls are untreated mice on Day 1. Bars: mean +/- SEM.

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11 Neuroinflammation Reduced in the Brain after PBFT02 - - Veh Veh 1 2 3 4 0 2000 4000 6000 8000 CD68 Area (μm2 ) WT Dose 1 Dose 2 Dose 3 Dose 4 Grn WT -/- V PBFT02 Baseline Grn -/- Day 90 V PBFT02 ## ### *** Thalamus CD68 Immunohistochemistry *** * Dose ranging in Grn-/- mice after intra-CSF delivery • From combined mouse data, Dose 1 established as minimum effective dose • Dose 2, 3 and 4 equivalents taken forward into NHP studies Activated microglia reduced in both cortical and sub-cortical brain regions after ICV PBFT02 ## p < 0.01; ### p < 0.005 vs WT; *p < 0.05, ***p < 0.005 vs Grn–/– + V , one-way ANOVA then Tukey’s multiple comparisons test. Abbreviations; GRN, granulin gene; ICV, Intra-cerebroventricular; V, vehicle; WT, wildtype Grn–/– and WT mice (n=14-15/gp) ICV-administered PBFT02 or vehicle (V). Baseline controls are untreated mice on Day 1. Bars: mean +/- SEM.

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12 Intra-Cisterna Magna (ICM) Administration of PBFT02 Enables PGRN Delivery Throughout CNS Cisterna magna Abbreviations: CNS, central nervous system; CSF, cerebrospinal fluid; CT, computed tomography; h, hour; ICM, intra-cisterna magna; IV, intra-venous; PNS, peripheral nervous system; PGRN, progranulin. Reference: 1Hinderer et al, Human Gene Therapy. 2018, 29:15-24 •Directly delivers vector into the CSF via a single infusion, to reach CNS, PNS, and peripheral tissues1 – Allows for broad CNS biodistribution – Lower doses compared to IV systemic delivery – Reduced impact of neutralizing antibodies • Brief, < 1 h, non-surgical, CT-guided procedure – Infusion catheter does not enter brain tissue • Expressed PGRN directly impacts transduced cells • Secreted PGRN cross-corrects proximal cells

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13 ICM Administration to NHPs Achieved High Levels of Gene Distribution Throughout the Nervous System • Robust vector delivery to cortical and sub-cortical brain regions affected in FTD •NHP PBFT02 dose 1 (equivalent to upliFT-D clinical Dose 1) resulted in ~10e4 GC/ug DNA throughout the brain Abbreviations: CBL, cerebellum; Cerv, cervical; DRG, dorsal root ganglion; FCX, frontal cortex; GC, genome copies; Hipp, hippocampus; ICM, intra-cisterna magna; LLoQ, lower limit of quantitation; Lumb, lumbar; NHP, non-human primate; OCX, occipital cortex; PCX, parietal cortex; TCX, temporal cortex; TRG, trigeminal root ganglio; Thor, thoracic; Veh, vehicle Vector Biodistribution 90 days post-PBFT02 to NHPs LLoQ Brain Spinal Cord DRG, TRG PBFT02, n=3/group; Veh, n=2/group. Data are mean +/- SEM.

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14 PBFT02 Dose-Dependently Increased PGRN in NHP CSF 0 30 60 90 0 5 10 15 Human PGRN in CSF Days hPGRN (ng/mL) Veh Dose 1 Dose 2 Dose 3 7 14 28 • Human PGRN was detected in NHP CSF shortly after ICM PBFT02 administration • Dose-dependent increases in PGRN seen up to day 14 • Thereafter, an immune response to the human protein in NHPs attenuated PGRN levels ‒ Not relevant when dosing FTD-GRN haploinsufficient individuals 0 30 60 90 0 300 600 900 1200 Anti-Human PGRN Antibody Response Days Anti-Human PGRN (AU) Veh Dose 1 Dose 2 Dose 3 7 14 28 PBT02, n=3/group; Veh, n=2. Data: mean +/- SEM. Dashed line is mean healthy adult human PGRN (n=61) Abbreviations: AU, arbitrary units; CSF, cerebrospinal fluid; ICM, intra-cisterna magna; NHP, non-human primate; PGRN, progranulin; SEM, standard error of mean; Veh, vehicle

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15 Assessments Observations in NHPs Abnormal clinical, neurological, or behavioral signs None Blood and CSF clinical pathology Mild and transient increases in CSF leukocytes only DRG, TRG, sensory nerve histopathology Typically minimal to mild • Consistent with NHP AAV responses • No clinical correlates observed NOAEL Not reached Abbreviations: CSF, cerebrospinal fluid; DRG, dorsal root ganglion; ICM, intra-cisterna magna; NOAEL, no observed adverse effect level; TRG, trigeminal root ganglion Dose 1 equivalent taken forward into a Ph1/2 clinical study, upliFT-D PBFT02 was Well Tolerated in NHPs Followed for 90 days after a single ICM delivery of one of 3 doses

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16 upliFT-D: Global Phase 1/2 Trial with PBFT02 Dose 1: 3.3e10 GC/g estimated brain weight. IDMC review COHORT 1 Dose 1 COHORT 2 OPTIONAL COHORT 3 Dosing Complete Enrolling •Phase 1/2 multi-center, open label dose-escalation study •Primary endpoints: Safety and tolerability Progress •FTD-GRN Cohort 1 (n = 5) dosing complete •Longest followed 12 months Safety Observations •All four Cohort 1 participants who received a revised immunosuppression regimen* had no SAEs or significant immune responses •No patients showed evidence of DRG toxicity, as measured by nerve conduction studies •No complications of ICM administration *Revised steroid regimen: 1 g methylprednisolone IV daily to day 3, then 60 mg oral prednisone to day 60; Participant 1 received 60 mg oral prednisone to day 60 and had 2 SAEs. Safety cut-off: 08/20/2024 Dose 1 Find more information on the upliFT-D trial here Abbreviations: DRG, dorsal root ganglion ICM, intra-cisterna magna; SAE, severe adverse event

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17 0 3 6 9 12 15 18 21 24 27 30 33 36 0 30 60 180 360 CSF PGRN, ng/mL Time (days) CSF Progranulin Dose 1 Patient 1 Patient 2 Patient 3 Patient 4 Patient 5 Healthy adult range Cohort 1 Interim Data: PBFT02 Administration Leads to Robust and Sustained Increases in CSF PGRN Shading: Healthy adult human sample range of PGRN levels in CSF, n=61 (Passage Bio data) Abreviations: CSF, Cerebrospinal fluid; M, month; PGRN, progranulin • Continued elevation of CSF PGRN at 6 M (n=2) and 12 M (n=1) ‒Rate of increase slowing over time • Consistent response across all five treated patients • Plasma PGRN remained below healthy adult control levels • Potential for best-in-class profile

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18 PBFT02 Preclinical and Clinical Development Summary Strong preclinical profile of PBFT02, a gene therapy to elevate PGRN in FTD-GRN •PBFT02 improved lysosomal histopathology and neuroinflammation in Grn-/- mice •Broad transduction across the brain and spinal cord in NHPs after ICM administration into the CSF •Well-tolerated in NHPs with no clinical adverse effects PBFT02 shows clinical potential as a one-time, CSF-delivered gene therapy approach •Consistent, durable elevation of CSF PGRN at 6-months and 12-months •Dose 1 well-tolerated among all Cohort 1 patients who received the revised steroid regimen* •Continuing to assess Dose 1 in Cohort 2, given the robust effects on PGRN expression *Revised steroid regimen: 1 g methylprednisolone IV daily up to day 3, followed by 60 mg oral prednisone to day 60. Safety cut-off: 08/20/2024 Abbreviations: CSF, cerebrospinal fluid; GRN/Grn, granulin gene; ICM, intra-cisterna magna; NHP, non-human primate; PGRN, progranulin

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We would like to thank the patients, families, caregivers, investigators, and our collaborators at Penn’s GTP

v3.24.3
Document and Entity Information
Oct. 24, 2024
Document and Entity Information [Abstract]  
Document Type 8-K
Document Period End Date Oct. 24, 2024
Entity File Number 001-39231
Entity Registrant Name PASSAGE BIO, INC.
Entity Incorporation, State or Country Code DE
Entity Tax Identification Number 82-2729751
Entity Address, Address Line One One Commerce Square
Entity Address, Adress Line Two 2005 Market Street, 39th Floor
Entity Address, City or Town Philadelphia
Entity Address, State or Province PA
Entity Address, Postal Zip Code 19103
City Area Code 267
Local Phone Number 866-0311
Written Communications false
Soliciting Material false
Pre-commencement Tender Offer false
Pre-commencement Issuer Tender Offer false
Title of 12(b) Security Common Stock, $0.0001 Par Value Per Share
Trading Symbol PASG
Security Exchange Name NASDAQ
Entity Emerging Growth Company true
Entity Ex Transition Period false
Entity Central Index Key 0001787297
Amendment Flag false

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