Form 8-K

8-K — Passage BIO, Inc.

Accession: 0001104659-26-045219

Filed: 2026-04-20

Period: 2026-04-20

CIK: 0001787297

SIC: 2836 (BIOLOGICAL PRODUCTS (NO DIAGNOSTIC SUBSTANCES))

Item: Regulation FD Disclosure

Item: Financial Statements and Exhibits

Documents

8-K — tm2612152d1_8k.htm (Primary)

EX-99.1 — EXHIBIT 99.1 (tm2612152d1_ex99-1.htm)

EX-99.2 — EXHIBIT 99.2 (tm2612152d1_ex99-2.htm)

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2026-04-20

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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):

April 20, 2026

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 Capital 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 ¨

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

PBFT02 Program Updates

On April 20, 2026, Passage Bio, Inc.

(the “Company”) announced updated interim data from the ongoing Phase 1/2 upliFT-D clinical trial evaluating

PBFT02 for the treatment of frontotemporal dementia caused by progranulin deficiency (“FTD-GRN”) and

provided regulatory and corporate updates.

Updated interim data from FTD-GRN patients

treated with PBFT02

Biomarkers

· PBFT02-treated patients with a global Clinical Dementia Rating (“CDR”)

score of 1 at baseline experienced an average of 3.1% (n=2) whole brain atrophy at 12 months, representing a 64% reduction in whole brain

atrophy as compared to volumetric Magnetic Resonance Imaging (“vMRI”) analysis of global CDR 1 patients from

the ALLFTD natural history data (n=7).

· PBFT02-treated patients with a global CDR score of 1 at baseline experienced

an average of 4.6% (n=2) frontotemporal cortex atrophy at 12 months, representing a 54% reduction in frontotemporal cortex atrophy as

compared to vMRI analysis of global CDR 1 patients from the ALLFTD natural history data (n=7).

· Patients who received PBFT02 showed stabilization of plasma neurofilament

(“NfL”) levels at 12 months post-treatment, comparing favorably to natural history.

· Plasma NfL levels among PBFT02-treated patients showed an average reduction

of 1.0 pg/mL (n=6) at 12 months compared to baseline.

· Untreated symptomatic FTD-GRN patients from the ALLFTD natural history

data showed an average increase of 13.5 pg/mL (n=7) at 12 months compared to baseline.

· Dose 1 PBFT02 (4.5e13 total genome copies) resulted in a robust and durable

increase in cerebrospinal fluid (“CSF”) progranulin (“PGRN”) expression through 18

months post-treatment.

· Dose 1 PBFT02 increased CSF PGRN in all patients from below 3 ng/mL at baseline

to a mean of 22.8 ng/mL (n=6) at 12 months and 24.2 ng/mL (n=3) at 18 months.

· Dose 2 PBFT02 (2.2e13 total genome copies) achieved comparable CSF PGRN levels

as Dose 1 at six months post-treatment.

· Dose 2 PBFT02 increased CSF PGRN to a mean of 8.6 ng/mL (n=2) at one month,

above the upper limit of a healthy adult reference range, and 22.6 ng/mL (n=1) at six months.

Safety (as of March 23, 2026)

· No new treatment-related serious adverse events (“SAEs”)

reported since the Company’s previous update.

· As previously disclosed, two patients who received Dose 1 PBFT02 experienced

a total of three asymptomatic SAEs related to PBFT02: venous sinus thrombosis (n=2) and hepatotoxicity (n=1).

· No evidence of dorsal root ganglion toxicity, as measured by nerve conduction

studies, and no complications from intra-cisterna magna administration have been reported.

Regulatory Update

The Company has completed a Type C meeting with the U.S. Food and Drug

Administration (“FDA”) to seek guidance on key elements of a potential future registrational trial of PBFT02

for FTD-GRN patients. Based on the feedback received, the FDA has indicated that a randomized controlled registrational study design

is required for PBFT02 in this indication. In light of the ethical, logistical, and financial challenges posed by a randomized controlled

registrational trial, the Company is evaluating potential next steps in the clinical development of PBFT02 in FTD-GRN and FTD-C9orf72

in the upliFT-D trial.

Corporate Update

The Company has initiated a review of strategic alternatives to maximize

shareholder value. These strategic alternatives may include merger or acquisition transactions, a reverse merger, a sale of assets of

the Company, strategic partnerships, licensing opportunities, or other potential paths. The strategic review is underway, and the Company

does not intend to provide updates until the Company’s board of directors approves a specific action or otherwise determines that

disclosure is appropriate or required. There can be no assurance that the process will result in any such transaction.

The Company has engaged Wedbush PacGrow as a financial advisor to assist

in the strategic review process.

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 Securities

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 April 20, 2026.

99.2

Corporate Presentation,

dated April 20, 2026.

104

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

Forward-Looking Statements

This Current Report on Form 8-K 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 evaluation of strategic

alternatives, the entry into or completion of any strategic alternative transaction, our expectations about timing and execution of anticipated

milestones, including the progress of clinical studies and the availability of clinical data from such trials; enrollment timing; timing

of engagement with, and feedback from, regulatory authorities; our expectations about our collaborators’ and partners’ ability

to execute key initiatives; our expectations about our cash runway; the ability of our product candidates to treat their respective target

CNS disorders; and the potential development of other product candidates. These forward-looking statements may be accompanied by such

words as “aim,” “anticipate,” “believe,” “continue,” “could,” “should,”

“target,” “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: uncertainties inherent in the strategic review process, our ability to

identify and consummate a suitable strategic alternative, 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.

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: April 20, 2026

By:

/s/ Kathleen Borthwick

Kathleen Borthwick

Chief Financial Officer

EX-99.1 — EXHIBIT 99.1

EX-99.1

Filename: tm2612152d1_ex99-1.htm · Sequence: 2

Exhibit 99.1

PASSAGE BIO REPORTS UPDATED INTERIM DATA FROM

UPLIFT-D TRIAL AND PROVIDES REGULATORY AND CORPORATE UPDATES

PBFT02 administration resulted in improvements

in two disease progression biomarkers, as compared to natural history, reducing brain atrophy and stabilizing plasma NfL levels

FDA feedback from recent Type C meeting indicated

a randomized controlled registrational trial will be required for PBFT02 in FTD-GRN

The Company initiated a strategic review process

intended to maximize shareholder value

PHILADELPHIA – April 20, 2026 – Passage Bio, Inc.

(NASDAQ: PASG), a clinical stage genetic medicines company focused on improving the lives of patients with neurodegenerative diseases,

today reported updated data from the ongoing Phase 1/2 upliFT-D clinical trial evaluating PBFT02 for the treatment of frontotemporal dementia

(FTD) with granulin (GRN) mutations. In addition, the Company shared feedback from a recent Type C meeting with the United States Food

and Drug Administration (FDA) on the likely registrational pathway for PBFT02 in FTD-GRN. The Company has also announced it has

engaged Wedbush PacGrow as a financial advisor and has initiated a review of strategic alternatives to maximize shareholder

value.

Will Chou, M.D., president and chief executive officer of Passage Bio

commented, “the data shared today suggest that PBFT02 may slow neurodegeneration in patients with FTD-GRN, with improvements

observed in both brain atrophy and plasma neurofilament levels, two well-established biomarkers of disease progression. Further, we continue

to observe durable and robust elevations in progranulin, the target protein, and are encouraged by the emerging data from Dose 2 patients,

which indicate that this lower dose level can achieve similar progranulin expression as observed with Dose 1, our higher dose.”

Dr. Chou continued, “As we look towards late-stage

development of the program, we recently completed a Type C meeting with the FDA to gain feedback on the design of a future

registrational trial for PBFT02 in FTD-GRN. Despite the rare, underserved nature of this devastating disease and the

availability of robust natural history data, FDA did not support a single-arm trial design for this indication and instead indicated

that a randomized controlled trial would be required for registrational purposes. In light of this outcome and the associated

ethical, logistical, and financial challenges, we are currently evaluating potential next steps for the PBFT02 clinical development

program and for the company.”

Updated interim upliFT-D data from FTD-GRN patients treated

with PBFT02:

Brain Atrophy as Measured by Volumetric Magnetic Resonance Imaging

(vMRI)

Patients earlier in their disease progression (global score of 1 at

baseline on the Clinical Dementia Rating scale, or CDR) who received PBFT02 exhibited reduced rates of whole brain atrophy and frontotemporal

cortex atrophy compared to natural history data from patients at the same stage of disease progression. In contrast, patients with more

advanced disease progression (global CDR score of 2 at baseline) showed no improvements on either atrophy measure versus natural history

data from a comparable global CDR 2 population. Patients with global CDR scores of 0.5 and 1 at baseline are the intended target population

for PBFT02, and patients with global CDR scores of 2 or greater have been excluded from future enrollment in the ongoing upliFT-D study.

Whole Brain Atrophy

· PBFT02-treated patients with a global CDR score of 1 at baseline experienced

a 64% reduction in whole brain atrophy at 12 months, on average, as compared to vMRI analysis of untreated global CDR 1 patients from

the ALLFTD natural history data.

o PBFT02-treated global CDR 1 patients (n=2): 3.1% atrophy at 12 months

o ALLFTD natural history global CDR 1 sample (n=7): 8.7% atrophy at 12 months

Frontotemporal Cortex Atrophy

· PBFT02-treated patients with a global CDR score of 1 at baseline experienced

a 54% reduction in frontotemporal cortex atrophy at 12 months, on average, as compared to vMRI analysis of untreated global CDR 1 patients

from the ALLFTD natural history data.

o PBFT02-treated global CDR 1 patients (n=2): 4.6% atrophy at 12 months

o ALLFTD natural history global CDR 1 sample (n=7): 9.9% atrophy at 12 months

Plasma Neurofilament (NfL)

Patients who received PBFT02 showed stabilization of plasma NfL levels

at 12 months post-treatment, comparing favorably to natural history.

· Plasma NfL levels among PBFT02 treated patients showed an average reduction

of 1.0 pg/mL (n=6) at 12 months compared to baseline.

· In contrast, analysis of untreated symptomatic FTD-GRN patients from

the ALLFTD natural history data showed an average increase of 13.5 pg/mL (n=7) at 12 months compared to baseline.

Cerebrospinal Fluid (CSF) Progranulin (PGRN)

· Dose 1 PBFT02 (4.5e13 total genome copies) resulted in a robust and durable

increase in CSF PGRN expression through 18 months post-treatment.

· Dose 1 PBFT02 increased CSF PGRN in all patients from below 3 ng/mL at baseline

to a mean of 22.8 ng/mL (n=6) at 12 months and 24.2 ng/mL (n=3) at 18 months.

· Dose 2 PBFT02 (2.2e13 total genome copies) achieved comparable CSF PGRN levels

as Dose 1 at six months post-treatment.

· Dose 2 PBFT02 increased CSF PGRN to a mean of 8.6 ng/mL (n=2) at one month,

above the upper limit of a healthy adult reference range, and 22.6 ng/mL (n=1) at 6 months.

Safety (as of March 23, 2026; n=10 FTD-GRN patients

and n=1 FTD-C9orf72 patient)

· PBFT02 continued to be generally well-tolerated, with no new treatment-related

serious adverse events (SAEs) reported.

o As previously disclosed, two patients who received Dose 1 PBFT02 experienced a total of three asymptomatic SAEs related to PBFT02:

venous sinus thrombosis (n=2) and hepatotoxicity (n=1).

· No evidence of dorsal root ganglion (DRG) toxicity and no complications from

intracisterna magna (ICM) administration have been reported.

A presentation summarizing the interim data update can be accessed

on the Events and Presentations page of the Investors and News section of the Company’s website.

Regulatory & Program Update

The Company has completed a Type C meeting with the FDA to seek guidance

on key elements of a future registrational trial of PBFT02 for FTD-GRN patients. Based on the feedback received, the FDA

has indicated that a randomized controlled registrational study design is required for PBFT02 in this indication. A randomized controlled

registrational trial poses substantial ethical concerns for patients and their families as well as logistical and financial challenges.

As such, the Company is evaluating potential next steps in the clinical development of PBFT02 in FTD-GRN and FTD-C9orf72

in the upliFT-D trial.

Corporate Update

The Company has initiated a review of strategic alternatives to maximize

shareholder value. These strategic alternatives may include merger or acquisition transactions, a reverse merger, a sale of assets of

the Company, strategic partnerships, licensing opportunities, or other potential paths.

The strategic review is underway, and the Company does not intend to

provide updates until the Board approves a specific action or otherwise determines that disclosure is appropriate or required. There can

be no assurance that the process will result in any such transaction.

The Company has engaged Wedbush PacGrow as a financial advisor to assist

in the strategic review process.

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: 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 evaluation of strategic alternatives, the entry into or completion of any strategic alternative transaction, our

expectations about timing and execution of anticipated milestones, including the progress of clinical studies and the availability of

clinical data from such trials; enrollment timing; timing of engagement with, and feedback from, regulatory authorities; our expectations

about our collaborators’ and partners’ ability to execute key initiatives; our expectations about cash runway; the ability

of our product candidates to treat their respective target CNS disorders; and the potential development of other product candidates. These

forward-looking statements may be accompanied by such words as “aim,” “anticipate,” “believe,” “continue,”

“could,” “should,” “target,” “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: uncertainties inherent in strategic

review processes, such as the risk that no suitable strategic alternative will be identified or consummated; 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

shenderson@passagebio.com

Passage Bio Media:

Mike Beyer

Sam Brown Inc. Healthcare Communications

312.961.2502

mikebeyer@sambrown.com

EX-99.2 — EXHIBIT 99.2

EX-99.2

Filename: tm2612152d1_ex99-2.htm · Sequence: 3

Exhibit 99.2

Corporate Presentation

Redefining the Course

of Neurodegenerative

Conditions

April 2026

Forward-Looking Statement

This 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 expectations about timing and execution of anticipated milestones,

including the progress of clinical studies and the availability of clinical data from such trials; enrollment timing; timing of engagement with

regulatory authorities; the potential of our product candidates versus other treatment options and clinical candidates; our expectations about

cash runway; the ability of PBFT02 to treat FTD-GRN or FTD-C9orf72, and the potential development of other product candidates. 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, the timing of and our ability to obtain and maintain regulatory approvals; our expectations about the willingness of

healthcare professionals to use our product candidates, the timing, or amount, 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; the timing, or amount, of receipt of any potential future milestone and royalty payments; 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.

2 April 2026

3 April 2026

Redefining the Course of Neurodegenerative Conditions

* Based on cash, cash equivalents, and marketable securities as of December 31, 2025.

Advancing clinical stage,

potential best-in-class, one-time progranulin raising gene

therapy for FTD

Pursuing preclinical

development of differentiated

gene therapy approach in

Huntington’s disease

Cash runway expected

through 1Q 2027*

Validating the Therapeutic Potential of PBFT02

4 April 2026

* Based on interim data.

Urgent Patient Need

in FTD-GRN

Differentiated, Potential

Best-in-Class Profile

Fast Track and

Orphan Drug Designation

Promising data from initial clinical

study of PBFT02 in FTD-GRN

Genetic form of FTD

caused by GRN mutations,

which lead to progranulin

(PGRN) deficiency

No approved

disease-modifying

therapies

One-time, gene

replacement therapy

Proprietary

AAV1 construct

Nonsurgical injection

directly to cerebrospinal

fluid (CSF)

Durable, elevated CSF

PGRN levels*

Significant Market Opportunity Addressing Neurodegenerative Diseases

Estimated Prevalence (US and EU)

5 April 2026

Huntington’s disease5

FTD-C9orf722–4

FTD-GRN1–3 ~18K

~21K

~70K

1. Greaves CV, et al. J Neurol 2019; 266:2075-2086. 2. Galvin JE, et al. Neurology 2017; 89:2049-2056. 3. Onyike CU, et al. Int Rev Psychiatry 2013; 25:130-137.

4. Moore KM, et al. Lancet Neurol 2020; 19: 145–156. 5. Crowell et al. Neuroepi. 2021; 55:361-368.

CURRENT

PRECLINICAL

PROGRAM

CURRENT

CLINICAL

PROGRAM

CURRENT

CLINICAL

PROGRAM

PBFT02

Frontotemporal

Dementia

OVERVIEW

• Fatal adult-onset neurodegenerative disease affecting the frontal and

temporal lobes of the brain, characterized by a decline in behavior,

language, and executive function

• One of the most common causes of early-onset dementia worldwide,

disproportionately affecting individuals aged 40–65 years

CLINICAL SYMPTOMS

Disease progression is rapid and degenerative, including loss of speech,

loss of expression, behavioral changes, and immobility

Frontotemporal Dementia (FTD):

A Devastating Adult Disease

On average,

people with

FTD live 8 years

after the onset

of symptoms

7 April 2026

Loss of

inhibition

Apathy Social

withdrawal

Hyperorality

(mouthing of objects)

Ritualistic compulsive

behaviors

Progranulin Deficiency is the Defining Characteristic of FTD-GRN and

Leads to Neurodegeneration

8 April 2026

Progranulin is critical to maintaining CNS cell homeostasis

Rhinn H et al. Trends Pharmacol Sci. 2022, 43:641-652.

Decrease in

PGRN levels

Neuronal dysfunction,

pathological changes, and inflammation

Vulnerability of

neurons in

affected regions

Neurodegeneration

Elevated PGRN Increases Potential for Improved Cellular Function

9 April 2026

Paushter et al. Acta Neuropathol. 2018;136:1-17. Rhinn et al. Trends Pharmacol Sci. 2022; 43:641-652.

Driving elevated PGRN levels in the extracellular

space increases the amount of PGRN available to

enter target CNS cells

Able to leverage cross-correction mechanism:

secreted PGRN can be taken up by non-transduced

cells

Progranulin is a secreted protein that binds to cell

membrane receptors to affect multiple intracellular

pathways

• Major role is regulating intracellular lysosomal activity

• Extracellular PGRN is endocytosed via multiple receptors

TRIAL DESIGN

upliFT-D: Global Phase 1/2 Trial with PBFT02

Currently enrolling patients in Cohort 3 and Cohort 4

10 April 2026

DURATION 2 years; with additional 3 years of follow-up for safety and durability of effect

PRIMARY

ENDPOINTS Safety and tolerability

SECONDARY

ENDPOINTS

Biomarkers

• Progranulin (CSF, plasma)

• vMRI

• NfL (CSF, plasma)

Clinical

• CDR + NACC FTLD sum of boxes

EXPLORATORY

BIOMARKERS

• Cathepsin D (CSF)

• GFAP (CSF, plasma)

• LAMP 1 (CSF)

• Lys-GL1 (CSF)

Multicenter Open-label Dose exploration

study

Phase

1/2

Complete IDMC review Dose 1: 4.5e13 GC

Dose 2: 2.2e13 GC

COHORT 1

(n=5)

Dose 1

COHORT 2

(n=4)

Dose 1 / Dose 2

COHORT 3

(n=5-10)

FTD

Dose 2

-GRN

COHORT 4

(n=3-5)

Dose 2

COHORT 5

(n=3-5)

FTD-C9orf72

Cisterna

magna

Intra-Cisterna Magna (ICM) Administration

11 April 2026

Directly deliver vector into the CSF via a single injection

• Allows for broad CNS biodistribution1

• Lower doses compared to IV systemic delivery

• Reduced impact of neutralizing antibodies

Brief (<60 min), non-surgical, CT-guided procedure for

precise delivery to the cisterna magna

Procedure avoids penetration of brain tissue

1. Hinderer et. al, Hum Gene Ther. 2018; 29:15-24.

Key Baseline Demographics for FTD-GRN Participants*

Dose 1 (n=7); Dose 2 (n=2)

12 April 2026

(n=9) PBFT02

Dose 1 Dose 2

Age, years, mean (range) 63.3 (51–71) 69.0 (66-72)

Sex, n (%) Male 4 (57%) 0

Female 3 (43%) 2 (100%)

FTD-GRN phenotype, n bvFTD 5 1

PPA 2 1

Disease duration at baseline, years, mean (range) 2.9 (1–5) 2.0 (1-3)

PGRN, CSF, ng/mL, mean (range) 2.2 (1.5–2.9) 1.8 (1.5 – 2.0)

PGRN, plasma, ng/mL, mean (range) 38.5 (22.4–89.0) 36.2 (23.6 – 48.7)

NfL, plasma, pg/mL, mean (range) 43.4 (12.4–105.0) 90.4 (69.8-111)

Clinical Dementia Rating Scale1

, Global

(%)

1 57% 50%

2 43% 50%

Clinical Dementia Rating Scale, Sum of Boxes, mean (range) 9.6 (5–17) 10.5 (6 – 15)

*Data as of January 26, 2026.

1. CDR® +NACC FTLD. Dose 1: 4.5e13 GC. Dose 2: 2.2e13 GC

bvFTD, behavioral variant; PPA, primary progressive aphasia.

Healthy adult range

0 3 6 9 12 15 18

CSF PGRN, ng/mL

Time, Month

Dose 1 Dose 2

PBFT02, at Both Dose Levels, Generated Robust Increases in CSF PGRN

in FTD-GRN Patients

13 April 2026

Dose 1

• Continued durability to 18 months

Dose 2

• First 2 patients with consistent Day 30

levels at high end of normal range

• First M6 data: Dose 2 generating a

robust PGRN response

• Potential for similar target

engagement as Dose 1 with half the

dose/capsid load

Data as of February 9, 2026. Mean +/- SEM

Shading: Healthy adult sample range for CSF PGRN (range: 3.28 – 8.15 ng/mL, mean: 4.76 ng/mL, n = 61) (Passage Bio data)

Dose 1: 4.5e13 GC; Dose 2: 2.2e13 GC

CSF, cerebrospinal fluid; M, month.

Progranulin, CSF

Dose 1 N: 7 6 6 6 3

Dose 2 N: 2 2 1

Brain Atrophy (as measured with vMRI) is Associated with Clinical

Deterioration in FTD-GRN Natural History

vMRI assesses volume of brain tissue across various

regions of interest (e.g. frontal and temporal lobes)

• Volume loss (atrophy) is considered to represent synaptic and

cell loss in the region of interest and is a common outcome

measure employed in neurodegenerative diseases

• In FTD-GRN, brain atrophy begins prior to symptom onset and

is most rapid after early symptom onset before slowing with

disease progression1

• In a sample of 218 GRN+ individuals (asymptomatic and FTD-GRN), atrophy was strongly associated with clinical

progression1

• Although longitudinal data are limited, FTD-GRN carries the

most aggressive atrophy rate across genetic FTD subtypes2,3

1. Staffaroni 2022. 2. Gordon et al. J. Neuroimage Clin. 2021. 3. Whitwell 2015.

vMRI, volumetric MRI

April 2026

Our Approach:

• Analyze PBFT02-treated patients vs.

ALLFTD natural history data to determine

rates of whole brain and frontotemporal

cortex atrophy at 12-months

• Segment analysis by CDR global score at

baseline (i.e., CDR global 1 only)

• Passage is only known analysis to report NH

brain atrophy rate by CDR score

• No statistical modelling applied to data

given small sample size

Early Biomarker Signal that PBFT02 Slowed Disease Progression in

Target Population

Longitudinal changes in whole brain volume1 and frontotemporal cortex volume2 have been shown to correlate with clinical changes in FTD

-9.9%

-4.6%

-14%

-12%

-10%

-8%

-6%

-4%

-2%

-8.7%

-3.1%

-12%

-10%

-8%

-6%

-4%

-2%

Data as of January 26, 2026.

Note: Volume is the difference between BL and 12month data, as a percentage of the baseline volume.

1. Knopman et al., 2009; Gordon et al., 2010 2. Staffaroni 2019; 3. ALLFTD: CDR 1 patients at baseline

Whole Brain Atrophy

Volumetric MRI 12 month change from baseline

CDR 1

Natural Hx3

(n=7)

CDR 1

PBFT02

(n=2)

Frontotemporal Cortex Atrophy

Volumetric MRI 12 month change from baseline

64%

reduction of

atrophy

54% reduction

of atrophy

April 2026

• PBFT02 global CDR 2 patients at baseline lost 9% of volume at Month 12, with no

improvement vs. CDR 2 natural history

• PBFT02 global CDR 2 patients at baseline lost 10% of volume at Month 12, with

no improvement vs. CDR 2 natural history

CDR 1

Natural Hx3

(n=7)

CDR 1

PBFT02

(n=2)

Plasma NfL Showed Early Evidence of Improvement in a Disease

Progression Biomarker vs. Natural History

• Plasma NfL remains stable in treated

patients at Month 12

• Absolute pNfL change from baseline is

the metric to be analyzed in

registrational study

Natural History

Natural history data supported by the ALLFTD Consortium (funded by NIA and NINDS)

Plasma NfL Change from Baseline at 12M

(Dose 1)

Data as of January 26, 2026. Mean +/- SEM

PBFT02 patients (n=6, Dose 1): Mean, SD for Baseline plasma NfL (neurofilament

light chain) 48.6 ± 27.0 pg/mL. Mean time since diagnosis 2.7 years.

1. Passage Bio analysis of ALLFTD natural history sample comprised of individuals

with a pathogenic GRN mutation and a CDR+NACC FTLD global score between

0.5 and 2, inclusive. Mean, SD for Baseline plasma NfL 57.8 + 20.2 pg/mL.

-10

-5

Plasma NfL CFB, pg/mL

ALLFTD (n=7)

PBFT02 (n=6)

+13.5 pg/mL

-1.0 pg/mL

April 2026

PBFT02 Interim Safety Profile

PBFT02 was generally well tolerated

• SAEs related to PBFT02 all asymptomatic; all occurred at Dose 1

• Venous sinus thrombosis (2)

• LFT increase (1)

• No evidence of thrombotic microangiopathy

• No evidence of dorsal root ganglion (DRG) toxicity

• No complications from ICM procedure

PBFT02 immune response profile

• As expected, T-cell responses against AAV1 were observed in majority of

participants by Day 30

• No association with any clinical findings

• No responses against hPGRN

• Anti-AAV1 antibodies observed in both serum and CSF by Day 30; stable out to

18 months

• 1 participant experienced transient low-titer anti-hPGRN antibodies in serum

only that had resolved at last testing

Data as of March 23, 2026 (n=10 FTD-GRN and n=1 FTD-C9orf72 patients)

SAE, serious adverse event; LFT, liver function test; ICM, intracisterna magna; TEAE, treatment emergent adverse event.

April 2026

N Events

TEAE considered

related to PBFT02 8 32

Serious TEAE unrelated

to PBFT02 1 3

Serious TEAE related

to PBFT02 2 3

PBFT02 Offers Best-in-Class Therapeutic Potential

PBFT02

Product Candidate AAV1 gene therapy delivering GRN AAV9 gene therapy delivering GRN PGRN replacement therapy via

protein transport vehicle

Stage of Development Phase 1/2 Phase 1/2 Phase 1/2

Route of Administration ICM

(non-surgical, 1 hour procedure)

Intrathalamic

(neurosurgery, lengthy procedure) IV

Frequency of

Administration One-time One-time Chronic dosing

(~every 4 weeks)1

CSF PGRN Level at 12m 22.8 ng/mL

(mean; n=6) – –

Durability of CSF PGRN

Elevation1

Durable at 18 m

(n=3) – –

PBFT02 uniquely positioned to offer a one-time therapy capable of achieving highest progranulin levels

18 April 2026

Data for PBFT02 as of January 26, 2026. Information for competitor programs based on publicly available information.

1 https://memory.ucsf.edu/research-trials/dnl593#:~:text=What%20to%20Expect,garages%20for%20all%20study%20visits (accessed on Feb 12, 2026).

PBFT02 has Potential to Correct Underlying Pathology in FTD-GRN, FTD-C9orf72 and ALS

19 April 2026

TDP-43 pathology is a hallmark of multiple

neurodegenerative diseases1

• TDP-43 mislocalizes from nucleus to cytoplasm

• Forms inclusion bodies associated with

neurodegeneration

1. Rhinn H et al. Trends Pharmacol Sci. 2022; 43:641-652

Elevated PGRN Ameliorates TDP-43 Pathology in Preclinical Models

20 April 2026

TDP-43 pathology due to lysosomal dysfunction (GRN/

TMEM106 double knockout, DKO) reduced by AAV.hPGRN1

AAV delivered hPGRN

to mouse brain

TDP-43 pathology in DKO mice

reduced by AAV.hPGRN

Elevated PGRN reduced insoluble

TDP-43 in mouse spinal cord

Elevated PGRN extended survival

of TDP-43 mutant mice

Elevated PGRN ameliorated TDP-43 pathology

and disease course in a preclinical model2

• Elevated PGRN also prevented degeneration of large axon fibers in

TDP-43 mice

• PGRN neuroprotection from pleiotropic effect, not single pathway

1. Reich et al. Sci Transl Med. 2024; 16(750); 2. Beel et al. Mol Neurodegen. 2018: 13:55.; Laird et al. PLoS One 2010; 5:e13368.

DKO, double gene knockout; GRN, granulin gene; PGRN, progranulin; TDP-43, transactive response DNA binding protein 43 kDa

† PGRN increased to >2x endogenous levels

• AAV delivery of functional GRN gene to express new PGRN,

increasing levels both intra- and extra-cellularly

• Preserves all natural pathways to properly traffic PGRN intracellularly

where it is needed

• ICM route of administration enables low doses of AAV and

broad CNS biodistribution

• Non-surgical, brief procedure (< 60 minutes)

• Potential for a one-time therapy for patients

• Durable elevation of CSF PGRN seen through 18 months1

PBFT02: Summary of Approach

21 April 2026

1. Interim data from upliFT-D as of January 26, 2026.

A novel and

potentially

transformative

therapy for

FTD-GRN patients

Completed development of high-productivity, suspension-based

manufacturing process

Single production lot estimated

to yield >1,000 doses1 with >70%

full capsids

Robust Manufacturing Process

Aligned with the FDA on an

analytical approach to establish

comparability of suspension-based

process

Process Comparability Plan

Developed assay and reached

alignment with FDA on suitability of

assay for PBFT02 release

Functional Potency Assay

Critical Manufacturing Milestones Achieved to Enable Late-Stage

Development of PBFT02

22 April 2026

1. Estimated yield based on Dose 2.

Huntington’s Disease

Preclinical Program

OVERVIEW

• Fatal, monogenic, autosomal dominant neurodegenerative disease

• Caused by trinucleotide (CAG) expansion in the huntingtin (HTT)

gene resulting in mutant huntingtin (mHTT) protein expression

• More than 200,000 people estimated to be at risk in the US1

CLINICAL SYMPTOMS

• Symptom onset typically occurs between 30–50 years old

• Characterized by progressive motor, cognitive, and behavioral

deterioration, due to neuronal dysfunction then degeneration

Huntington’s Disease: A Fatal Neurodegenerative

Disease with No Disease-Modifying Therapy

Average life

expectancy

after symptom

onset is

15–20 years

24 April 2026

Motor

deterioration

Cognitive

deterioration

Behavioral

deterioration

1. HDSA; Fisher and Hayden Mov Disord. 29:105-14, 2014.

Unaffected

HD Is Caused By A Mutation In Huntingtin (HTT) Gene:

A Stretch Of CAG Nucleotides Is Expanded

CAG repeat expansion leads to production of mutant huntingtin protein (mHTT)

25 April 2026

Normal huntingtin gene, HTT, CAG </= 35 Mutant huntingtin gene, mHTT, CAG > 35

GLUTAMINES

Exon 1 Exons 2–67

SHORT

CAG

HTT

DNA

LONG GLUTAMINE STRETCH

HTT

PROTEIN

Exon 1 Exons 2–67

LONG

CAG

mHTT

DNA

mHTT

PROTEIN

Huntington’s Disease

DNA Repair (DR) Proteins Play a Key Role in CAG Repeat Expansion

• CAG expansion above a certain threshold leads to neurodegeneration

• Longer CAG repeats associated with worse disease pathology

• CAG expansion occurs at different rates in different neurons, and is fastest in the

caudate and putamen brain regions which degenerate first

26 April 2026

1. Genetic Modifiers of Huntington’s Disease (GeM-HD) Consortium, Nat Genet. 2025; 57:1426-36.

2. Dragileva E et. al, Neurobio Dis. 2009; 33:37-47. 3. Mouro Pinto et. al, Nat Genet. 2025; 57:314-322.

In Huntington’s disease

(HD), the CAG repeat in the

HTT gene can elongate

over time, termed somatic

instability

• In the presence of certain CAG motifs, MSH3 can erroneously incorporate CAGs into

DNA, leading to CAG expansion

• In HD: certain genetic variants altering MSH3 function are associated with delayed

onset and slowed progression1

• In HD mice: MSH3 is essential for CAG expansion, and MSH3 knock-down reduced

somatic instability and HTT pathology2,3

MSH3, a DR protein, is a

key driver of somatic

instability

Our Approach: Decrease MSH3 to Reduce Somatic Instability in the HTT

Gene

Program Status

27 April 2026

Developing a differentiated approach to decrease MSH3

expression via AAV delivery of a miRNA

Proof-of-concept studies completed, with additional

preclinical studies ongoing

Plan to utilize an optimized intraparenchymal delivery approach

• One-time delivery

• Direct delivery to critical brain regions

• Reduced total procedure time

• Limited peripheral exposure to reduce safety risks

passagebio.com

Thank you!

Program Indication US/EU

prevalence Discovery Preclinical Phase 1/2 Pivotal

PBFT02

Frontotemporal dementia —

GRN 18,0001-3

Frontotemporal dementia —

C9orf72 21,0002-4

Unnamed Huntington’s disease 70,0005

Focused Pipeline Addressing Rare and Prevalent Neurodegenerative Indications

1. Greaves CV, et al. J Neurol 2019; 266:2075-2086. 2. Galvin JE, et al. Neurology 2017; 89:2049-2056. 3. Onyike CU, et al. Int Rev Psychiatry 2013; 25:130-137. 4. Moore KM, et al. Lancet Neurol 2020; 19: 145–156.

5. Crowell et al. Neuroepi. 2021; 55:361-368.

29 April 2026

ALS and Alzheimer’s disease represent additional pipeline expansion opportunities for PBFT02

LEADERSHIP TEAM

Demonstrated Leadership

BOARD OF DIRECTORS

Maxine Gowen, Ph.D.

Chairwoman

Athena Countouriotis, M.D.

Avenzo Therapeutics

Derrell Porter, M.D.

cTRL Therapeutics

Dolan Sondhi, Ph.D.

Weill Cornell Medicine

Sandip Kapadia

Former CFO Harmony Biosciences

Thomas Kassberg

Former CBO Ultragenyx

William Chou, M.D.

President and Chief Executive Officer

Deep experience in rare disease, CNS disorders and genetic medicines

Eden Fucci

SVP Technical Operations

Stuart Henderson

Chief Business Officer

William Chou, M.D.

President and

Chief Executive Officer

Kathleen Borthwick

Chief Financial Officer

Karl Whitney, Ph.D.

SVP Global Regulatory Affairs

Sue Browne, Ph.D.

Chief Scientific Officer

30 April 2026

Preclinical NHP: AAV1 Achieved the Highest Levels of CSF PGRN

31 April 2026

After ICM administration to NHPs:

• AAV1 capsid resulted in CSF hPGRN levels

5x higher than AAVhu68 (an AAV9 variant)

• Superior hPGRN response led to selection

of AAV1 capsid for PBFT02

Rhesus macaques (n=2/gp) 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 sample range for CSF PGRN, n = 61 (Passage Bio data)

CSF, cerebrospinal fluid; GC, genome copies; ICM, intra-cisterna magna; NHP, non-human primate. Reference: Hinderer et al., Ann Clin Trans Neurol. 2020; 7:1843-1853.

Human PGRN in NHP CSF

Vector Comparison

Healthy adult range

Days

BL 0 7 14 21 28 35

hPGRN *ng/mL)

AAV1.CB7.hGRN

AAV5.CB7.hGRN

AAVhu68.CB7.hGRN

AAVhu68.UbC.hGRN

Preclinical NHP: ICM Administration of PBFT02 Led to Broad Distribution

of Vector Throughout Brain/Spinal Cord

• Robust, dose-dependent vector

delivery to cortical and sub-cortical brain regions affected

in FTD

• NHP low dose, equivalent to

clinical Dose 1 of PBFT02 in

upliFT-D study, resulted in ~10⁴

GC/μg DNA in all sampled areas

throughout the brain

32 April 2026

n=3/gp. Data are mean +/- SEM.

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; OCX, occipital cortex;

PCX, parietal cortex; TCX, temporal cortex; Thor, thoracic; TRG, trigeminal root ganglion; Veh, vehicle

Vector Biodistribution in NHPs 90 Days Post-ICM PBFT02

GC/µg DNA

107

106

105

104

103

102

101

FCX PCX TCX OCX Hipp Medulla CBL Cerv Lumb Thor Cerv Lumb Thor TRG

LLoQ

Veh

Low

Medium

High dose

Cortex DRG

Preclinical Grn–/– Mice: Expression of hPGRN Improved Lysosomal

Dysfunction and Neuroinflammation in the Brain

33 April 2026

Greatest pathological benefit was associated with the highest PGRN levels in the CSF

Lipofuscin deposition and microglial activation are hallmark pathologies seen in FTD; Improvements in both measures were seen in cerebral cortex, thalamus, and hippocampus after PBFT02 administration

Grn–/– and WT mice (n=14-15/gp) ICV-administered PBFT02 or vehicle (V). Baseline controls were untreated mice on Day 1. Bars: mean +/- SEM.

# ## p < 0.01, ### p < 0.005 vs WT control; *p < 0.05, ***p < 0.005 vs Grn-/-+ V , one-way ANOVA followed by Tukey’s multiple comparisons test.

Grn, granulin gene; ICV, Intra-cerebroventricular; PGRN, progranulin; WT, wildtype

Thalamus Lipofuscin Thalamus CD68 Immunohistochemistry

PBFT02 Reduced Lipofuscin Deposition at All Doses,

Suggesting Improved Lysosomal Dysfunction

Dose-Dependent Elevations in CSF PGRN after PBFT02

Led to Progressive Reductions in Microglial Activation

Lipofuscin Count

1000

800

600

400

200

Baseline Day 90 Baseline Day 90 CD68 Area (µm2

)

5000

4000

3000

2000

1000

PBFT02

Dose 1

Dose 2

Dose 3

Dose 4

PBFT02

Dose 1

Dose 2

Dose 3

Dose 4

WT Grn-/- WT Grn-/- WT Grn-/- WT Grn-/-

V V PBFT02 V V PBFT02

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v3.26.1

Cover

Apr. 20, 2026

Cover [Abstract]

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Entity File Number

001-39231

Entity Registrant Name

PASSAGE

BIO, INC.

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Commerce Square

Entity Address, Address Line Two

2005 Market Street, 39th Floor

Entity Address, City or Town

Philadelphia

Entity Address, State or Province

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

false

- Definition

Boolean flag that is true when the XBRL content amends previously-filed or accepted submission.

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No definition available.

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Area code of city

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No definition available.

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Cover page.

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No definition available.

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For the EDGAR submission types of Form 8-K: the date of the report, the date of the earliest event reported; for the EDGAR submission types of Form N-1A: the filing date; for all other submission types: the end of the reporting or transition period. The format of the date is YYYY-MM-DD.

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No definition available.

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- Definition

The type of document being provided (such as 10-K, 10-Q, 485BPOS, etc). The document type is limited to the same value as the supporting SEC submission type, or the word 'Other'.

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No definition available.

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Name:

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- Definition

Address Line 1 such as Attn, Building Name, Street Name

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No definition available.

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Address Line 2 such as Street or Suite number

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No definition available.

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Name of the City or Town

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No definition available.

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Code for the postal or zip code

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- Definition

Name of the state or province.

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No definition available.

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- Definition

A unique 10-digit SEC-issued value to identify entities that have filed disclosures with the SEC. It is commonly abbreviated as CIK.

+ References

Reference 1: http://www.xbrl.org/2003/role/presentationRef

-Publisher SEC

-Name Exchange Act

-Number 240

-Section 12

-Subsection b-2

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- Definition

Indicate if registrant meets the emerging growth company criteria.

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Reference 1: http://www.xbrl.org/2003/role/presentationRef

-Publisher SEC

-Name Exchange Act

-Number 240

-Section 12

-Subsection b-2

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- Definition

Commission file number. The field allows up to 17 characters. The prefix may contain 1-3 digits, the sequence number may contain 1-8 digits, the optional suffix may contain 1-4 characters, and the fields are separated with a hyphen.

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No definition available.

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- Definition

Two-character EDGAR code representing the state or country of incorporation.

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No definition available.

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- Definition

The exact name of the entity filing the report as specified in its charter, which is required by forms filed with the SEC.

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Reference 1: http://www.xbrl.org/2003/role/presentationRef

-Publisher SEC

-Name Exchange Act

-Number 240

-Section 12

-Subsection b-2

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- Definition

The Tax Identification Number (TIN), also known as an Employer Identification Number (EIN), is a unique 9-digit value assigned by the IRS.

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Reference 1: http://www.xbrl.org/2003/role/presentationRef

-Publisher SEC

-Name Exchange Act

-Number 240

-Section 12

-Subsection b-2

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- Definition

Local phone number for entity.

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No definition available.

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- Definition

Boolean flag that is true when the Form 8-K filing is intended to satisfy the filing obligation of the registrant as pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act.

+ References

Reference 1: http://www.xbrl.org/2003/role/presentationRef

-Publisher SEC

-Name Exchange Act

-Number 240

-Section 13e

-Subsection 4c

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- Definition

Boolean flag that is true when the Form 8-K filing is intended to satisfy the filing obligation of the registrant as pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act.

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Reference 1: http://www.xbrl.org/2003/role/presentationRef

-Publisher SEC

-Name Exchange Act

-Number 240

-Section 14d

-Subsection 2b

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- Definition

Title of a 12(b) registered security.

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-Publisher SEC

-Name Exchange Act

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-Section 12

-Subsection b

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- Definition

Name of the Exchange on which a security is registered.

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-Publisher SEC

-Name Exchange Act

-Number 240

-Section 12

-Subsection d1-1

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- Definition

Boolean flag that is true when the Form 8-K filing is intended to satisfy the filing obligation of the registrant as soliciting material pursuant to Rule 14a-12 under the Exchange Act.

+ References

Reference 1: http://www.xbrl.org/2003/role/presentationRef

-Publisher SEC

-Name Exchange Act

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-Section 14a

-Subsection 12

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- Definition

Trading symbol of an instrument as listed on an exchange.

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- Definition

Boolean flag that is true when the Form 8-K filing is intended to satisfy the filing obligation of the registrant as written communications pursuant to Rule 425 under the Securities Act.

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Reference 1: http://www.xbrl.org/2003/role/presentationRef

-Publisher SEC

-Name Securities Act

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-Section 425

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