Form 8-K

8-K — Entrada Therapeutics, Inc.

Accession: 0001104659-26-063325

Filed: 2026-05-19

Period: 2026-05-18

CIK: 0001689375

SIC: 2834 (PHARMACEUTICAL PREPARATIONS)

Item: Regulation FD Disclosure

Item: Financial Statements and Exhibits

Documents

8-K — tm2614944d1_8k.htm (Primary)

EX-99.1 — EXHIBIT 99.1 (tm2614944d1_ex99-1.htm)

GRAPHIC (tm2614944d1_ex99-1img001.jpg)

GRAPHIC (tm2614944d1_ex99-1img002.jpg)

GRAPHIC (tm2614944d1_ex99-1img003.jpg)

GRAPHIC (tm2614944d1_ex99-1img004.jpg)

GRAPHIC (tm2614944d1_ex99-1img005.jpg)

GRAPHIC (tm2614944d1_ex99-1img006.jpg)

GRAPHIC (tm2614944d1_ex99-1img007.jpg)

GRAPHIC (tm2614944d1_ex99-1img008.jpg)

GRAPHIC (tm2614944d1_ex99-1img009.jpg)

GRAPHIC (tm2614944d1_ex99-1img010.jpg)

GRAPHIC (tm2614944d1_ex99-1img011.jpg)

GRAPHIC (tm2614944d1_ex99-1img012.jpg)

GRAPHIC (tm2614944d1_ex99-1img013.jpg)

GRAPHIC (tm2614944d1_ex99-1img014.jpg)

GRAPHIC (tm2614944d1_ex99-1img015.jpg)

GRAPHIC (tm2614944d1_ex99-1img016.jpg)

GRAPHIC (tm2614944d1_ex99-1img017.jpg)

GRAPHIC (tm2614944d1_ex99-1img018.jpg)

GRAPHIC (tm2614944d1_ex99-1img019.jpg)

GRAPHIC (tm2614944d1_ex99-1img020.jpg)

GRAPHIC (tm2614944d1_ex99-1img021.jpg)

GRAPHIC (tm2614944d1_ex99-1img022.jpg)

GRAPHIC (tm2614944d1_ex99-1img023.jpg)

GRAPHIC (tm2614944d1_ex99-1img024.jpg)

GRAPHIC (tm2614944d1_ex99-1img025.jpg)

GRAPHIC (tm2614944d1_ex99-1img026.jpg)

GRAPHIC (tm2614944d1_ex99-1img027.jpg)

GRAPHIC (tm2614944d1_ex99-1img028.jpg)

GRAPHIC (tm2614944d1_ex99-1img029.jpg)

GRAPHIC (tm2614944d1_ex99-1img030.jpg)

GRAPHIC (tm2614944d1_ex99-1img031.jpg)

GRAPHIC (tm2614944d1_ex99-1img032.jpg)

GRAPHIC (tm2614944d1_ex99-1img033.jpg)

GRAPHIC (tm2614944d1_ex99-1img034.jpg)

GRAPHIC (tm2614944d1_ex99-1img035.jpg)

GRAPHIC (tm2614944d1_ex99-1img036.jpg)

GRAPHIC (tm2614944d1_ex99-1img037.jpg)

GRAPHIC (tm2614944d1_ex99-1img038.jpg)

GRAPHIC (tm2614944d1_ex99-1img039.jpg)

GRAPHIC (tm2614944d1_ex99-1img040.jpg)

GRAPHIC (tm2614944d1_ex99-1img041.jpg)

GRAPHIC (tm2614944d1_ex99-1img042.jpg)

GRAPHIC (tm2614944d1_ex99-1img043.jpg)

GRAPHIC (tm2614944d1_ex99-1img044.jpg)

GRAPHIC (tm2614944d1_ex99-1img045.jpg)

GRAPHIC (tm2614944d1_ex99-1img046.jpg)

GRAPHIC (tm2614944d1_ex99-1img047.jpg)

GRAPHIC (tm2614944d1_ex99-1img048.jpg)

GRAPHIC (tm2614944d1_ex99-1img049.jpg)

GRAPHIC (tm2614944d1_ex99-1img050.jpg)

GRAPHIC (tm2614944d1_ex99-1img051.jpg)

XML — IDEA: XBRL DOCUMENT (R1.htm)

8-K — FORM 8-K

8-K (Primary)

Filename: tm2614944d1_8k.htm · Sequence: 1

false

0001689375

2026-05-18

iso4217:USD

xbrli:shares

iso4217:USD

xbrli:shares

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):

May 18, 2026

ENTRADA

THERAPEUTICS, INC.

(Exact name of registrant as specified in its

charter)

Delaware

001-40969

81-3983399

(State or other jurisdiction

(Commission

(I.R.S. Employer

of incorporation)

File Number)

Identification No.)

One Design Center Place

Suite 17-500

Boston, MA

02210

(Address

of principal executive offices)

(Zip

Code)

Registrant’s telephone number, including area

code: (857) 520-9158

Not Applicable

(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

TRDA

The Nasdaq Global 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 x

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 May 18, 2026, Entrada Therapeutics, Inc. updated its corporate presentation

for use in meetings with investors, analysts and others. A copy of the updated corporate presentation is furnished as Exhibit 99.1 to

this Current Report on Form 8-K (this “Current Report”) and is incorporated by reference herein.

The information in Item 7.01 of this Current Report, including the

accompanying Exhibit 99.1, is intended to be furnished and shall not be deemed “filed” for purposes of Section 18 of the Exchange

Act or otherwise subject to the liability of such section, nor shall it be deemed incorporated by reference in any filing under the Securities

Act or the Exchange Act, except as expressly set forth by specific reference in such filing.

Item 9.01 Financial Statements and Exhibits.

(d) Exhibits.

The following exhibit relating to Item 7.01 of this Current Report

shall be deemed to be furnished and not filed:

99.1

Corporate Presentation of Entrada Therapeutics, Inc., dated May 2026.

104

Cover Page Interactive Data File (embedded within the Inline XBRL document).

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.

Entrada Therapeutics, Inc.

Date: May 18, 2026

/s/ Dipal Doshi

Dipal Doshi

Chief Executive Officer

EX-99.1 — EXHIBIT 99.1

EX-99.1

Filename: tm2614944d1_ex99-1.htm · Sequence: 2

Exhibit 99.1

Meet Andrew and JJ, living with Duchenne muscular dystrophy

Corporate Presentation

May 2026

Disclaimer

May 2026 2

This presentation has been prepared by Entrada Therapeutics, Inc. (“Entrada”) and shall not constitute an offer to sell or a solicitation of an offer to buy securities or an invitation or inducement to engage in investment

activity nor shall there be any sale of securities in any jurisdiction in which such offer, solicitation or sale would be unlawful prior to registration or qualification of such securities under the securities law of any such

jurisdiction. Before you invest in any securities of Entrada, you should read any documents Entrada has filed with the SEC for more complete information about Entrada and the offering. You may get these documents for

free by visiting EDGAR on the SEC website at www.sec.gov.

This presentation contains express and implied forward-looking statements that involve substantial risks and uncertainties. All statements, other than statements of historical facts, contained in this presentation, including

statements regarding Entrada's strategy, future operations, prospects and plans, objectives of management, the validation, differentiation and superiority of Entrada’s approach and EEV platform and its ability to provide a

potential best-in-class outcomes in high unmet need diseases, expectations regarding Entrada’s Phase 1/2 MAD clinical study of ENTR-601-44, including the completion of the open-label period by year-end 2026 and the

reporting, translatability, and ability to achieve a clinically meaningful effect from additional metrics data, including 10-meter walk/run, stride velocity 95th centile, 4-stair climb, north star ambulatory, and performance upper

limb, the translatability of dystrophin concentrations and exon skipping based on juvenile NHP data, the timing of competitive data from Cohort 2 by year-end 2026, with expected higher levels of plasma and muscle

exposure (linear or better), substantially higher dystrophin levels, increases in muscle function and continued functional response over time, with the timing of Cohort 3 to follow, expectations regarding the data from the

clinical study of ENTR-601-44, including expected results such as higher dystrophin restoration and positive safety data, expectations regarding muscle regeneration, muscle stabilization, and greater strength in patients

as measured by Time to Rise velocity, expectations regarding the connection between EEV-PMO uptake in satellite cells and muscle regeneration, speed and durability of functional improvement, expectations of lower

risk of anti-drug antibody response and lower cost of goods from EEV-PMO conjugates, translatability of current data to de-risk Entrada’s DMD clinical portfolio, support dose escalations, and its ability to support U.S.

Accelerated Approval, expectations regarding Entrada’s Phase 1/2 MAD clinical study of ENTR-601-45 and the timing of first-in-class data from Cohort 1 in mid-2026, expectations regarding the timing to market of ENTR-601-45 and it’s potential best-in-class clinical profile, expectations regarding regulatory filings in the EU for the planned Phase 1/2 MAD clinical study of ENTR-601-50, expectations regarding the global regulatory filings for

the planned clinical study of ENTR-601-51, the ability to recruit for and complete global Phase 2 clinical studies of ENTR-601-44, ENTR-601-45, ENTR-601-50 and ENTR-601-51 and to obtain U.S. Accelerated Approval

and/or full approval for each program, the ability of EEV therapies to provide a 25-50-fold improvement in endosomal escape and lower whole drug requirements compared to antibody-based therapies, the ability to

continue to expand and develop additional therapeutic programs and modalities, including further exon skipping programs, the potential therapeutic benefits of Entrada’s EEV product candidates and the ability to advance

therapeutic candidates in indications beyond neuromuscular disease, including but not limited to ocular disease, expectations regarding the timing of nomination of a second clinical candidate for inherited retinal disease in

the second half of 2026, the continued development and advancement of ENTR-601-44, -45, -50 and -51 for the potential treatment of DMD and ENTR-801 for the potential treatment of Usher syndrome type 2A and the

partnered product candidate VX-670 for the potential treatment of DM1, expectations regarding the progress and success of Entrada’s collaboration with Vertex, including expected proceeds from program milestones plus

royalties and completion of the MAD portion of the global Phase 1/2 study of the VX-670 program and results shared in the second half of 2026, the size of the DMD market opportunity in the U.S., and the sufficiency of

Entrada’s cash resources into the third quarter of 2027, constitute forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995. The words “anticipate,” “believe,” “continue,”

“could,” “estimate,” “expect,” “intend,” “may,” “might,” “objective,” “ongoing,” “plan,” “predict,” “project,” “potential,” “should,” or “would,” or the negative of these terms, or other comparable terminology are intended to identify

forward-looking statements, although not all forward-looking statements contain these identifying words. Entrada may not actually achieve the plans, intentions or expectations disclosed in these forward-looking statements

and you should not place undue reliance on these forward-looking statements. Actual results or events could differ materially from the plans, intentions and expectations disclosed in these forward-looking statements as a

result of various important factors, including: uncertainties inherent in the identification and development of product candidates, including the conduct of research activities and the initiation and completion of preclinical

studies and clinical studies; uncertainties as to the availability and timing of results from preclinical and clinical studies; the timing of and Entrada’s ability to submit and obtain regulatory clearance and initiate clinical

studies; whether results from preclinical studies or clinical studies will be predictive of the results of later preclinical studies and clinical studies; whether Entrada's cash resources will be sufficient to fund Entrada's

foreseeable and unforeseeable operating expenses and capital expenditure requirements; as well as the risks and uncertainties identified in Entrada's filings with the SEC, including Entrada's most recent Form 10-K and in

subsequent filings Entrada may make with the SEC. In addition, the forward-looking statements included in this presentation represent Entrada's views as of the date of this presentation. Entrada anticipates that

subsequent events and developments will cause its views to change. However, while Entrada may elect to update these forward-looking statements at some point in the future, it specifically disclaims any obligation to do

so. These forward-looking statements should not be relied upon as representing Entrada's views as of any date subsequent to the date of this presentation.

2026 is a transformational year for Entrada

May 2026

Entrada is a clinical-stage biopharma company developing proprietary genetic medicines to deliver

best-in-class outcomes in high unmet need diseases

*ELEVATE-44-201 Cohort 1, DMD: Duchenne muscular dystrophy; DM1: Myotonic dystrophy type 1; Cash runway based on current operating plans and ending cash, cash

equivalents and marketable securities as of March 31, 2026.

• 5 clinical-stage programs in DMD and DM1

• 4 clinical data catalysts in DMD and DM1 patients achieved or expected in 2026

• 2 development candidates in inherited retinal diseases projected by year-end 2026

• Cash runway into Q3 2027

• Up to $485 million in DM1 milestones, plus royalties associated with Vertex partnership

• $5 billion U.S. DMD market, with limited competitive penetration; Untapped global markets

• FDA Accelerated Approval strategy to be supported by Phase 1/2 data from ex-U.S. DMD studies

• Proprietary and differentiated delivery and active moiety sequences in all candidate programs

• Favorable safety data and early but compelling functional improvement results*

• Best-in-class preclinical data in all declared clinical and preclinical programs

Deep pipeline with

value inflection

points in 2026

Differentiated

programs in

untapped markets

Capitalized to realize

value catalysts

May 2026 *All references in this presentation regarding planned regulatory filings and clinical study designs are subject to ongoing discussion with regulatory authorities;

DMD: Duchenne muscular dystrophy; DM1: Myotonic dystrophy type 1; SAD: Single ascending dose; MAD: Multiple ascending dose.

ENTR-601-44

• Cohort 1 dosing complete; All patients

transitioned to open-label dosing

• Cohort 2 dose escalation cleared to

initiate at 12 mg/kg and dosing ongoing

• Cohort 1 open-label and Cohort 2 MAD

data expected by year-end 2026

ENTR-601-45

• Cohort 1 data expected mid-2026

ENTR-601-50 and ENTR-601-51

• Additional regulatory filings expected

following a review of data from the

ongoing DMD clinical studies

• Completed SAD portion of global

Phase 1/2 study

• MAD portion to evaluate safety and

efficacy is ongoing

• Vertex to share study results in H2 2026

• Partnership terms include up to $485

million in milestones, plus royalties

Inherited Retinal Diseases

• Nominated first ocular candidate,

ENTR-801 for Usher syndrome type 2A

• Second program in lead optimization;

Candidate declaration in H2 2026

Additional Discovery Efforts

• Expansion of neuromuscular and

ocular franchises leveraging next-generation EEVs and oligonucleotides

• Range of undisclosed diseases, targets

and modalities

Rapidly Expanding DMD

Clinical Franchise

Vertex Advancing VX-670 for

the Treatment of DM1

Advancing Innovative

Preclinical Pipeline

Clinical inflection points for ENTR-601-44, ENTR-601-45 and VX-670 in 2026; ENTR-601-44 safety

data fundamentally de-risks the neuromuscular portfolio

Multiple clinical milestones achieved or expected in 2026

Each target disease

has a substantial patient

population with a significant

unmet medical need

May 2026

Phase 1/2

ENTR-801: USH2A

Undisclosed

Duchenne Muscular Dystrophy (DMD)

Inherited Retinal Diseases

Myotonic Dystrophy Type 1 (DM1) – Partnered with

ENTR-601-44

ENTR-601-45

ENTR-601-50

ENTR-601-51

VX-670

Preclinical Phase 2/3

Pipeline and Platform Expansion

Phase 1/2 data from ex-U.S.

DMD studies to support

Accelerated Approval

regulatory filings in the U.S.

Advancing five fully

owned programs and

one partnered program

Duchenne Muscular Dystrophy (DMD)

Entrada’s DMD strategy is to de-risk a differentiated

portfolio and commercially launch best-in-class drugs

May 2026 7

• Novel EEV and PMO sequences

• Best-in-class non-clinical data

translated into compelling safety and

functional data

• Progenitor cell uptake supports

regenerative potential, speed and

durability of functional improvement

• Lower whole drug exposure supports

lower risk of anti-drug antibody

response and lower cost of goods

• Favorable ENTR-601-44 Phase 1

healthy volunteer safety profile

• Favorable ENTR-601-44 Phase 1/2

patient safety data for Cohort 1

• Statistically significant

improvement in functional benefit*

observed in ENTR-601-44 Cohort 1

• All neuromuscular programs leverage

the same EEV

• ENTR-601-44 Cohort 1 data de-risks the DMD franchise

• Phase 1/2 data from ex-U.S.

studies to support

U.S. Accelerated Approval**

• ENTR-601-44 Cohort 1 open-label and Cohort 2 MAD

expected to deliver competitive

data by year-end 2026

• First-in-class clinical program

in exon 45 projected to deliver

Cohort 1 MAD data by mid-2026

Differentiated EEV Platform

and Novel PMO Conjugates

De-risked and Rapid

Clinical Development

Potential for “Best-in-class”

Commercial Opportunities

*Time to Rise velocity (TTRV), nominal p-value, post hoc analysis; **Accelerated Approval is subject to regulatory feedback; PMO: Phosphorodiamidate morpholino oligomer; Healthy

volunteer may also be described as HNV (healthy normal volunteer).

Three strategic pillars: Differentiation, de-risking and best-in-class opportunities

Entrada is developing genetic medicines to correct the

mechanism of disease and slow, halt or reverse progression

May 2026 8

~8% ~9% ~4% ~15%

The portfolio covers ~35% of the total population totaling

~11,500 patients in the U.S. and EU*

DMD Mutations and Tissues

of Focus in the Entrada Portfolio

PMO, phosphorodiamidate morpholino oligomer.

Individuals with Duchenne Entrada Approach

Pre-mRNA

mRNA

Protein

With exon deletion, protein program is miscoded

Reading frame disrupted and body reads STOP!

Resultant mRNA sequence stops the production

of functional dystrophin protein

No Translation

DMD

Pre-mRNA

mRNA

Protein

Treatment enables skipping of exon

Reading frame restored

Functional dystrophin protein is translated

and muscle membrane regains integrity

Translation

Missing code Oligo blocks inclusion of an exon

Splice modulation

Entrada addresses mutations which result in a lack of dystrophin,

muscle breakdown, progressive disability and death

Entrada’s Approach: Modulate RNA Splicing and Produce

Functional Protein to Preserve and Rebuild Muscle

~35% = ~11,500 Patients*

Heart Diaphragm Skeletal muscle

44 45 50 51

*Sub-mutation estimates rounded, from Bladen et al., HGVS Journal, January 2015; DMD population estimated to be ~7-8 per 100,000 males per Crisafulli et al., Orphanet J. Rare

Disease, June 2020; Calculation based on estimates of U.S. and EU (defined as EU27 population).

U.S. Annual Market Opportunity

$ Millions

$1,000

$2,000

$3,000

$4,000

$5,000

$6,000

May 2026 9

Entrada’s DMD franchise is positioned to address ~1/3 of all U.S. DMD patients, representing

a potential ~$5B annual market opportunity in the U.S. alone

Entrada’s DMD franchise unlocks a potential $5B U.S.

market opportunity, with significant further upside ex-U.S.

*$1M per patient per year market price estimated based on Lin et al., Institute for Clinical and Economic Review, April 2022, Posner et al., Journal of Manag. Care and Spec. Pharm. 2025;

**Bladen et al., HGVS Journal, January 2015; Total U.S. DMD population estimated to be ~7-8 per 100,000 males (~13,800) per Crisafulli et al., Orphanet J. Rare Disease, June 2020.

~$5 Billion Annual U.S. Commercial Opportunity*

ENTR-601-44 ENTR-601-45 ENTR-601-50 ENTR-601-51 U.S. DMD

Franchise Total

~$1.1B

~$1.3B

~$0.6B

~$1.9B ~$4.8B

~1,100

Patients

~1,250

Patients

~550

Patients

~1,900

Patients

• Few available treatment options and

limited competitive penetration to date

• ~5,000 U.S. patients addressable

with exon skipping therapies 44, 45,

50 and 51**

• ~6,500 European patients

addressable with exon skipping

therapies 44, 45, 50 and 51**

• Ex-U.S. market not factored into

projections and represents further

upside potential

~4,800 Patients

ELEVATE-44-201

Cohort 1: Study Results Summary

Executive summary and key takeaways

ELEVATE-44-201 Cohort 1 results

May 2026

• Favorable safety and tolerability profile at 6 mg/kg; All AEs were mild to moderate

▪ No reported SAEs nor AEs leading to discontinuation

▪ Renal markers within normal range and comparable to placebo

• Functional benefit demonstrated at 6 mg/kg via Time to Rise and Time to Rise Velocity (TTR and TTRV) measures

▪ TTR is a secondary endpoint of the ELEVATE-44-201 study

▪ Cohort 1 resulted in a statistically significant* impact on TTR and TTRV versus placebo

▪ TTRV levels were several fold above MCID after only 3 doses (127 days, 6 weeks after the last dose administered)

• Mechanistic advantages support early functional benefit observations

▪ EEV-PMO uptake in satellite cells can lead to the proliferation, activation and asymmetric division which is the basis of muscle regeneration

▪ Continued benefit in muscle function expected in the open-label period of Cohort 1 and future Cohorts

• Updated PK modeling, based on recently received juvenile NHP data, supports higher dystrophin in Cohorts 2 and 3

▪ Due to lower plasma drug exposures, dystrophin levels in Cohort 1 were lower than predicted

11 AE: Adverse event; SAE: Serious adverse events TTR: Time to Rise; TTRV: Time to Rise velocity; 10MWR: 10-meter walk/run; MCID: Minimal clinically important difference;

Pharmacokinetics may be abbreviated to PK and Pharmacodynamics may be abbreviated to PD; *Wilcoxon rank-sum (one sided) test, nominal p-values, post hoc analysis.

Early functional benefit response is compelling and statistically significant

Cohort 1 achieved the objective of demonstrating safety/tolerability; Importantly, Cohort 1 achieved

functional benefit at the lowest dose with dystrophin levels expected to increase in Cohorts 2 and 3

ELEVATE-44-201

Cohort 1: Trial Design and Treatment Population

May 2026 13 *Expansion cohort and potential for Accelerated Approval is subject to regulatory feedback; Global registration and approval will require Phase 3 studies to follow the Phase 1/2

studies; Phase 3 studies will likely include functional measures as the primary endpoint (U.S. confirmatory study/EU registrational study).

Screening Double-Blind Period Open-Label Period Follow-up Period

Up to 6 weeks 19 weeks 31 weeks 6 weeks

N=24 participants across three

cohorts, n=8 per cohort

Within each cohort, randomization 3:1

(ENTR-601-44 to placebo)

✓ Cohort 1: 6 mg/kg or placebo

• Cohort 2: 12 mg/kg or placebo

• Cohort 3: ≤18 mg/kg or placebo

x3 doses

Days 1, 43 and 85

Muscle biopsy #2

Day 127

Part

Ambulatory

participants with DMD

who are exon 44

skipping amenable

Muscle biopsy #1

Participants who complete Part A are able to continue

into open-label period

• Receive 6 doses of ENTR-601-44 at the level that was

administered in participant’s Part A cohort

• Dosing initiated

• Study blinded to end of open-label period

Expansion Cohort

ELEVATE-44-201 is a global, two-part,

randomized, double-blind placebo-controlled Phase 1/2 study in

ambulatory patients*

Primary objective: Safety and tolerability of ENTR-601-44

Secondary objectives: Evaluation of pharmacokinetics,

exon skipping, dystrophin production and measures of function

ENTR-601-44

• Cohort 2: 12 mg/kg or placebo

✓ Cohort 1: 6 mg/kg or placebo

• Ongoing

✓ Complete

ELEVATE-44-201 is designed to support U.S. Accelerated

Approval and forms the basis of a global registrational program*

Demographics and baseline characteristics

May 2026

ELEVATE-44-201

Placebo

n=2

ENTR-601-44

6 mg/kg

n=6

Age, mean 13.5 9.3

Body mass index, mean, kg/m2 17.96 20.00

Age at disease onset, mean, years 1.0 2.2

Corticosteroid use, n (%) 2 (100%) 6 (100%)

Ambulatory, n (%) 2 (100%) 6 (100%)

Baseline dystrophin 4.6% 4.0%

• Baseline dystrophin levels seen in Cohort 1 were the lowest levels observed in recent Exon 44 studies

• Higher levels of baseline dystrophin correlate to higher treatment responses and vice versa

ELEVATE-44-201

Cohort 1: Safety Data

Safety was consistent and unremarkable at the 6 mg/kg dose

May 2026

ELEVATE-44-201

TEAE: Treatment emergent adverse event. 16

Participants with ≥1 TEAE, n (%) Placebo

n=2

ENTR-601-44

6 mg/kg

n=6

Any TEAE 2 (100%) 6 (100%)

TEAEs related to study drug 1 (50%) 5 (83%)

Serious TEAEs 0 0

TEAEs leading to study discontinuation 0 0

TEAEs leading to death 0 0

All TEAEs were mild to moderate

• Headache was the most common study

drug–related TEAE, reported in 50% of

the treatment group and 50% of the

placebo group

• All events resolved

• There were no serious TEAEs and no

study discontinuation due to any causes

• No hypomagnesemia or renal safety

concerns were noted

A highly favorable safety profile supports a de-risking of DMD programs

May 2026 Data from ELEVATE-44-201; eGFR: Estimated glomerular filtration rate; LLN: Lower limit of normal; ULN: Upper limit of normal; Serum creatinine reference range shown is 27–106

μmol/L and is dependent on age of the participant enrolled in Cohort 1; Serum creatinine is below normal in participants with DMD due to reduced muscle mass.

ELEVATE-44-201

eGFR Serum Cystatin C

Serum Magnesium Serum Creatinine

Renal markers were within normal range and comparable

to placebo

Renal marker results further de-risk current and future DMD programs and support dose

escalation to drive a higher therapeutic index

ELEVATE-44-201

Cohort 1: Functional Efficacy Data

Functional benefit summary

May 2026

• Time to Rise and Time to Rise Velocity are the first functional measurements to ”move”

• Functional benefit demonstrated via Time to Rise and Time to Rise Velocity measurements

▪ TTRV is a calculation based on TTR that minimizes any imputation, outliers and noise associated with TTR

▪ TTRV is a clinically significant and accepted regulatory endpoint

▪ Cohort 1 resulted in a statistically significant impact on TTRV versus placebo at levels several fold above MCID after only 3 doses (127

days, 6 weeks after the last dose administered)

▪ TTR and TTRV generally precede improvements in other functional measures (10MWR, etc.)

• Positive trends observed in 10MWR and will be tracked and reported at the end of the open-label period (year-end 2026)

• Additional metrics (e.g., 4SC) to be reported at the end of the open-label period (year-end 2026)

4SC: 4 stair climb. 19

Early functional benefit response is compelling and statistically significant

Cohort 1 achieved functional benefit via statistically significant measurements in both TTR and

TTRV; 10MWR trending favorably with additional metrics to be shared by year-end 2026

Functional improvement

The importance and meaning of Time to Rise velocity

May 2026 20

Time to Rise, a secondary endpoint in this study, is a robust, prognostic factor that predicts disease

progression; Time to Rise velocity reduces the impact of imputation, outliers and noise

1.Cicala et al., Italian DMD Network (WMS 2025); 2.McDonald et al., CINRG DNHS (PPMD 2021); NSAA: North Star Ambulatory Assessment.

TTR

baseline

(seconds)

TTR end of

study

(seconds)

Improvement

(seconds) TTRV calculation Δ TTRV

(rises/sec)

6.0 3.89 2.11 1/3.89 – 1/6.0 = 0.257 – 0.167 +0.09

8.0 4.65 3.35 1/4.65 – 1/8.0 = 0.215 – 0.125 +0.09

10.0 5.26 4.74 1/5.26 – 1/10.0 = 0.190 – 0.100 +0.09

Explanation: A boy starting at a TTR of 6 seconds needs to improve by ~2 seconds to achieve

+0.09 ΔTTRV, but a boy starting at a TTR of 10 seconds needs to improve by ~4.5 seconds for

the same velocity change

• TTR declines rapidly over time in patients with DMD and is

an early prognostic factor for disease progression and

loss of ambulation1

▪ The largest absolute and proportional annual signal among

functional measures and early prognostic factor for disease

progression and loss of ambulation

▪ Robust, as rising from the floor depends on proximal strength and

postural control, functions affected early in disease progression1

▪ Precedes improvements in 4-stair climb or 10-meter walk test and

less complicated than NSAA2

• TTRV is calculated as 1/TTR, expressed as rises/second

and is designed to reduce the impact of outliers and imputed

data (illustration at right)

▪ Handles the unable to perform problem by scoring that

observation at zero avoiding arbitrary scoring

▪ Dampens clinically meaningless scoring noise between visits

▪ Compresses the long tail and produces a distribution that is much

closer to normal, which matters for parametric statistics

Illustrative Data and Representative Calculation of TTRV

Functional cascade: TTR velocity is a robust indicator of

treatment effect and the earliest measurement to move

May 2026 21

Proximal functional measures, including TTR and 4SC, detect changes before composite/distal

measures like PUL and NSAA; TTR and TTRV were statistically significant versus placebo in Cohort 1

Sources: Duong et al., J Neuromuscul Dis 2021;8(6):939–948; Gupta et al., PLOS ONE 2023; Rabbia et al., J Neuromuscul Dis 2024; EMA SV95C Qualification Opinion 2022;

McDonald et al., Muscle Nerve 2013; Mercuri et al., NMD 2016; OLE: Open-label extension.

Relevant Functional

Readout

ENTR-601-44 Cohort 1 detected a statistically significant TTRV signal at Day 127 (18 weeks) which is

consistent with TTRV being the earliest timed function test to detect treatment effect

4SC Velocity

4 Stair Climb

• Baseline not collected in Cohort 1 MAD; To be reported at the end of the open-label period

10MWR Velocity

10-Meter Walk/Run

• Trend towards functional improvement in Cohort 1 MAD portion of the study;

Will be assessed at the end of the open-label period

SV95C

Stride Velocity 95th Centile

• Not collected during Cohort 1 MAD; To be reported at the end of the open-label period

PUL 2.0

Performance Upper Limb

• Less sensitive in ambulatory participants; To be reported at the end of the open-label period

NSAA

North Star Ambulatory

• Composite measure; Will be assessed at the end of the open-label period

TTR Velocity

Time to Rise (TTSTAND)

• Statistically significant improvement versus placebo demonstrated in Cohort 1

MAD portion of the study

Status Of Functional Measure

Collection and Readout

MAD

(18 weeks)

Open-Label

(~1 year)

OL – OLE*

(≥1 year)

Relevant Study

Period

Disease-modifying functional benefit seen at lowest dose

TTRV results

May 2026 22

*Analysis on TTRV versus placebo shown rather than TTR in order to maintain the study blind, Wilcoxon rank-sum (one sided) test, nominal p-values, post hoc analysis; MCID: “The

Minimal Clinical Important Difference (MCID) in Annual Rate of Change of Timed Function Tests in Boys with DMD," Duong T, Canbek J, Birkmeier M, Nelson L, Siener C, Fernandez-Fernandez A, Henricson E, McDonald CM, Gordish-Dressman H and the CINRG-DNHS Investigators; Journal of Neuromuscular Diseases. 2021;8(6):939–948; Updated from

previously disclosed topline data to reflect subsequently received information.

0.01

0.02

0.03

0.04

0.05

0.06

0.07

0.08

0.09

0.1

TTRV Improvement Versus Placebo MCID

• TTR is a pre-specified secondary endpoint in the

ELEVATE-44-201 study

• Change in TTR and in TTRV was seen across the

majority of treated participants, irrespective of age

• The mean change in TTRV versus placebo was 0.09,

~3.5x higher than the MCID threshold of 0.023

• End of Cohort 1 dystrophin levels correlated with the end

of Cohort 1 TTRV, suggesting that dystrophin production

may have crossed a critical threshold for functional

improvement

• The magnitude of the overall response supports the

hypothesis that Cohort 1’s functional benefit represents a

true drug-related effect

• In addition, 10MWR also demonstrated positive trends

versus placebo

Change in Time to Rise velocity

Versus Placebo (rises/second)

TTRV Improvement Versus Placebo*

p<0.05*

~3.5x MCID

Significant improvements in TTR and TTRV were observed*; TTRV is a widely accepted Phase 3

endpoint in DMD, with good statistical properties for evaluating motor function in patients

Key Takeaways

ENTR-601-44 delivered a differentiated impact on TTRV

TTRV is a validated registrational endpoint

May 2026 23

Sources: *VISION-DMD (JAMA 2022) registrational study; DELIVER (Dyne Company presentation); EMBARK (FDA Decisional Memo 2024); ENTR-601-44 (Cohort 1); No head-to-head trials have been conducted; Cross-trial comparisons may not be reliable based on differences in study designs, compound formulation and mechanism, patient

populations, etc.; **Supplement to original Phase 3 filing in U.S.

0.01

0.02

0.03

0.04

0.05

0.06

0.07

0.08

0.09

0.1

Vamorolone Elevidys Dyne 251 ENTR-601-44

TTRV Change from Baseline

Versus Placebo (rises/sec)

Reported TTRV Competitive Comparisons

• Phase 3 trials using TTRV as the primary endpoint: Novartis: del-zota, Phase 3 (initiating);

Solid Biosciences: SGT-003, Phase 3 (ongoing); Roche: Elevidys, Phase 3 (to initiate in EU)

Phase 2b* Phase 3** Phase 1/2

ENTR-601-44’s TTRV versus placebo is superior to reported numbers from steroids, gene therapy

and second-generation exon skipping therapies

Phase 1/2

ELEVATE-44-201:

Pharmacokinetics and Biomarkers

May 2026

Lower-than-expected plasma exposures resulted in lower-than-expected exon skipping and dystrophin expression

AUC: Area under the curve (proportions are approximate); 1.Healthy normal volunteer, single dose 6 mg/kg, 2.Pediatric DMD participants following third dose of 6 mg/kg every 6

weeks (similar, proportionally lower levels seen in juvenile NHP 55 week study); Note: As biopsies were taken 6 weeks post-final dose, muscle concentration levels were 10-fold

below projected peak, in line with plasma concentration and expectations.

Cmax (ng/mL) AUC (hr*ng/mL)

Adult (HNV) Pediatric (Cohort 1 patients)

Originally expected

participant exposures,

based on HNV1 and adult

NHP exposures

Actual participant

exposure observed2

4.58

5.40

4.00

6.36

0.00

1.00

2.00

3.00

4.00

5.00

6.00

7.00

Placebo

Baseline

Placebo D127 6 mg/kg

Baseline

6 mg/kg D127

Mean Percent MHC Normalized Dystrophin

1.34 1.76

2.66

4.97

0.00

1.00

2.00

3.00

4.00

5.00

6.00

Placebo

Baseline

Placebo D127 6 mg/kg

Baseline

6 mg/kg D127

Mean Percent Exon Skipping

Percent Exon Skipping Percent MHC Normalized

Dystrophin

2.31% Increase

2.36% Increase

Lower Cmax and AUC observed in pediatric participants when compared with healthy adults

~60% of Adult

~40% of Adult

Cmax (ng/mL)

A linear (or better) increase in exposure is expected in Cohort 2 at 12 mg/kg which should result in substantially

higher dystrophin levels and continued muscle function

ENTR-601-44:

Mechanistic Rationale

May 2026 Source: Servais L, et al. ICNMD 2026.

Healthy

muscle

The DMD challenge: Muscle damage and impaired repair

An ideal treatment is regenerative – replacing damaged, dystrophic muscle with healthy muscle;

This requires satellite cell correction which then promotes asymmetric differentiation

DMD muscle

lacking dystrophin

• Muscle fibers susceptible to damage

• Stem cells and regeneration impaired

• Muscle replaced with fat and scar tissue

• Dystrophin supports stabilizing and repairing muscle

fibers and stem cell replenishment and function The dystrophin “double hit” results in a decline

in function

• Lack of dystrophin results in muscle damage

• Lack of dystrophin also results in the inability to repair

and regenerate new fibers

• Lack of normal regeneration results in the replacement

of muscle with fat and fibrosis

Satellite (stem) cells require dystrophin to

efficiently promote muscle regeneration

• Deficit inhibits asymmetric differentiation and activation,

thus impairing regeneration

May 2026

Enhanced satellite cell activity would result in the regeneration of healthy fibers and the stabilization

of the overall muscle; In turn, this may convert into greater strength, as measured by TTRV

D2-mdx: Dystrophic mouse model; D2-mdx mice were treated with 3 IV doses of EEV-PMO administered every six weeks; Gastrocnemius was collected 12 weeks after the third

dose and analyzed by immunohistochemistry; Data presented at International Conference on Muscle Wasting 2025; CK: Creatine kinase; Q6W: Every 6 weeks.

Entrada differentiation

• Immunohistochemistry data demonstrates

PMO in satellite cells and newly regenerated

centrally nucleated fibers 12 weeks post-washout after 3 Q6W doses (D2-mdx mice)

Antibody and gene therapy competitors

• No transferrin receptor expressed on these cells

so the antibodies cannot reach them

• AAV-enabled gene therapies lack ability to

efficiently reach satellite cells which limits

response durability

Immunohistochemistry data demonstrates PMO in satellite cells and newly regenerated

centrally nucleated fibers 12-weeks post-washout after 3 Q6W doses (D2-mdx mice)

EEV-enabled stem cell uptake implies the potential for the

return of healthy muscle and function

Myotonic Dystrophy Type 1 (DM1)

May 2026 30

DM1 partnership established with Vertex in Q1 2023

• Entrada received an upfront payment of $224M and an equity investment of $26M upon initiation of the collaboration

• Agreement provided for up to $485M for the achievement of milestones

• Tiered royalties on future net sales

VX-670 differentiation

• Unlike antibody-based approaches, VX-670's targeted and specific blocking of pathogenic CUG repeats drives global transcriptome

correction while preserving healthy DMPK levels

• Satellite cell uptake may improve outcomes as CUG repeat length correlates with progenitor cell activation, proliferation and differentiation*

Vertex advancing a placebo-controlled Phase 1/2 clinical program at over 25 global sites

• MAD portion of the clinical study to assess safety and efficacy is on track to read out in the second half of 2026

• Open-label extension study is enrolling

• Same EEV utilized for VX-670 as in DMD franchise

DM1: A transformational partnership with Vertex

*Hasuike et al., Front. Genet., March 2022; MBNL: Muscleblind-like proteins; CUG repeat: Repeating sequence of cytosine, uracil and guanine in RNA; DMPK: Dystrophia

myotonica protein kinase.

No disease-modifying treatments are currently available for the more than 110,000 people in the U.S.

and Europe living with DM1

Inherited Retinal Diseases (IRDs)

Addressing areas of high unmet need in IRDs with new

oligonucleotide-based therapeutics

May 2026

Usher Syndrome Type 2A (USH2A)

• An inherited eye condition caused by changes in the USH2A gene

• In some patients, mutations in exon 13 prevent production of the

usherin protein

• Without usherin, photoreceptors (the light-sensing cells in the eye)

gradually degenerate

• Lack of usherin leads to vision loss in early adulthood and legal

blindness in mid-adulthood

• No disease-modifying treatments are currently available that

can slow or stop disease progression

About

ENTR-801

• Proprietary exon 13 skipping therapy designed to restore functional usherin protein production with the goal

of preserving photoreceptor health and function

• Demonstrated robust exon skipping and usherin protein production, with the potential for quarterly dosing IVT

• IND-enabling studies will be initiated and clinical strategies will be shared in 2026

• ~15,000 patients in the U.S. and Europe are exon 13 skipping amenable*

Note: IRD: Inherited Retinal Disorders; *Delmaghani et al., Hum Genet., Apr. 2022; Sanjurjo-Soriano et al., HGG Advance, Oct. 2023; Su et al., Front Aging Neurosci.,

Aug. 2022; IVT: Intravitreal. 32

Low Dose High Dose

Entrada’s first IRD clinical candidate, ENTR-801, will target Usher syndrome type 2A;

Addressable population is ~15,000 patients* in the U.S. and Europe with no approved therapeutics

Duration of Truncated Usherin Protein Generation

in phUSH2A WT Mice

2026 Inflection Points

May 2026

ELEVATE-44-201 Cohort 1 open-label functional data, Cohort 2 dystrophin and functional data and

ELEVATE-45-201 Cohort 1 data represent additional 2026 catalysts

• All ELEVATE-44-201 Cohort 1 participants have rolled over into the open-label portion of the study

▪ Placebo participants crossed over into treatment via the open-label period

▪ Company expects continued functional response with additional measurements collected during open-label period

▪ Completion of open-label period expected by year-end 2026

• ELEVATE-44-201 Cohort 2 at 12 mg/kg continues to enroll with readout expected by year-end 2026

▪ Higher levels of plasma and muscle exposure expected

▪ Concomitant increases in exon skipping and dystrophin production are expected

▪ Continued functional responses expected at higher doses

• ELEVATE-45-201 Cohort 1 at 5 mg/kg fully enrolled with readout expected in mid-2026

2026 inflection points

Note: All references in this presentation regarding planned regulatory filings and clinical study designs are subject to ongoing discussion with regulatory authorities; *Based on May 2026 current operating plans and ~$255M in cash, cash equivalents and marketable securities as of March 31, 2026. 35

VX-670

MAD portion of global

Phase 1/2 ongoing

Multiple 2026 near-term value drivers anticipated

across expanding pipeline of intracellular therapeutics

ENTR-601-45

Multiple clinical

study sites activated

in U.K. and EU

FPD with Cohort 1 data

expected mid-2026

ENTR-601-44

Global Phase 1/2 MAD

study ongoing

Cohort 1 data

demonstrated safety,

dystrophin production and

functional improvement

Cohort 2 data expected by

year-end 2026

ENTR-601-45

Global Phase 1/2 MAD

study ongoing

Cohort 1 data expected

mid-2026

VX-670

Vertex is on track to share

results in H2 2026

ENTR-601-51

Global regulatory filings

expected following a review

of data from the ongoing

DMD clinical studies

Cash runway

into Q3 2027*

ENTR-601-50

Received authorization for

Phase 1/2 MAD study (U.K.)

EU regulatory filing

expected following a review

of data from the ongoing

DMD clinical studies

ENTR-801

Initial IRD candidate focused

on Usher syndrome type 2A

Additional data and clinical

plans will be shared in 2026

Second IRD candidate

declaration in H2 2026

Pipeline Expansion

Next-generation EEVs for

neuromuscular expansion

Ocular expansion into

larger disease areas

Range of undisclosed

diseases and modalities

Appendix

EEV Platform

Understanding EEV endosomal escape advantages

May 2026 38

Unique pH-dependent membrane binding affinity enhances EEV endosomal escape

Sahni, A. et al. ACS Chem. Biol. 2021; CPP: Cell-penetrating peptide.

• EEVs have a higher affinity to phospholipids compared to traditional linear CPPs; The interaction of EEVs with phospholipids is pH-dependent

• The specific interaction of EEVs with the endosomal membrane facilitates the escape of EEVs from early endosomes, as demonstrated by

the correlation between endosomal escape efficiency and endosomal membrane binding affinity

This results in “Saddle Splay”

Binding of Arg-rich

peptides induces

negative curvature

Post

Collapse

DextranAlexa

Merge

EEV12TMR

Nucleation

Zones

Binding to

Endosome

Membrane

Budding

Positive

curvature Negative

curvature

Insertion of hydrophobic

groups induces positive

curvature

High Intracellular

Uptake

~90% uptake

Unique Budding Mechanism

Conserves endosomal integrity

pH 7.4

pH ~6.5

Efficient Endosomal Escape

~25-50-fold increase in endosomal

escape vs. other competitive approaches

Concept Mechanism Visualization

R6-PMO EEV-PMO

100

Exon Skipping (%)

• PMO sequences are the same, cell penetrating peptides are different (linear vs. cyclic)

• EEV-PMO significantly improved exon skipping after 3 days in mdx mice as compared

to competitive R6-PMO

EEV Optimization PMO Optimization

• EEVs are the same, PMO sequences are different (casimersen vs. Entrada proprietary)

• Proprietary PMO significantly improved exon skipping after 3 days in mdx mice as compared

to competitive casimersen sequence

May 2026

Entrada optimizes both the EEV delivery vehicle and the

active conjugate to create best-in-class medicines

*p<0.05, **p<0.01, ***p<0.001, ****p<0.0001; relative to saline; Concentrations provided are PMO equivalent; Data presented at 2024 World Muscle Society conference. 39

In the below DMD example, Entrada has optimized the EEV and the PMO sequence;

The data represents the superiority of each component against other approaches and sequences

Saline EEV-PMO45

(45 mg/kg) ENTR-601-45

(45 mg/kg)

100

Exon Skipping (%)

✱✱

✱✱✱✱

✱✱✱✱ Casimersen PMO Sequence Proprietary PMO Sequence

Casimersen PMO Sequence

Proprietary PMO Sequence

DMD Approach

Inflammation

Necrosis Fibrogenesis

Atrophy

Entrada addresses the underlying cause of DMD and

restores dystrophin in muscle fibers and muscle stem cells

May 2026 Adapted from Front. Cell Dev. Biol., 18 August 2021; Sec. Molecular and Cellular Pathology; Volume 9, 2021; 1.No other exon skippers nor gene therapy fit all the

disease-modifying criteria; 2.ENTR-601-44 data.

DMD Gene Mutation

Dysfunctional Dystrophin

Membrane Damage

Calcium

Dysregulation

Progenitor

Senescence

Oxidative

Stress

2. Supportive care agents only address downstream biology

• Myosin(i), AAK1(i), HDAC(i) may potentially enhance disease-modifying therapies and complement

dystrophin restoration

• Mechanisms include membrane protection/repair and stem cell proliferation

• Symptomatic care, led by steroids, have served as standard of care despite long-term tolerability and

safety concerns

1. Disease-modifying agents address the root cause of morbidity and mortality

• Double-digit high-quality dystrophin production protects healthy muscle and restores regenerative capacity

• Must be safe, potent, reach both mature and progenitor cells, be infrequently dosed, be redosable and

dosing is weight based to meet the needs of a growing child

• Entrada is developing the only disease-modifying agents with the potential to meet ALL of the above1

The Duchenne Disease Cascade Current and Emerging Treatment Options

Signaling Perturbation

Mitochondrial

Dysfunction

Entrada’s next-generation exon skippers

• Established safety at a therapeutic dose of 6 mg/kg with escalation to 12 mg/kg underway2

• Expected to provide durable and significant access to skeletal and cardiac muscle

• Target progenitor cells (satellite) needed to regenerate muscle and provide functional benefit

• Flexible to dose escalate and redose

Final Common Pathway

Competitive Comparison

Design

Dose

Uptake

Target

engagement

Anti-TfR1-mAb-PMO (exon 44)

Novartis/Avidity

Anti-TfR1-Fab-PMO (exon 51)

Dyne

Full-length antibody

~150 kDa

TfR1 specific deliver; Non-cleavable linker

Fragment antibody

~50 kDa

TfR1 specific delivery; Cleavable linker

Large conjugate doses

5 mg/kg PMO (registrational dose) +

~23 mg/kg mAb = ~28 mg/kg whole

drug dose1

Large conjugate doses

20 mg/kg PMO (registrational dose) +

undisclosed mg/kg Fab = undisclosed

mg/kg whole drug dose2

Apparent limit on dose response

No increase in dystrophin from 5 to 10 mg/kg

PMO dose in DMD exon 44 patients:

25% vs. 26%4,5

Apparent limit on dose response

No increase in dystrophin from 10 to 20

mg/kg PMO dose in DMD exon 51 patients:

2.97% vs. 3.14%2,4

No enhanced endosomal escape

Once dissociated from the mAb in the

lysosome, the unconjugated PMO escapes at

<2% efficiency6

No enhanced endosomal escape

Once dissociated from the Fab in the

endosome, the unconjugated PMO escapes

at <2% efficiency6

EEV therapies are expected to show superior dystrophin

production and dose-dependent increases in therapeutic index

May 2026 43

TfR1: Transferrin receptor 1; 1.Etxaniz et al., Nucleic Acid Res., 2025; 2.Dyne corporate materials from DELIVER Clinical Update investor call September 2025; 3.Total mean exon

skipping; Entrada internal data from Phase 1 SAD study of ENTR-601-44 in HNV; 4.Unadjusted dystrophin, mean change from baseline; 5.Avidity corporate materials from del-zota

Topline Data investor call March 2025; 6.Dowdy et al., Nucleic Acid Ther., 2022.

EEV-PMO

Entrada

Cyclic, arginine-light peptide

2.6 kDa

Tissue-specific delivery; Increases stability and half-life

Low conjugate doses

~5 mg/kg PMO + 1 mg/kg EEV = 6 mg/kg

whole drug (ELEVATE-44-201 Cohort 1 dose)

No limit on dose response seen

48.3% increase in exon skipping from 3 to 6

mg/kg whole drug dose in HNV3

Enhanced endosomal escape

~25-fold increase in endosomal escape vs.

other competitive approaches

A 25-50-fold improvement in endosomal escape, novel PMO sequences, non-linear increases in

PK/PD, satellite cell uptake and lower whole drug requirements compared to antibody-based therapies

Pharmacokinetic Modeling

May 2026

Lower Cmax and AUC observed in juvenile humans and NHPs; A linear (or better) increase in

exposure is expected in Cohort 2 at 12 mg/kg (double dose = double exposure)

Predictive pharmacokinetics

*Healthy normal volunteer, single dose 6mg/kg, pediatric DMD patients following third dose; **Adult: 13-week 25 mg/kg repeat dose study, Q6W, 3 doses; Juvenile: 55-week 20

mg/kg repeat dose study, Q6W,10 doses.

Cmax (ng/mL) AUC (hr*ng/mL)

Adult (HNV) Juvenile (Cohort 1 patients)

Human (HNVs and Patients)*

Cmax (ng/mL) AUC (hr*ng/mL)

Adult (NHP) Juvenile (NHP)

Non-Human Primate**

~60% of Adult

~40% of Adult ~50% of Adult

~50% Adult

Proportional Difference

(Juvenile = ~60% of Adult)

Cmax (ng/mL) Cmax (ng/mL)

May 2026 46

Juvenile NHP Plasma Concentration and Exon Skipping

Expected AUC in

Cohort 1

• Juvenile NHP data suggest a right-shifted

double-digit dystrophin expectation

starting at 12 mg/kg in Cohort 2

• As the exposure to exon skipping

relationship has not changed, updated

projections indicate significantly increased

exon skipping and dystrophin expression

expected in Cohorts 2 and 3

• Cohorts 2 and 3 dystrophin levels will be

assessed for registrational potential,

when combined with observed

functional outcomes

NHP data from 55 weeks, QW6, 10 doses, chronic juvenile toxicology study.

Cohort 1

Participant Data

Extrapolation

Juvenile NHP data suggest an increase of AUC should result in substantially higher dystrophin levels

and increases in muscle function

Improved, predictive modeling based on new data point to

higher dystrophin levels in Cohorts 2 and 3

Cohort 2 Model

Cohort 3 Model

% Exon Skipping

Plasma Concentration

(AUC, hr*ng/mL)

10%

20%

30%

40%

50%

60%

70%

20,000

40,000

60,000

80,000

100,000

120,000

5 mg/kg 20 mg/kg 30 mg/kg

Expected AUC in

Cohort 1

DMD Functional Data

Preclinical Models

Preclinical data support potential for best-in-class clinical

profile for ENTR-601-45

May 2026 48 Data are shown as mean ± SD; *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001; 25 mg/kg correlates to ~5 mg/kg human equivalent dose (HED), 50 mg/kg correlates to ~10 mg/kg

HED, 75 mg/kg correlates to ~15 mg/kg HED; Data presented at the 2024 World Muscle Society conference.

• Active and vehicle del44hDMD.mdx mice, n=5 per cohort, EEV-PMO-45 (Q6W x 3 doses); Control saline treated hDMD.mdx mice, n=10 (Q6W x 3 doses)

• Skipping (ddPCR) and dystrophin production (JESS) is significantly increased 6 weeks after the third dose of ENTR-601-45 (gastrocnemius muscle shown)

Exon Skipping Dystrophin Restoration Functional Correction

ENTR-601-45

100

kip

****

Dose in mg/kg

100

stro

hin

storatio

n (%)

orm

alize

d to

D.m

****

** *

Dose in mg/kg

100

stro

hin

sitiv

Fib

ers

****

Dose in mg/kg

100 ****

****

***

Dose in mg/kg

Dose-dependent increase in exon skipping and dystrophin expression correlates to complete

functional correction

% Force before injury

Dose-dependent and durable improvements in muscle

function observed in del44hDMD.mdx mice

May 2026 49

del44hDMD.mdx mice were treated with three Q6W IV injections of ENTR-601-45 or vehicle; ECC-induced muscle force loss generated by repeated eccentric force (ECC) contraction of the gastrocnemius muscle was assessed 5

weeks (left/center) or 4 and 8 weeks (right) after the third dose; Data (mean ± standard deviation) shown across 10 ECC contractions normalized into a percentage of the initial force before any ECC contractions and as the percentage

of force retained after the tenth contraction; Vehicle-treated hDMD.mdx mice were used as a control group for normal muscle function; One-way ANOVA (Analysis of variance) was used for statistical comparison to vehicle-treated

del44hDMD.mdx mice; **p < 0.01, ***p < 0.001, ****p < 0.0001 vs. vehicle; Data presented at the 2024 World Muscle Society conference.

Skeletal Muscle Membrane Stability Stability After Washout

ENTR-601-45

Dose-dependent increase in percent force retention following 10 contractions; Increase maintained

for at least 8 weeks after the third Q6W dose of ENTR-601-45

% Force before injury

Efficacy of ENTR-601-50 in exon 50 skipping amenable mice

Single dose of ENTR-601-50 produced robust human DMD exon 50 skipping and dystrophin;

Translated into improvements in muscle function within 2 weeks post-dose

ENTR-601-50

Exon Skipping and Dystrophin in the Gastrocnemius Percent Force After 10 Contractions

del51hDMD.mdx mice were treated with a single IV injection of ENTR-601-50 or vehicle. Human DMD exon 50 skipping (top) and dystrophin protein expression (bottom) were analyzed in the gastrocnemius, diaphragm and heart 2

weeks post-dose; Percent dystrophin protein restoration is normalized to total protein and normalized to hDMD.mdx controls; Data shown as mean ± standard deviation; One-way ANOVA was used for statistical comparison; ECC-induced muscle force loss generated by repeated ECC contraction of the gastrocnemius muscle was assessed 2 weeks after dosing. Data (mean ± standard deviation) are shown across ten ECC contractions normalized as the

percentage of force retained after the tenth contraction; Data presented at the 2025 World Muscle Society conference; IV: Intravenous.

May 2026 50

100

150

orc

efore injury

✱✱✱✱

✱✱

✱✱✱✱

del51hDMD.mdx mice

Vehicle 25 45

stro

hin re

storatio

n (%)

orm

aliz

d to

m. dx

del51hDMD.mdx mice

****

Vehicle 25 45

kip

del51hDMD.mdx mice

****

45 mg/kg ENTR-601-50

25 mg/kg ENTR-601-50

del51hDMD.mdx vehicle

45 mg/kg ENTR-601-50

25 mg/kg ENTR-601-50

del51hDMD.mdx vehicle

***

ENTR-601-50_45 mg/kg

ENTR-601-50_25 mg/kg

ENTR-601-50_15 mg/kg

del51hDMD.mdx vehicle

hDMD.mdx vehicle

Learn more at

EntradaTx.com

GRAPHIC

Filename: tm2614944d1_ex99-1img001.jpg · Sequence: 3

Binary file (198973 bytes)

Download tm2614944d1_ex99-1img001.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img002.jpg · Sequence: 4

Binary file (423423 bytes)

Download tm2614944d1_ex99-1img002.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img003.jpg · Sequence: 5

Binary file (215957 bytes)

Download tm2614944d1_ex99-1img003.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img004.jpg · Sequence: 6

Binary file (226766 bytes)

Download tm2614944d1_ex99-1img004.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img005.jpg · Sequence: 7

Binary file (139787 bytes)

Download tm2614944d1_ex99-1img005.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img006.jpg · Sequence: 8

Binary file (111251 bytes)

Download tm2614944d1_ex99-1img006.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img007.jpg · Sequence: 9

Binary file (241495 bytes)

Download tm2614944d1_ex99-1img007.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img008.jpg · Sequence: 10

Binary file (211164 bytes)

Download tm2614944d1_ex99-1img008.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img009.jpg · Sequence: 11

Binary file (188099 bytes)

Download tm2614944d1_ex99-1img009.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img010.jpg · Sequence: 12

Binary file (79743 bytes)

Download tm2614944d1_ex99-1img010.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img011.jpg · Sequence: 13

Binary file (242258 bytes)

Download tm2614944d1_ex99-1img011.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img012.jpg · Sequence: 14

Binary file (85569 bytes)

Download tm2614944d1_ex99-1img012.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img013.jpg · Sequence: 15

Binary file (207332 bytes)

Download tm2614944d1_ex99-1img013.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img014.jpg · Sequence: 16

Binary file (121217 bytes)

Download tm2614944d1_ex99-1img014.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img015.jpg · Sequence: 17

Binary file (77063 bytes)

Download tm2614944d1_ex99-1img015.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img016.jpg · Sequence: 18

Binary file (141672 bytes)

Download tm2614944d1_ex99-1img016.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img017.jpg · Sequence: 19

Binary file (152818 bytes)

Download tm2614944d1_ex99-1img017.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img018.jpg · Sequence: 20

Binary file (81139 bytes)

Download tm2614944d1_ex99-1img018.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img019.jpg · Sequence: 21

Binary file (188771 bytes)

Download tm2614944d1_ex99-1img019.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img020.jpg · Sequence: 22

Binary file (257803 bytes)

Download tm2614944d1_ex99-1img020.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img021.jpg · Sequence: 23

Binary file (636168 bytes)

Download tm2614944d1_ex99-1img021.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img022.jpg · Sequence: 24

Binary file (210771 bytes)

Download tm2614944d1_ex99-1img022.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img023.jpg · Sequence: 25

Binary file (143318 bytes)

Download tm2614944d1_ex99-1img023.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img024.jpg · Sequence: 26

Binary file (83598 bytes)

Download tm2614944d1_ex99-1img024.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img025.jpg · Sequence: 27

Binary file (175314 bytes)

Download tm2614944d1_ex99-1img025.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img026.jpg · Sequence: 28

Binary file (77341 bytes)

Download tm2614944d1_ex99-1img026.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img027.jpg · Sequence: 29

Binary file (196911 bytes)

Download tm2614944d1_ex99-1img027.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img028.jpg · Sequence: 30

Binary file (228051 bytes)

Download tm2614944d1_ex99-1img028.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img029.jpg · Sequence: 31

Binary file (109193 bytes)

Download tm2614944d1_ex99-1img029.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img030.jpg · Sequence: 32

Binary file (185205 bytes)

Download tm2614944d1_ex99-1img030.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img031.jpg · Sequence: 33

Binary file (109928 bytes)

Download tm2614944d1_ex99-1img031.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img032.jpg · Sequence: 34

Binary file (221119 bytes)

Download tm2614944d1_ex99-1img032.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img033.jpg · Sequence: 35

Binary file (70070 bytes)

Download tm2614944d1_ex99-1img033.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img034.jpg · Sequence: 36

Binary file (163015 bytes)

Download tm2614944d1_ex99-1img034.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img035.jpg · Sequence: 37

Binary file (192418 bytes)

Download tm2614944d1_ex99-1img035.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img036.jpg · Sequence: 38

Binary file (64018 bytes)

Download tm2614944d1_ex99-1img036.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img037.jpg · Sequence: 39

Binary file (65814 bytes)

Download tm2614944d1_ex99-1img037.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img038.jpg · Sequence: 40

Binary file (195742 bytes)

Download tm2614944d1_ex99-1img038.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img039.jpg · Sequence: 41

Binary file (161310 bytes)

Download tm2614944d1_ex99-1img039.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img040.jpg · Sequence: 42

Binary file (66397 bytes)

Download tm2614944d1_ex99-1img040.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img041.jpg · Sequence: 43

Binary file (242460 bytes)

Download tm2614944d1_ex99-1img041.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img042.jpg · Sequence: 44

Binary file (71712 bytes)

Download tm2614944d1_ex99-1img042.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img043.jpg · Sequence: 45

Binary file (243549 bytes)

Download tm2614944d1_ex99-1img043.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img044.jpg · Sequence: 46

Binary file (72412 bytes)

Download tm2614944d1_ex99-1img044.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img045.jpg · Sequence: 47

Binary file (122364 bytes)

Download tm2614944d1_ex99-1img045.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img046.jpg · Sequence: 48

Binary file (156904 bytes)

Download tm2614944d1_ex99-1img046.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img047.jpg · Sequence: 49

Binary file (77645 bytes)

Download tm2614944d1_ex99-1img047.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img048.jpg · Sequence: 50

Binary file (166809 bytes)

Download tm2614944d1_ex99-1img048.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img049.jpg · Sequence: 51

Binary file (181420 bytes)

Download tm2614944d1_ex99-1img049.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img050.jpg · Sequence: 52

Binary file (173185 bytes)

Download tm2614944d1_ex99-1img050.jpg

GRAPHIC

Filename: tm2614944d1_ex99-1img051.jpg · Sequence: 53

Binary file (165345 bytes)

Download tm2614944d1_ex99-1img051.jpg

XML — IDEA: XBRL DOCUMENT

XML

Filename: R1.htm · Sequence: 58

v3.26.1

Cover

May 18, 2026

Cover [Abstract]

Document Type

8-K

Amendment Flag

false

Document Period End Date

May 18, 2026

Entity File Number

001-40969

Entity Registrant Name

ENTRADA

THERAPEUTICS, INC.

Entity Central Index Key

0001689375

Entity Tax Identification Number

81-3983399

Entity Incorporation, State or Country Code

Entity Address, Address Line One

One Design Center Place

Entity Address, Address Line Two

Suite 17-500

Entity Address, City or Town

Boston

Entity Address, State or Province

Entity Address, Postal Zip Code

02210

City Area Code

857

Local Phone Number

520-9158

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

TRDA

Security Exchange Name

NASDAQ

Entity Emerging Growth Company

true

Elected Not To Use the Extended Transition Period

false

- Definition

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

+ References

No definition available.

+ Details

Name:

dei_AmendmentFlag

Namespace Prefix:

dei_

Data Type:

xbrli:booleanItemType

Balance Type:

Period Type:

duration

- Definition

Area code of city

+ References

No definition available.

+ Details

Name:

dei_CityAreaCode

Namespace Prefix:

dei_

Data Type:

xbrli:normalizedStringItemType

Balance Type:

Period Type:

duration

- Definition

Cover page.

+ References

No definition available.

+ Details

Name:

dei_CoverAbstract

Namespace Prefix:

dei_

Data Type:

xbrli:stringItemType

Balance Type:

Period Type:

duration

- Definition

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.

+ References

No definition available.

+ Details

Name:

dei_DocumentPeriodEndDate

Namespace Prefix:

dei_

Data Type:

xbrli:dateItemType

Balance Type:

Period Type:

duration

- 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'.

+ References

No definition available.

+ Details

Name:

dei_DocumentType

Namespace Prefix:

dei_

Data Type:

dei:submissionTypeItemType

Balance Type:

Period Type:

duration

- Definition

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

+ References

No definition available.

+ Details

Name:

dei_EntityAddressAddressLine1

Namespace Prefix:

dei_

Data Type:

xbrli:normalizedStringItemType

Balance Type:

Period Type:

duration

- Definition

Address Line 2 such as Street or Suite number

+ References

No definition available.

+ Details

Name:

dei_EntityAddressAddressLine2

Namespace Prefix:

dei_

Data Type:

xbrli:normalizedStringItemType

Balance Type:

Period Type:

duration

- Definition

Name of the City or Town

+ References

No definition available.

+ Details

Name:

dei_EntityAddressCityOrTown

Namespace Prefix:

dei_

Data Type:

xbrli:normalizedStringItemType

Balance Type:

Period Type:

duration

- Definition

Code for the postal or zip code

+ References

No definition available.

+ Details

Name:

dei_EntityAddressPostalZipCode

Namespace Prefix:

dei_

Data Type:

xbrli:normalizedStringItemType

Balance Type:

Period Type:

duration

- Definition

Name of the state or province.

+ References

No definition available.

+ Details

Name:

dei_EntityAddressStateOrProvince

Namespace Prefix:

dei_

Data Type:

dei:stateOrProvinceItemType

Balance Type:

Period Type:

duration

- 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

+ Details

Name:

dei_EntityCentralIndexKey

Namespace Prefix:

dei_

Data Type:

dei:centralIndexKeyItemType

Balance Type:

Period Type:

duration

- Definition

Indicate if registrant meets the emerging growth company criteria.

+ References

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

-Publisher SEC

-Name Exchange Act

-Number 240

-Section 12

-Subsection b-2

+ Details

Name:

dei_EntityEmergingGrowthCompany

Namespace Prefix:

dei_

Data Type:

xbrli:booleanItemType

Balance Type:

Period Type:

duration

- Definition

Indicate if an emerging growth company has elected not to use the extended transition period for complying with any new or revised financial accounting standards.

+ References

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

-Publisher SEC

-Name Securities Act

-Number 7A

-Section B

-Subsection 2

+ Details

Name:

dei_EntityExTransitionPeriod

Namespace Prefix:

dei_

Data Type:

xbrli:booleanItemType

Balance Type:

Period Type:

duration

- 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.

+ References

No definition available.

+ Details

Name:

dei_EntityFileNumber

Namespace Prefix:

dei_

Data Type:

dei:fileNumberItemType

Balance Type:

Period Type:

duration

- Definition

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

+ References

No definition available.

+ Details

Name:

dei_EntityIncorporationStateCountryCode

Namespace Prefix:

dei_

Data Type:

dei:edgarStateCountryItemType

Balance Type:

Period Type:

duration

- Definition

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

+ References

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

-Publisher SEC

-Name Exchange Act

-Number 240

-Section 12

-Subsection b-2

+ Details

Name:

dei_EntityRegistrantName

Namespace Prefix:

dei_

Data Type:

xbrli:normalizedStringItemType

Balance Type:

Period Type:

duration

- Definition

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

+ References

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

-Publisher SEC

-Name Exchange Act

-Number 240

-Section 12

-Subsection b-2

+ Details

Name:

dei_EntityTaxIdentificationNumber

Namespace Prefix:

dei_

Data Type:

dei:employerIdItemType

Balance Type:

Period Type:

duration

- Definition

Local phone number for entity.

+ References

No definition available.

+ Details

Name:

dei_LocalPhoneNumber

Namespace Prefix:

dei_

Data Type:

xbrli:normalizedStringItemType

Balance Type:

Period Type:

duration

- 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

+ Details

Name:

dei_PreCommencementIssuerTenderOffer

Namespace Prefix:

dei_

Data Type:

xbrli:booleanItemType

Balance Type:

Period Type:

duration

- 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.

+ References

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

-Publisher SEC

-Name Exchange Act

-Number 240

-Section 14d

-Subsection 2b

+ Details

Name:

dei_PreCommencementTenderOffer

Namespace Prefix:

dei_

Data Type:

xbrli:booleanItemType

Balance Type:

Period Type:

duration

- Definition

Title of a 12(b) registered security.

+ References

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

-Publisher SEC

-Name Exchange Act

-Number 240

-Section 12

-Subsection b

+ Details

Name:

dei_Security12bTitle

Namespace Prefix:

dei_

Data Type:

dei:securityTitleItemType

Balance Type:

Period Type:

duration

- Definition

Name of the Exchange on which a security is registered.

+ References

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

-Publisher SEC

-Name Exchange Act

-Number 240

-Section 12

-Subsection d1-1

+ Details

Name:

dei_SecurityExchangeName

Namespace Prefix:

dei_

Data Type:

dei:edgarExchangeCodeItemType

Balance Type:

Period Type:

duration

- 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

-Number 240

-Section 14a

-Subsection 12

+ Details

Name:

dei_SolicitingMaterial

Namespace Prefix:

dei_

Data Type:

xbrli:booleanItemType

Balance Type:

Period Type:

duration

- Definition

Trading symbol of an instrument as listed on an exchange.

+ References

No definition available.

+ Details

Name:

dei_TradingSymbol

Namespace Prefix:

dei_

Data Type:

dei:tradingSymbolItemType

Balance Type:

Period Type:

duration

- 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.

+ References

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

-Publisher SEC

-Name Securities Act

-Number 230

-Section 425

+ Details

Name:

dei_WrittenCommunications

Namespace Prefix:

dei_

Data Type:

xbrli:booleanItemType

Balance Type:

Period Type:

duration