US Patent 11,690,853 Scope and Claims: Methods for Treating Muscular Dystrophy via EF/FS Improvement at ≥2 mg/kg/day

US 11,690,853 covers a tightly defined therapeutic method: treating muscular dystrophy by administering an unspecified “compound” (defined only by a structural formula and salts) at a daily dose at or above 2 mg/kg/day, where treatment is evidenced by improved cardiac performance endpoints, specifically increased ejection fraction (EF) and increased fraction shortening (FS), measured by echocardiography, with oral dosing and treatment duration at least about 8 weeks appearing in dependent claims.

The claim set is narrow on indication framing and outcome metrics (EF/FS) but broad in muscular dystrophy subtype coverage (multiple dystrophies), delivery route (oral in dependent claims), and evidentiary method (echocardiography in a dependent claim). The enforceable “center of gravity” is the combination of (i) muscular dystrophy treatment, (ii) ≥2 mg/kg/day exposure, and (iii) post-treatment EF and FS improvements.

What does US 11,690,853 claim: a method that improves ejection fraction and fraction shortening in muscular dystrophy?

Core independent claim construct (Claim 1).
Claim 1 is structured as a classic therapeutic method claim with:

Condition: muscular dystrophy
Activity: administering a “therapeutically effective amount” of the claimed compound (or salt)
Dose floor: therapeutically effective amount is ≥ 2 mg/kg/day
Outcome framing: method is “treating or reducing symptoms” by increasing EF and increasing FS in a patient

Outcome endpoints are integral to infringement.
The claim language ties treatment success to physiologic measures:

EF increase
FS increase Those endpoints are not merely background; they define the method’s functional result. A system that administers the compound at ≥2 mg/kg/day without EF/FS improvement would have a weaker fit to the literal claim language.

Structural definition of the compound is claim-limiting but not reproduced in your text.
Claim 1 limits the “compound” to one having the “structural formula or a salt thereof.” Without the chemical structure in the prompt, the scope analysis below focuses on claim architecture and required elements rather than identifying the exact chemical identity.

How broad is muscular dystrophy coverage under Claim 1 vs dependent claims? (Claim 2-3)

Claim 2 (subtype sweep). It enumerates multiple muscular dystrophies:

Duchenne
Becker
limb girdle
congenital
facioscapulohumeral
myotonic
oculopharyngeal
distal
Emery-Dreifuss

This is a multi-indication, multi-genotype list that can support enforcement across many orphan and non-orphan muscular dystrophy programs, assuming the clinical population shows the EF/FS improvement after dosing.

Claim 3 locks to Duchenne.
Claim 3 narrows Claim 2 to Duchenne muscular dystrophy.

Practical scope effect.

If an accused regimen targets Duchenne only, it can still fall within the broader Claim 1 if the method elements are met, but Claim 3 provides a more specific target.
If an accused program targets other dystrophies in the list, Claim 2 provides coverage, and Claim 1 can serve as the independent hook.

What symptoms does the claim require: cardiac metrics rather than muscular symptoms? (Claim 4)

Claim 4 specifies symptoms from this set:

muscle wasting
muscle degeneration
muscle inflammation
decreased EF
decreased FS

This creates two layers:

The independent claim already frames improvement as EF and FS increases.
Claim 4 makes explicit that the symptoms include decreased EF/FS, tying muscular dystrophy symptomatology to cardiac function metrics.

Litigation implication.
The symptom list can be used to argue that EF/FS reductions are a defined “symptom” of muscular dystrophy for purposes of the method. That supports a position that EF/FS improvements are part of “treating or reducing symptoms.”

Does the claim require echocardiographic measurement? (Claim 5)

Claim 5 states EF and FS improvements are measured by echocardiography.

Scope consequence.

Claim 1, by itself, does not force echocardiography as the measurement method.
Claim 5 adds that requirement as a dependent limitation.
If an accused study uses an alternative cardiac imaging modality, Claim 5 would be harder to match, but Claim 1 could still be asserted if the endpoints are nevertheless EF and FS in substance and result.

Dose floor and “therapeutically effective amount”: what does that mean for design-around?

Claim 1 requires the therapeutically effective amount to be ≥2 mg/kg/day.

Design-around pressure points.

A regimen at <2 mg/kg/day is outside the literal dose floor.
But “therapeutically effective amount” is typically context-dependent. Still, the claim makes the threshold explicit, so accused products attempting to hit clinical effect below 2 mg/kg/day can argue non-infringement on dose limitation.

Do not confuse formulation dose with patient dose.
The claim is patient-dose framed: mg/kg/day. That is typically governed by actual administered dose, not theoretical dose.

Oral administration and duration: how restrictive are Claim 6 and Claim 7?

Claim 6: compound administered orally
Claim 7: administration duration of at least about eight weeks

These are dependent claims. They do not limit Claim 1 or Claim 8 unless those dependents are asserted. They create additional pathways to infringement in programs that use oral dosing and trial durations consistent with at least ~8 weeks.

How does Claim 8 expand the method: includes oral administration plus measured improvement post-dosing?

Claim 8 is another method claim that adds the following structural elements:

Oral administration (explicit in Claim 8)
Dose floor again: ≥2 mg/kg/day
Outcome after administration: patient has improved EF and FS as measured by echocardiography

Claim 8 therefore operationalizes the method: it requires both administration route and post-dosing measurement framing.

Relationship to Claim 1.

Claim 1 is broader (no explicit oral requirement, no explicit “post administration” wording, and echocardiography only via dependent Claim 5).
Claim 8 is narrower but more evidentiary: it hardwires oral dosing and echocardiographic measurement into the independent claim text.

Subtypes and symptoms in Claim 9-11: same enumeration, same cardiac functional endpoints

Claim 9: dystrophy chosen from the same nine subtypes
Claim 10: Duchenne
Claim 11: symptoms chosen from the same symptom set (including decreased EF/FS)

Route and duration in Claim 12-13: oral and ≥8 weeks again

Claim 12: oral administration
Claim 13: duration at least about eight weeks

Again, those are dependent limitations within the Claim 8 family.

What is the practical claim scope for enforcement: which elements must match in an accused muscular dystrophy program?

A simplified infringement-fit checklist, focused on literal claim elements:

Minimum elements likely required for any asserted claim (Claim 1 / Claim 8 family):

Patient has muscular dystrophy (one of the stated types if asserted via dependent claims)
Treatment is performed by administering a compound with the claimed structural formula or a salt
Dose administered is ≥2 mg/kg/day
The method results in increased EF and increased FS
In Claim 8 family, oral dosing and echocardiographic measurement are required by the claim structure

Additional elements if asserted via dependents:

Echocardiography measurement (Claim 5 or Claim 8)
Oral administration (Claim 6 or Claim 8/12)
Treatment duration ≥ about 8 weeks (Claim 7 or Claim 13)
Specific dystrophy subtype matching (Claims 2-3 and 9-10)
Symptom framing (Claims 4 and 11)

How strong is US 11,690,853 as a patent estate for muscular dystrophy cardiac outcomes (EF/FS)?

Based on claim architecture alone, the patent’s strength trends toward high enforceability against clinical regimens that are designed to show cardiac functional improvement in muscular dystrophy at or above a defined dose.

Why the claim is enforceable when programs track trial endpoints:

Drug developers often align trial endpoints with clinically meaningful metrics like EF/FS.
If a clinical protocol includes echocardiography and reports EF/FS improvements, it becomes easier to map results back to the method claims.

Key vulnerability vectors:

Programs that use the compound for muscular dystrophy without EF/FS endpoints (or without showing improvement) can reduce literal claim mapping.
Dosing below 2 mg/kg/day creates a clean non-infringement argument.
Use of non-oral route avoids Claim 6/12 but does not avoid Claim 1 unless the broader claim is also used without oral limitations.
If measurement is performed by methods that do not operationalize EF and FS as claimed, evidentiary disputes may arise.

What formulation and compound-scope limits exist: is the patent about a specific drug entity or just a method using a compound?

The claim text is method-focused and references the compound only by a structural formula and salts, without additional formulation limitations (e.g., excipients, crystalline form, salt polymorph, dosing regimen beyond dose floor, oral dosage form details).

So US 11,690,853 is best read as:

a compound-anchored method claim, not a formulation patent in the typical sense
with infringement primarily tied to administration and clinical outcomes

If a company uses the same compound (or salt within the defined scope), the method claims can still be implicated regardless of formulation details, unless formulation changes are used to change dose delivered, route, or duration below claim thresholds.

What patent landscape could be surrounding this method: how does a EF/FS muscular dystrophy claim typically position against earlier or later IP?

Even without the file wrapper text, this claim set suggests a landscape where:

Earlier patents may have covered the compound itself (chemical entity, salts, and general therapeutic use).
Later patents may focus on specific disease settings and specific clinical endpoints like EF/FS.

US 11,690,853 appears tailored to capture competitive activity where EF/FS improvements are demonstrated in muscular dystrophy populations. This style of drafting often complements:

method-of-use patents that broaden beyond one dystrophy subtype
cardiac function endpoint-driven patents that distinguish from generic muscular dystrophy treatment claims

Because you provided only the claims text and not the patent’s specification, priority data, assignees, or citations, a complete “landscape” mapping to specific related US applications and families cannot be produced here.

Key Takeaways

US 11,690,853 covers a method of treating muscular dystrophy by administering a specific compound (structural formula or salt) at ≥2 mg/kg/day to increase ejection fraction (EF) and fraction shortening (FS).
Claim 2 and Claim 9 expand coverage across nine muscular dystrophy subtypes, with Duchenne singled out in Claims 3 and 10.
Echocardiography is an explicit requirement in the dependent Claim 5 and in Claim 8’s post-treatment framing.
Oral administration and ≥about 8 weeks are covered as dependent limitations (Claim 6-7 and Claim 12-13), enabling layered enforcement depending on accused protocols.
The enforceable “center of gravity” is the combination of dose floor + EF/FS improvement + muscular dystrophy treatment, with claim strength highest when clinical protocols measure EF/FS by echocardiography.

FAQs

1) Does US 11,690,853 require the compound to be administered orally?
No for Claim 1. Oral administration is required for Claim 6 and Claim 8/12, but Claim 1 is not limited to oral dosing.

2) Is echocardiography required for every claim in the patent?
No. Echocardiography is explicitly required in Claim 5 and Claim 8’s post-administration measurement language.

3) What is the lowest dose permitted by the claims?
The claims require a therapeutically effective amount of ≥2 mg/kg/day.

4) Which muscular dystrophy types are enumerated in the claim set?
Duchenne, Becker, limb girdle, congenital, facioscapulohumeral, myotonic, oculopharyngeal, distal, and Emery-Dreifuss muscular dystrophy.

5) Can a provider avoid infringement by changing imaging methods used to assess EF/FS?
Changing imaging methods may avoid dependent claims that require echocardiography (e.g., Claim 5/Claim 8), but the broader claims still require EF and FS increases as functional outcomes.

References

United States Patent No. 11,690,853.

Title:	Non-hormonal steroid modulators of NF-κβ for treatment of disease
Abstract:	The present invention relates to compounds and methods which may be useful as treatments of diseases.
Inventor(s):	John M. McCall, Eric Hoffman, Kanneboyina Nagaraju, Jesse Damsker
Assignee:	Reveragen Biopharma Inc
Application Number:	US17/008,237
Patent Claim Types: see list of patent claims	Use; Delivery; Dosage form;
Patent landscape, scope, and claims:	US Patent 11,690,853 Scope and Claims: Methods for Treating Muscular Dystrophy via EF/FS Improvement at ≥2 mg/kg/day US 11,690,853 covers a tightly defined therapeutic method: treating muscular dystrophy by administering an unspecified “compound” (defined only by a structural formula and salts) at a daily dose at or above 2 mg/kg/day, where treatment is evidenced by improved cardiac performance endpoints, specifically increased ejection fraction (EF) and increased fraction shortening (FS), measured by echocardiography, with oral dosing and treatment duration at least about 8 weeks appearing in dependent claims. The claim set is narrow on indication framing and outcome metrics (EF/FS) but broad in muscular dystrophy subtype coverage (multiple dystrophies), delivery route (oral in dependent claims), and evidentiary method (echocardiography in a dependent claim). The enforceable “center of gravity” is the combination of (i) muscular dystrophy treatment, (ii) ≥2 mg/kg/day exposure, and (iii) post-treatment EF and FS improvements. What does US 11,690,853 claim: a method that improves ejection fraction and fraction shortening in muscular dystrophy? Core independent claim construct (Claim 1). Claim 1 is structured as a classic therapeutic method claim with: Condition: muscular dystrophy Activity: administering a “therapeutically effective amount” of the claimed compound (or salt) Dose floor: therapeutically effective amount is ≥ 2 mg/kg/day Outcome framing: method is “treating or reducing symptoms” by increasing EF and increasing FS in a patient Outcome endpoints are integral to infringement. The claim language ties treatment success to physiologic measures: EF increase FS increase Those endpoints are not merely background; they define the method’s functional result. A system that administers the compound at ≥2 mg/kg/day without EF/FS improvement would have a weaker fit to the literal claim language. Structural definition of the compound is claim-limiting but not reproduced in your text. Claim 1 limits the “compound” to one having the “structural formula or a salt thereof.” Without the chemical structure in the prompt, the scope analysis below focuses on claim architecture and required elements rather than identifying the exact chemical identity. How broad is muscular dystrophy coverage under Claim 1 vs dependent claims? (Claim 2-3) Claim 2 (subtype sweep). It enumerates multiple muscular dystrophies: Duchenne Becker limb girdle congenital facioscapulohumeral myotonic oculopharyngeal distal Emery-Dreifuss This is a multi-indication, multi-genotype list that can support enforcement across many orphan and non-orphan muscular dystrophy programs, assuming the clinical population shows the EF/FS improvement after dosing. Claim 3 locks to Duchenne. Claim 3 narrows Claim 2 to Duchenne muscular dystrophy. Practical scope effect. If an accused regimen targets Duchenne only, it can still fall within the broader Claim 1 if the method elements are met, but Claim 3 provides a more specific target. If an accused program targets other dystrophies in the list, Claim 2 provides coverage, and Claim 1 can serve as the independent hook. What symptoms does the claim require: cardiac metrics rather than muscular symptoms? (Claim 4) Claim 4 specifies symptoms from this set: muscle wasting muscle degeneration muscle inflammation decreased EF decreased FS This creates two layers: The independent claim already frames improvement as EF and FS increases. Claim 4 makes explicit that the symptoms include decreased EF/FS, tying muscular dystrophy symptomatology to cardiac function metrics. Litigation implication. The symptom list can be used to argue that EF/FS reductions are a defined “symptom” of muscular dystrophy for purposes of the method. That supports a position that EF/FS improvements are part of “treating or reducing symptoms.” Does the claim require echocardiographic measurement? (Claim 5) Claim 5 states EF and FS improvements are measured by echocardiography. Scope consequence. Claim 1, by itself, does not force echocardiography as the measurement method. Claim 5 adds that requirement as a dependent limitation. If an accused study uses an alternative cardiac imaging modality, Claim 5 would be harder to match, but Claim 1 could still be asserted if the endpoints are nevertheless EF and FS in substance and result. Dose floor and “therapeutically effective amount”: what does that mean for design-around? Claim 1 requires the therapeutically effective amount to be ≥2 mg/kg/day. Design-around pressure points. A regimen at <2 mg/kg/day is outside the literal dose floor. But “therapeutically effective amount” is typically context-dependent. Still, the claim makes the threshold explicit, so accused products attempting to hit clinical effect below 2 mg/kg/day can argue non-infringement on dose limitation. Do not confuse formulation dose with patient dose. The claim is patient-dose framed: mg/kg/day. That is typically governed by actual administered dose, not theoretical dose. Oral administration and duration: how restrictive are Claim 6 and Claim 7? Claim 6: compound administered orally Claim 7: administration duration of at least about eight weeks These are dependent claims. They do not limit Claim 1 or Claim 8 unless those dependents are asserted. They create additional pathways to infringement in programs that use oral dosing and trial durations consistent with at least ~8 weeks. How does Claim 8 expand the method: includes oral administration plus measured improvement post-dosing? Claim 8 is another method claim that adds the following structural elements: Oral administration (explicit in Claim 8) Dose floor again: ≥2 mg/kg/day Outcome after administration: patient has improved EF and FS as measured by echocardiography Claim 8 therefore operationalizes the method: it requires both administration route and post-dosing measurement framing. Relationship to Claim 1. Claim 1 is broader (no explicit oral requirement, no explicit “post administration” wording, and echocardiography only via dependent Claim 5). Claim 8 is narrower but more evidentiary: it hardwires oral dosing and echocardiographic measurement into the independent claim text. Subtypes and symptoms in Claim 9-11: same enumeration, same cardiac functional endpoints Claim 9: dystrophy chosen from the same nine subtypes Claim 10: Duchenne Claim 11: symptoms chosen from the same symptom set (including decreased EF/FS) Route and duration in Claim 12-13: oral and ≥8 weeks again Claim 12: oral administration Claim 13: duration at least about eight weeks Again, those are dependent limitations within the Claim 8 family. What is the practical claim scope for enforcement: which elements must match in an accused muscular dystrophy program? A simplified infringement-fit checklist, focused on literal claim elements: Minimum elements likely required for any asserted claim (Claim 1 / Claim 8 family): Patient has muscular dystrophy (one of the stated types if asserted via dependent claims) Treatment is performed by administering a compound with the claimed structural formula or a salt Dose administered is ≥2 mg/kg/day The method results in increased EF and increased FS In Claim 8 family, oral dosing and echocardiographic measurement are required by the claim structure Additional elements if asserted via dependents: Echocardiography measurement (Claim 5 or Claim 8) Oral administration (Claim 6 or Claim 8/12) Treatment duration ≥ about 8 weeks (Claim 7 or Claim 13) Specific dystrophy subtype matching (Claims 2-3 and 9-10) Symptom framing (Claims 4 and 11) How strong is US 11,690,853 as a patent estate for muscular dystrophy cardiac outcomes (EF/FS)? Based on claim architecture alone, the patent’s strength trends toward high enforceability against clinical regimens that are designed to show cardiac functional improvement in muscular dystrophy at or above a defined dose. Why the claim is enforceable when programs track trial endpoints: Drug developers often align trial endpoints with clinically meaningful metrics like EF/FS. If a clinical protocol includes echocardiography and reports EF/FS improvements, it becomes easier to map results back to the method claims. Key vulnerability vectors: Programs that use the compound for muscular dystrophy without EF/FS endpoints (or without showing improvement) can reduce literal claim mapping. Dosing below 2 mg/kg/day creates a clean non-infringement argument. Use of non-oral route avoids Claim 6/12 but does not avoid Claim 1 unless the broader claim is also used without oral limitations. If measurement is performed by methods that do not operationalize EF and FS as claimed, evidentiary disputes may arise. What formulation and compound-scope limits exist: is the patent about a specific drug entity or just a method using a compound? The claim text is method-focused and references the compound only by a structural formula and salts, without additional formulation limitations (e.g., excipients, crystalline form, salt polymorph, dosing regimen beyond dose floor, oral dosage form details). So US 11,690,853 is best read as: a compound-anchored method claim, not a formulation patent in the typical sense with infringement primarily tied to administration and clinical outcomes If a company uses the same compound (or salt within the defined scope), the method claims can still be implicated regardless of formulation details, unless formulation changes are used to change dose delivered, route, or duration below claim thresholds. What patent landscape could be surrounding this method: how does a EF/FS muscular dystrophy claim typically position against earlier or later IP? Even without the file wrapper text, this claim set suggests a landscape where: Earlier patents may have covered the compound itself (chemical entity, salts, and general therapeutic use). Later patents may focus on specific disease settings and specific clinical endpoints like EF/FS. US 11,690,853 appears tailored to capture competitive activity where EF/FS improvements are demonstrated in muscular dystrophy populations. This style of drafting often complements: method-of-use patents that broaden beyond one dystrophy subtype cardiac function endpoint-driven patents that distinguish from generic muscular dystrophy treatment claims Because you provided only the claims text and not the patent’s specification, priority data, assignees, or citations, a complete “landscape” mapping to specific related US applications and families cannot be produced here. Key Takeaways US 11,690,853 covers a method of treating muscular dystrophy by administering a specific compound (structural formula or salt) at ≥2 mg/kg/day to increase ejection fraction (EF) and fraction shortening (FS). Claim 2 and Claim 9 expand coverage across nine muscular dystrophy subtypes, with Duchenne singled out in Claims 3 and 10. Echocardiography is an explicit requirement in the dependent Claim 5 and in Claim 8’s post-treatment framing. Oral administration and ≥about 8 weeks are covered as dependent limitations (Claim 6-7 and Claim 12-13), enabling layered enforcement depending on accused protocols. The enforceable “center of gravity” is the combination of dose floor + EF/FS improvement + muscular dystrophy treatment, with claim strength highest when clinical protocols measure EF/FS by echocardiography. FAQs 1) Does US 11,690,853 require the compound to be administered orally? No for Claim 1. Oral administration is required for Claim 6 and Claim 8/12, but Claim 1 is not limited to oral dosing. 2) Is echocardiography required for every claim in the patent? No. Echocardiography is explicitly required in Claim 5 and Claim 8’s post-administration measurement language. 3) What is the lowest dose permitted by the claims? The claims require a therapeutically effective amount of ≥2 mg/kg/day. 4) Which muscular dystrophy types are enumerated in the claim set? Duchenne, Becker, limb girdle, congenital, facioscapulohumeral, myotonic, oculopharyngeal, distal, and Emery-Dreifuss muscular dystrophy. 5) Can a provider avoid infringement by changing imaging methods used to assess EF/FS? Changing imaging methods may avoid dependent claims that require echocardiography (e.g., Claim 5/Claim 8), but the broader claims still require EF and FS increases as functional outcomes. References United States Patent No. 11,690,853. More… ↓ ⤷ Start Trial

Applicant	Tradename	Generic Name	Dosage	NDA	Approval Date	TE	Type	RLD	RS	Patent No.	Patent Expiration	Product	Substance	Delist Req.	Patented / Exclusive Use	Submissiondate
Catalyst Pharms	AGAMREE	vamorolone	SUSPENSION;ORAL	215239-001	Oct 26, 2023		RX	Yes	Yes	⤷ Start Trial	⤷ Start Trial				TREATMENT OF DUCHENNE MUSCULAR DYSTROPHY	⤷ Start Trial
>Applicant	>Tradename	>Generic Name	>Dosage	>NDA	>Approval Date	>TE	>Type	>RLD	>RS	>Patent No.	>Patent Expiration	>Product	>Substance	>Delist Req.	>Patented / Exclusive Use	>Submissiondate

Country	Patent Number	Estimated Expiration	Supplementary Protection Certificate	SPC Country	SPC Expiration
World Intellectual Property Organization (WIPO)	2017004205	⤷ Start Trial
>Country	>Patent Number	>Estimated Expiration	>Supplementary Protection Certificate	>SPC Country	>SPC Expiration

Details for Patent: 11,690,853

Which drugs does patent 11,690,853 protect, and when does it expire?

Summary for Patent: 11,690,853