Executive summary: US Drug Patent 11,813,255 claims a specific, patient- and assay-defined Fabry disease treatment method: administering migalastat (including migalastat hydrochloride) to patients whose α-galactosidase A (α-Gal A) protein contains HEK assay amenable mutations selected from A13T, D322N, and M421V, using every-other-day oral dosing (notably ~150 mg), and tying the regimen to biomarker and clinical effects (GL-3, lyso-Gb3, WBC α-Gal A activity, LVMi, renal stabilization). The claim set is structured to create multiple infringement hooks: mutation identity, dosing interval and dose range, formulation/salt and oral solid dosage form, and effect-based limitations (biomarkers and organ outcomes). This is a narrow-by-eligibility patent but broad across outcomes and subpopulations, which raises barriers to generic or “label-fidelity” at-launch copying if challengers cannot show the accused product is used for the claimed mutation cohort and dosing/effect scheme.

What is US Patent 11,813,255 scope for migalastat-treated Fabry disease with HEK assay amenable mutations?

US 11,813,255 is a method-of-treatment patent. The core independent claim (your Claim 1) has three principal structural elements:

Drug: “administering migalastat to a patient in need thereof”
Eligibility via α-Gal A mutation: patient has an α-galactosidase A protein comprising a HEK assay amenable mutation selected from:
- A13T
- D322N
- M421V
Disease: “method of treating Fabry disease”

Claim 1’s practical meaning (eligibility-first infringement)

Because the mutation is specifically enumerated and tied to “HEK assay amenable mutation,” infringement turns on whether the treated patient (or at least the patient cohort in which the regimen is administered) meets that eligibility definition. A generic maker’s labeling strategy matters less than what clinicians actually do for patients with those exact mutations and whether the claimed dosing and effect limitations are also met by the accused use.

Claim dependencies expand coverage by adding “AND” filters

The dependent claims then layer restrictions that can each serve as an additional infringement “path,” not necessarily requiring all dependent limitations to be present if another claim stands alone for infringement.

Which α-galactosidase A mutations are explicitly covered by claim 1 (A13T, D322N, M421V)?

Claim 1 explicitly limits the method to patients whose α-Gal A protein includes a mutation from the set {A13T, D322N, M421V} that is “HEK assay amenable.”

Mutation-specific coverage (claims 2–4)

Claim 2: mutation is A13T
Claim 3: mutation is D322N
Claim 4: mutation is M421V

This creates three single-mutation infringement pathways in addition to the “set” pathway in Claim 1.

Relationship to broader Fabry mutation categories

Claim 1 does not read on all Fabry-causing mutations. It reads on a subset defined by both:

being Fabry disease-causing (Claim 5 is a further dependency), and
being HEK assay amenable and falling in the listed mutation set.

What dosing regimen and amount limits are claimed (every other day, ~150 mg, and dose ranges)?

Claims 6–9 lock down timing and dosage form.

Dosing interval (claims 6, 8, 9)

Claim 6: migalastat (or salt) administered every other day
Claim 8: about 150 mg every other day
Claim 9: about 150 mg migalastat hydrochloride every other day

Dose range (claim 7)

Claim 7: about 123 to about 300 mg every other day

Infringement design

This combination supports two infringement strategies:

“Range” infringement (Claim 7) if accused dosing falls anywhere within ~123–300 mg QOD.
“Target dose” infringement (Claims 8–9) centered on ~150 mg QOD, which is the most label-likely dose profile.

Is oral administration and solid dosage form claimed?

Yes. Claims 20–22 require oral dosing in a solid dosage form.

Claim 20: migalastat (or salt) is administered orally
Claim 21: the oral administration is in a solid dosage form
Claim 22: the solid dosage form comprises a capsule

Formulation anchors

Claim 23: migalastat can be administered as a pharmaceutically acceptable salt (consistent with Claim 9 and implied with Claim 24–29 referencing migalastat hydrochloride)

A challenger attempting a non-capsule delivery or a non-oral route would aim to design around Claims 20–22. Many generic strategies, however, keep to capsule/oral because of bioequivalence requirements.

What biomarker and clinical endpoints are claimed (GL-3, lyso-Gb3, WBC α-Gal A, LVMi, renal stabilization)?

Claims 24–29 add effect-based limitations. These are important because they can tie infringement to measurable outcomes and may align with clinical trial endpoints typically used in product labeling.

Biomarker and outcome-specific dependent claims

Claim 24: orally administer ~150 mg migalastat HCl every other day to reduce organ GL-3 accumulation
Claim 25: the same regimen to reduce plasma lyso-Gb3
Claim 26: the same regimen to increase WBC α-Gal A activity
Claim 27: the same regimen to reduce LVMi
Claim 28: the same regimen to stabilize renal function
Claim 29: the same regimen to achieve the combined set:
1. reduce GL-3 in an organ
2. reduce plasma lyso-Gb3
3. increase WBC α-Gal A activity
4. reduce LVMi
5. stabilize renal function

How effect limitations change infringement risk

If an accused generic is used at the same dosing and within the mutation-defined population, it is likely to reproduce the same biomarker outcomes clinically. But effect-based dependent claims can become litigated on evidentiary record: whether the method in practice produced the claimed physiological changes in the treated patient(s). Claim 29 is the tightest composite because it requires a bundle of outcomes.

How do patient subpopulation limitations change claim coverage (male, female, renal impairment, ERT experienced/naïve)?

Claims 10–19 address treated-patient subgroups.

Sex-specific dependents

Claim 10: patient is male
Claim 11: patient is female

These are broad in the sense that most patients are one of these; they also reduce potential arguments about sex limitation escaping infringement.

Renal impairment dependents

Claim 12: patient has renal impairment
Claim 13: patient has mild or moderate renal impairment

Enzyme replacement therapy history

Claim 14: ERT-experienced patient
Claim 15: ERT-experienced with renal impairment
Claim 16: ERT-naïve patient

Proteinuria stratification (claims 17–19)

Claim 17: proteinuria <100 mg/24 hr
Claim 18: proteinuria 100 to 1,000 mg/24 hr
Claim 19: proteinuria >1,000 mg/24 hr

Infringement mapping

These dependents are not mutually exclusive in concept (some can overlap, such as ERT-experienced plus renal impairment plus a proteinuria band). A litigation record may show which patient subset was treated in the accused program and which dependent limitations were satisfied.

What does the claim structure imply about design-around strategies for generics or label revisions?

Likely design-around vectors based on the claim text

Mutation eligibility: If accused use is steered away from the enumerated A13T/D322N/M421V HEK assay amenable cohort, the claim 1 eligibility hook may be avoided. In practice, treating those mutations is core to the therapeutic positioning of migalastat in Fabry programs.
Dosing interval and dose: Avoiding every-other-day dosing and/or avoiding ~123–300 mg QOD could aim to evade Claims 6–9 and the biomass-linked Claims 24–29 (which specify ~150 mg QOD).
Oral capsule pathway: Non-oral or non-capsule delivery may target Claims 20–22.
Salt/form: Evading “migalastat hydrochloride” would attack Claims 9 and the ~150 mg HCl framing in Claims 24–29, though Claim 6 and Claim 7 cover “migalastat or salt thereof,” so generic substitution to other salts may not fully eliminate risk.
Effect requirements: Arguing no reproduction of claimed biomarker/clinical endpoints could be used against the effect-limited dependent claims, though Claim 1 itself is not outcome-based beyond “treating Fabry disease.”

What remains hard to avoid

Even if a challenger changes salt or formulation, the broad “administering migalastat” and “every other day” dosing concepts can remain within the claim perimeter unless the dosing regimen is materially changed.

What patents typically surround this type of migalastat method claim (and how could they overlap)?

Without the full prosecution history, specification, and the complete US family for 11,813,255, the tightest actionable reading is the claim scope itself.

Likely adjacent IP themes around this claim (based on claim content)

Mutation/assay-based eligibility: patents that define “HEK assay amenable” mutations or assay thresholds.
Patient stratification: ERT-naïve vs ERT-experienced, renal impairment bands, proteinuria strata.
Dosing regimens: QOD dosing and dose ranges.
Outcome claims: GL-3/lyso-Gb3/WBC α-Gal A/LVMi/renal stabilization.
Formulation/salt: migalastat hydrochloride capsule dosing or specific solid dosage formats.

In practice, such clusters often split across:

method-of-treatment claims (like this one),
compound and pharmaceutical composition claims,
assay/mutation testing claims, and
specific dosing regimens and patient-selection protocol claims.

How strong is the patent estate for US 11,813,255 claim coverage based on its own breadth and specificity?

Strengths (as a litigation asset)

Clear eligibility definition: limits to a small mutation set, making it easier to point to specific patient cohorts and clinical records.
Multiple dependent hooks: dosing interval, dose range, salt, oral capsule form, and multiple biomarker/clinical outcomes.
Comprehensive subpopulation coverage: male/female, renal impairment, ERT history, and proteinuria bands create fallback claim paths.

Weaknesses (as a scope limitation)

Narrow mutation universe: if an accused regimen targets different HEK assay amenable mutations or broader Fabry-causing mutations outside A13T/D322N/M421V, Claim 1’s eligibility element is not met.
Effect-dependent dependent claims: Claims 24–29 add physiological endpoints that may require stronger evidentiary demonstration.

Overall, the independent claim is not outcome-burdened; dependent claims add complexity. That pattern usually supports enforcement focused on the mutation-defined population and dosing protocol.

What are the key “infringement predicates” you can map to real-world prescribing?

From the claim text, infringement analysis can be reduced to five predicates:

Patient has Fabry disease and α-Gal A protein with HEK assay amenable mutation ∈ {A13T, D322N, M421V}
Treatment is migalastat (or salt) and is administered every other day
Dosing is within ~123–300 mg QOD, with special attention to ~150 mg and migalastat hydrochloride
Administration is oral and solid, specifically a capsule for claims 20–22
For dependent enforcement, the patient treatment produces biomarker/clinical changes (GL-3, lyso-Gb3, WBC α-Gal A activity, LVMi, renal stabilization)

This makes 11,813,255 most sensitive to real-world evidence: mutation confirmation approach, dosing documentation, formulation used, and the treatment outcomes recorded in patient charts.

Timeline and exclusivity questions: when does this method claim lose practical exclusivity?

Your prompt provides only claim text, not:

filing/priority dates,
issue date of 11,813,255,
terminal disclaimer status,
PTA, or
Orange Book or regulatory exclusivity data.

Without those facts, a correct “when exclusivity ends” timeline cannot be generated from the information provided.

Orange Book status, Paragraph IV challenges, and biosimilar risk for migalastat method claims

Your prompt provides no Orange Book listing details, listed patents, or any FDA regulatory pathway or exclusivity data for migalastat products tied to 11,813,255.

Biosimilar risk: Migalastat is a small molecule and is not a biologic; “biosimilar” framing is generally not applicable for migalastat, but that depends on product classification and labeling context.
Paragraph IV: Requires Orange Book listed patents and generic product filings linked to migalastat NDA(s).

A complete and accurate analysis cannot be produced from the supplied inputs.

Key Takeaways

US 11,813,255 is a patient-selection method patent: it requires migalastat administration for Fabry disease in patients with α-Gal A mutations A13T, D322N, or M421V that are HEK assay amenable.
The claim set creates multiple infringement hooks: QOD dosing (~123–300 mg; especially ~150 mg), oral capsule/salt delivery, and dependent claims tied to GL-3, lyso-Gb3, WBC α-Gal A activity, LVMi, and renal stabilization.
The independent claim is less outcome-burdened than dependent claims; enforcement risk is highest when an accused regimen is used in the enumerated mutation cohort at QOD dosing in oral capsule form.
Practical design-around focuses on escaping eligibility (other mutations), changing regimen (non-QOD and/or outside the dose window), or changing delivery (non-oral/non-capsule), though the effectiveness depends on how closely real-world prescribing matches the claim language.

FAQs

1) Does US 11,813,255 cover Fabry patients with other HEK assay amenable mutations beyond A13T, D322N, and M421V?
No, Claim 1 as provided is limited to the enumerated set in the eligibility element.

2) Is reducing lyso-Gb3 required for infringement of the independent claim?
No. Biomarker reduction (lyso-Gb3) appears in dependent Claims 25 and the composite Claim 29, not in Claim 1 as you provided it.

3) What dosing detail is most central to Claims 6–9?
The dosing interval (every other day) and dose framing (~123 to ~300 mg, with dependent coverage at ~150 mg, including migalastat hydrochloride).

4) Can infringement occur if migalastat is administered orally but not in capsule form?
Claims 20–22 require oral and solid dosage form and, in Claim 22, specifically a capsule. Claim 1 itself does not expressly require capsule form in the text provided, but dependent claim coverage does.

5) How do renal impairment and proteinuria limitations affect coverage?
They appear as dependent claim limitations (Claims 12–13 and 17–19), enabling narrower enforcement paths for specific patient subsets treated under those conditions.

References (APA)

US Patent 11,813,255 (method of treating Fabry disease with migalastat for HEK assay amenable α-galactosidase A mutations).

Title:	Methods of treating Fabry patients having renal impairment
Abstract:	Provided are methods for treatment of Fabry disease in patients having HEK assay amenable mutations in α-galactosidase A. Certain methods comprise administering migalastat or a salt thereof every other day, such as administering about 150 mg of migalastat hydrochloride every other day.
Inventor(s):	Jeff Castelli, Elfrida Benjamin
Assignee:	Amicus Therapeutics Inc
Application Number:	US18/069,716
Patent Litigation and PTAB cases:	See patent lawsuits and PTAB cases for patent 11,813,255
Patent Claim Types: see list of patent claims	Use; Delivery; Dosage form;
Patent landscape, scope, and claims:	Executive summary: US Drug Patent 11,813,255 claims a specific, patient- and assay-defined Fabry disease treatment method: administering migalastat (including migalastat hydrochloride) to patients whose α-galactosidase A (α-Gal A) protein contains HEK assay amenable mutations selected from A13T, D322N, and M421V, using every-other-day oral dosing (notably ~150 mg), and tying the regimen to biomarker and clinical effects (GL-3, lyso-Gb3, WBC α-Gal A activity, LVMi, renal stabilization). The claim set is structured to create multiple infringement hooks: mutation identity, dosing interval and dose range, formulation/salt and oral solid dosage form, and effect-based limitations (biomarkers and organ outcomes). This is a narrow-by-eligibility patent but broad across outcomes and subpopulations, which raises barriers to generic or “label-fidelity” at-launch copying if challengers cannot show the accused product is used for the claimed mutation cohort and dosing/effect scheme. What is US Patent 11,813,255 scope for migalastat-treated Fabry disease with HEK assay amenable mutations? US 11,813,255 is a method-of-treatment patent. The core independent claim (your Claim 1) has three principal structural elements: Drug: “administering migalastat to a patient in need thereof” Eligibility via α-Gal A mutation: patient has an α-galactosidase A protein comprising a HEK assay amenable mutation selected from: A13T D322N M421V Disease: “method of treating Fabry disease” Claim 1’s practical meaning (eligibility-first infringement) Because the mutation is specifically enumerated and tied to “HEK assay amenable mutation,” infringement turns on whether the treated patient (or at least the patient cohort in which the regimen is administered) meets that eligibility definition. A generic maker’s labeling strategy matters less than what clinicians actually do for patients with those exact mutations and whether the claimed dosing and effect limitations are also met by the accused use. Claim dependencies expand coverage by adding “AND” filters The dependent claims then layer restrictions that can each serve as an additional infringement “path,” not necessarily requiring all dependent limitations to be present if another claim stands alone for infringement. Which α-galactosidase A mutations are explicitly covered by claim 1 (A13T, D322N, M421V)? Claim 1 explicitly limits the method to patients whose α-Gal A protein includes a mutation from the set {A13T, D322N, M421V} that is “HEK assay amenable.” Mutation-specific coverage (claims 2–4) Claim 2: mutation is A13T Claim 3: mutation is D322N Claim 4: mutation is M421V This creates three single-mutation infringement pathways in addition to the “set” pathway in Claim 1. Relationship to broader Fabry mutation categories Claim 1 does not read on all Fabry-causing mutations. It reads on a subset defined by both: being Fabry disease-causing (Claim 5 is a further dependency), and being HEK assay amenable and falling in the listed mutation set. What dosing regimen and amount limits are claimed (every other day, ~150 mg, and dose ranges)? Claims 6–9 lock down timing and dosage form. Dosing interval (claims 6, 8, 9) Claim 6: migalastat (or salt) administered every other day Claim 8: about 150 mg every other day Claim 9: about 150 mg migalastat hydrochloride every other day Dose range (claim 7) Claim 7: about 123 to about 300 mg every other day Infringement design This combination supports two infringement strategies: “Range” infringement (Claim 7) if accused dosing falls anywhere within ~123–300 mg QOD. “Target dose” infringement (Claims 8–9) centered on ~150 mg QOD, which is the most label-likely dose profile. Is oral administration and solid dosage form claimed? Yes. Claims 20–22 require oral dosing in a solid dosage form. Claim 20: migalastat (or salt) is administered orally Claim 21: the oral administration is in a solid dosage form Claim 22: the solid dosage form comprises a capsule Formulation anchors Claim 23: migalastat can be administered as a pharmaceutically acceptable salt (consistent with Claim 9 and implied with Claim 24–29 referencing migalastat hydrochloride) A challenger attempting a non-capsule delivery or a non-oral route would aim to design around Claims 20–22. Many generic strategies, however, keep to capsule/oral because of bioequivalence requirements. What biomarker and clinical endpoints are claimed (GL-3, lyso-Gb3, WBC α-Gal A, LVMi, renal stabilization)? Claims 24–29 add effect-based limitations. These are important because they can tie infringement to measurable outcomes and may align with clinical trial endpoints typically used in product labeling. Biomarker and outcome-specific dependent claims Claim 24: orally administer ~150 mg migalastat HCl every other day to reduce organ GL-3 accumulation Claim 25: the same regimen to reduce plasma lyso-Gb3 Claim 26: the same regimen to increase WBC α-Gal A activity Claim 27: the same regimen to reduce LVMi Claim 28: the same regimen to stabilize renal function Claim 29: the same regimen to achieve the combined set: reduce GL-3 in an organ reduce plasma lyso-Gb3 increase WBC α-Gal A activity reduce LVMi stabilize renal function How effect limitations change infringement risk If an accused generic is used at the same dosing and within the mutation-defined population, it is likely to reproduce the same biomarker outcomes clinically. But effect-based dependent claims can become litigated on evidentiary record: whether the method in practice produced the claimed physiological changes in the treated patient(s). Claim 29 is the tightest composite because it requires a bundle of outcomes. How do patient subpopulation limitations change claim coverage (male, female, renal impairment, ERT experienced/naïve)? Claims 10–19 address treated-patient subgroups. Sex-specific dependents Claim 10: patient is male Claim 11: patient is female These are broad in the sense that most patients are one of these; they also reduce potential arguments about sex limitation escaping infringement. Renal impairment dependents Claim 12: patient has renal impairment Claim 13: patient has mild or moderate renal impairment Enzyme replacement therapy history Claim 14: ERT-experienced patient Claim 15: ERT-experienced with renal impairment Claim 16: ERT-naïve patient Proteinuria stratification (claims 17–19) Claim 17: proteinuria <100 mg/24 hr Claim 18: proteinuria 100 to 1,000 mg/24 hr Claim 19: proteinuria >1,000 mg/24 hr Infringement mapping These dependents are not mutually exclusive in concept (some can overlap, such as ERT-experienced plus renal impairment plus a proteinuria band). A litigation record may show which patient subset was treated in the accused program and which dependent limitations were satisfied. What does the claim structure imply about design-around strategies for generics or label revisions? Likely design-around vectors based on the claim text Mutation eligibility: If accused use is steered away from the enumerated A13T/D322N/M421V HEK assay amenable cohort, the claim 1 eligibility hook may be avoided. In practice, treating those mutations is core to the therapeutic positioning of migalastat in Fabry programs. Dosing interval and dose: Avoiding every-other-day dosing and/or avoiding ~123–300 mg QOD could aim to evade Claims 6–9 and the biomass-linked Claims 24–29 (which specify ~150 mg QOD). Oral capsule pathway: Non-oral or non-capsule delivery may target Claims 20–22. Salt/form: Evading “migalastat hydrochloride” would attack Claims 9 and the ~150 mg HCl framing in Claims 24–29, though Claim 6 and Claim 7 cover “migalastat or salt thereof,” so generic substitution to other salts may not fully eliminate risk. Effect requirements: Arguing no reproduction of claimed biomarker/clinical endpoints could be used against the effect-limited dependent claims, though Claim 1 itself is not outcome-based beyond “treating Fabry disease.” What remains hard to avoid Even if a challenger changes salt or formulation, the broad “administering migalastat” and “every other day” dosing concepts can remain within the claim perimeter unless the dosing regimen is materially changed. What patents typically surround this type of migalastat method claim (and how could they overlap)? Without the full prosecution history, specification, and the complete US family for 11,813,255, the tightest actionable reading is the claim scope itself. Likely adjacent IP themes around this claim (based on claim content) Mutation/assay-based eligibility: patents that define “HEK assay amenable” mutations or assay thresholds. Patient stratification: ERT-naïve vs ERT-experienced, renal impairment bands, proteinuria strata. Dosing regimens: QOD dosing and dose ranges. Outcome claims: GL-3/lyso-Gb3/WBC α-Gal A/LVMi/renal stabilization. Formulation/salt: migalastat hydrochloride capsule dosing or specific solid dosage formats. In practice, such clusters often split across: method-of-treatment claims (like this one), compound and pharmaceutical composition claims, assay/mutation testing claims, and specific dosing regimens and patient-selection protocol claims. How strong is the patent estate for US 11,813,255 claim coverage based on its own breadth and specificity? Strengths (as a litigation asset) Clear eligibility definition: limits to a small mutation set, making it easier to point to specific patient cohorts and clinical records. Multiple dependent hooks: dosing interval, dose range, salt, oral capsule form, and multiple biomarker/clinical outcomes. Comprehensive subpopulation coverage: male/female, renal impairment, ERT history, and proteinuria bands create fallback claim paths. Weaknesses (as a scope limitation) Narrow mutation universe: if an accused regimen targets different HEK assay amenable mutations or broader Fabry-causing mutations outside A13T/D322N/M421V, Claim 1’s eligibility element is not met. Effect-dependent dependent claims: Claims 24–29 add physiological endpoints that may require stronger evidentiary demonstration. Overall, the independent claim is not outcome-burdened; dependent claims add complexity. That pattern usually supports enforcement focused on the mutation-defined population and dosing protocol. What are the key “infringement predicates” you can map to real-world prescribing? From the claim text, infringement analysis can be reduced to five predicates: Patient has Fabry disease and α-Gal A protein with HEK assay amenable mutation ∈ {A13T, D322N, M421V} Treatment is migalastat (or salt) and is administered every other day Dosing is within ~123–300 mg QOD, with special attention to ~150 mg and migalastat hydrochloride Administration is oral and solid, specifically a capsule for claims 20–22 For dependent enforcement, the patient treatment produces biomarker/clinical changes (GL-3, lyso-Gb3, WBC α-Gal A activity, LVMi, renal stabilization) This makes 11,813,255 most sensitive to real-world evidence: mutation confirmation approach, dosing documentation, formulation used, and the treatment outcomes recorded in patient charts. Timeline and exclusivity questions: when does this method claim lose practical exclusivity? Your prompt provides only claim text, not: filing/priority dates, issue date of 11,813,255, terminal disclaimer status, PTA, or Orange Book or regulatory exclusivity data. Without those facts, a correct “when exclusivity ends” timeline cannot be generated from the information provided. Orange Book status, Paragraph IV challenges, and biosimilar risk for migalastat method claims Your prompt provides no Orange Book listing details, listed patents, or any FDA regulatory pathway or exclusivity data for migalastat products tied to 11,813,255. Biosimilar risk: Migalastat is a small molecule and is not a biologic; “biosimilar” framing is generally not applicable for migalastat, but that depends on product classification and labeling context. Paragraph IV: Requires Orange Book listed patents and generic product filings linked to migalastat NDA(s). A complete and accurate analysis cannot be produced from the supplied inputs. Key Takeaways US 11,813,255 is a patient-selection method patent: it requires migalastat administration for Fabry disease in patients with α-Gal A mutations A13T, D322N, or M421V that are HEK assay amenable. The claim set creates multiple infringement hooks: QOD dosing (~123–300 mg; especially ~150 mg), oral capsule/salt delivery, and dependent claims tied to GL-3, lyso-Gb3, WBC α-Gal A activity, LVMi, and renal stabilization. The independent claim is less outcome-burdened than dependent claims; enforcement risk is highest when an accused regimen is used in the enumerated mutation cohort at QOD dosing in oral capsule form. Practical design-around focuses on escaping eligibility (other mutations), changing regimen (non-QOD and/or outside the dose window), or changing delivery (non-oral/non-capsule), though the effectiveness depends on how closely real-world prescribing matches the claim language. FAQs 1) Does US 11,813,255 cover Fabry patients with other HEK assay amenable mutations beyond A13T, D322N, and M421V? No, Claim 1 as provided is limited to the enumerated set in the eligibility element. 2) Is reducing lyso-Gb3 required for infringement of the independent claim? No. Biomarker reduction (lyso-Gb3) appears in dependent Claims 25 and the composite Claim 29, not in Claim 1 as you provided it. 3) What dosing detail is most central to Claims 6–9? The dosing interval (every other day) and dose framing (~123 to ~300 mg, with dependent coverage at ~150 mg, including migalastat hydrochloride). 4) Can infringement occur if migalastat is administered orally but not in capsule form? Claims 20–22 require oral and solid dosage form and, in Claim 22, specifically a capsule. Claim 1 itself does not expressly require capsule form in the text provided, but dependent claim coverage does. 5) How do renal impairment and proteinuria limitations affect coverage? They appear as dependent claim limitations (Claims 12–13 and 17–19), enabling narrower enforcement paths for specific patient subsets treated under those conditions. References (APA) US Patent 11,813,255 (method of treating Fabry disease with migalastat for HEK assay amenable α-galactosidase A mutations). 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
Amicus Therap Us	GALAFOLD	migalastat hydrochloride	CAPSULE;ORAL	208623-001	Aug 10, 2018		RX	Yes	Yes	11,813,255	⤷ Start Trial				THE TREATMENT OF FABRY PATIENTS	⤷ 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
Argentina	111971	⤷ Start Trial
Argentina	131106	⤷ Start Trial
Argentina	131107	⤷ Start Trial
Australia	2009214648	⤷ Start Trial
Australia	2014221321	⤷ Start Trial
Australia	2016206297	⤷ Start Trial
>Country	>Patent Number	>Estimated Expiration	>Supplementary Protection Certificate	>SPC Country	>SPC Expiration

Summary for Patent: 11,813,255