Scope and Claims Analysis for U.S. Patent 11,260,053: Method for Increasing Distal GI Bile Acids Using an ASBT Inhibitor
U.S. Patent 11,260,053 claims a US-method-of-treatment for increasing bile acids and salts in the distal gastrointestinal tract by administering an apical sodium-dependent bile acid transporter inhibitor (ASBTI) with delivery to the distal ileum/colon/rectum, including explicit coverage of a specific ASBTI structure (a potassium salt/solvate form) and dependent claim support for combination regimens and timing/administration (preprandial; ≤60 or ≤30 minutes; oral ileal-pH sensitive/enteric delivery). The claim set is written to capture (i) core method mechanics (distal delivery + functional outcome), (ii) a defined chemical species (the ASBTI recited by name), and (iii) variant regimens that broaden to co-administered agents and to specific patient cohorts (e.g., premature/infants).
What does US Patent 11,260,053 claim: full scope of independent claim 1 and limiting elements?
Independent claim 1: required elements
Claim 1 is a method and requires all of the following, in combination:
- Therapeutic method objective: “increasing the concentration of bile acids and salts thereof”
- Target anatomy: “distal gastrointestinal tract of an individual”
- Mechanism via drug class: administering an Apical Sodium-dependent Bile Acid Transporter Inhibitor (ASBTI)
- Delivery location constraint: “therapeutically amount of the ASBTI is delivered to the distal ileum, the colon, or the rectum”
- An ASBTI selection limitation: ASBTI is selected from and includes a specific potassium-salt/solvate chemical species (recited by full IUPAC-like name)
ASBTI recited species:
potassium((2R,3R,4S,5R,6R)-4-benzyloxy-6-{3-[3-((3S,4R,5R)-3-butyl-7-dimethylamino-3-ethyl-4-hydroxy-1,1-dioxo-2,3,4,5-tetrahydro-1H-benzo[b]thiepin-5-yl)-phenyl]-ureido}-3,5-dihydroxy-tetrahydropyran-2-ylmethyl)sulphate ethanolate hydrate, plus “a pharmaceutically acceptable salt or solvate thereof” (as later reiterated in dependent claims)
Enforcement implication: A practicing party must satisfy both (a) pharmacology class (ASBT inhibition) and (b) site-specific delivery (distal ileum/colon/rectum exposure), not merely systemic ASBT inhibition.
Claim 1 functional outcome coupling
Claim 1 couples an outcome (“increasing bile acids and salts”) with a particular GI delivery pattern. In litigation, this often creates two distinct infringement pathways:
- Literal site-delivery path: the administered ASBTI formulation actually delivers drug levels to distal ileum/colon/rectum sufficient to achieve the claimed concentration increase.
- Doctrine-of-equivalents path: if delivery timing or formulation differs but still yields distal bile acid concentration increases in the defined regions.
Key claim-interpretation pressure points
- “Distal gastrointestinal tract” boundary: claim language explicitly lists distal ileum, colon, rectum, which narrows the anatomic interpretation.
- “Increasing the concentration”: does not require a named disease outcome; it is outcome functional. That tends to broaden reach, but it also invites disputes about measurement, biomarkers, and whether “increase” occurred.
- “Therapeutically amount”: requires more than trace dosing. Dose-range specifics are not provided in the claim text you supplied, but it is an element that can be contested.
How broad is the claim coverage beyond the specific ASBT inhibitor: what exactly is “selected from” in claim 1?
Is the independent claim restricted to one ASBTI species
Claim 1, as provided, indicates ASBTI is “selected from and potassium(… ) ethanolate hydrate,” which strongly suggests the claim is at least explicitly anchored to that species. Your excerpt does not show the full preceding “selected from” list items, so the safe technical interpretation from the provided text is:
- The named potassium ethanolate hydrate ASBTI is definitely inside claim scope.
- The possibility remains that other ASBTIs are also inside the “selected from” set, but the excerpt you provided includes only the single explicit chemical anchor.
Variant capture via “salt or solvate”
Dependent claim 13 (and later 21) reiterates coverage for:
- the exact named ASBTI and
- “a pharmaceutically acceptable salt or solvate thereof”
This expands infringement risk to:
- polymorph/solvate substitutions (to the extent courts treat them as “solvate”)
- counterion salt forms (as pharmaceutically acceptable salts)
- potential process-derived forms if they remain “solvate” or “salt” under claim construction
Risk posture: If a competitor uses different counterion/cocrystal/solvate forms, infringement turns on whether the form is captured as a “pharmaceutically acceptable salt or solvate” of the recited molecule.
What do the dependent claims add: combinations, timing, route, and patient populations?
Claim 2: combination with enteroendocrine/FXR/LRH-1/DPP-IV/PPI/H2/prokinetic/biguanide/incretin/THIA/mucoadhesion/GLP-1 or analog
Claim 2 adds a second agent “selected from” a wide set of drug classes, including:
- enteroendocrine peptide enhancing agent
- nuclear FXR agonist
- LRH-1
- DPP-IV inhibitor
- proton pump inhibitor
- H2 antagonist
- prokinetic agent
- biguanide
- incretin mimetic
- thiazolidinone
- mucoadhesive agent
- GLP-1 or analog
Scope expansion mechanics:
- Claim 2 is add-on: infringement requires both the ASBTI method of claim 1 and the co-administered second agent from the enumerated set.
- Because claim 2 enumerates classes and named exemplars for some (FXR), it supports multiple combination licensing strategies.
Claim 3: specific infant cohorts
Claim 3 limits the method target to:
- prematurely born infant
- enterally-fed infant
- formula-fed infant
This is commercially relevant because infant enteral nutrition strategies and bile acid physiology can diverge from adult populations. It also increases the evidentiary burden on proving delivery and physiological response in infants.
Claim 4: therapeutic effect framing about ileal architecture
Claim 4 recites:
- ASBTI “reduces intraenterocyte bile acids” or
- “reduces necrosis and/or damage to ileal architecture”
This is a notable dual framing. It broadens therapeutic language beyond “increase bile acids in distal tract” by adding a possible protective mechanism associated with ileal injury/architecture. This can be used to argue that the same dosing regimens achieve bile acid modulation with tissue-protective endpoints.
Potential tension to manage: Claim 1 says “increasing concentration of bile acids and salts” distally, while claim 4 suggests “reduces intraenterocyte bile acids.” Those can be reconciled if:
- luminal distal bile acid concentration increases, while
- intracellular bile acid concentrations decrease in ileal epithelial cells, or
- claim 4 represents an alternate effect within the overall method.
Claims 5–6: enteroendocrine peptide enhancing agent and FXR agonists
Claim 5 provides a very long list of candidate enteroendocrine peptide enhancing agents, including multiple bile acids/bile salts and multiple receptor agonists (TGR5 binding analog, M-BAR agonist, GPR119 agonist, GPR120 agonist, GPR131 agonist, GPR140 agonist, GPR143 agonist, GPBAR1 agonist, BG37 agonist, FXR agonist, etc.) and includes named compounds (e.g., INT-777, RG-239) plus “Formula (VII)” structural definitions.
Claim 6 specifies the FXR agonist can be among GW4064, GW9662, INT-747, T0901317, WAY-362450, fexaramine, and multiple bile acids/salts.
Breadth implication: Even if a competitor selects only a single FXR agonist or bile acid mimic, they can fall within claim 2.
Claims 7–9 and 15–17: preprandial timing
Claim set provides explicit timing windows:
- Claim 7: before ingestion of food
- Claim 8: less than about 60 minutes before ingestion
- Claim 9: less than about 30 minutes before ingestion
- Claims 15–17 mirror those timing limitations but tied specifically to claim 1 (ASBTI-only method)
This is a common infringement anchor because formulation and dosing schedules can be designed around or away from preprandial timing.
Claims 10, 18: route oral
Claim 10 (and 18 on claim 1) requires:
Claims 11 and 19: delivery form oral as ileal-pH sensitive or enterically coated
Claim 11 requires:
- oral administration as an ileal-pH sensitive release or an enterically coated formulation
This narrows infringement for oral competitors. If a competitor uses a different delivery system not properly characterized as ileal-pH sensitive or enteric coating, infringement risk decreases (though equivalence remains possible).
Claims 12, 20: truncated in your excerpt
Claims 12 and 20 are not displayed (“wherein the ASBTI is …” / “wherein the ASBTI is …”) which prevents a complete claim-by-claim coverage reconstruction from what you provided.
How does the claim language map to real-world product design and infringement risk?
Formulation design levers that matter most
- Site delivery to distal ileum/colon/rectum
- Supports infringement for ileal-release and enteric coating approaches.
- Oral route
- Excludes many non-oral routes from literal coverage.
- Preprandial dosing (<60 minutes, <30 minutes)
- Competitors can attempt to shift dosing after meals to avoid the timing elements, though claim scope may still be asserted under equivalence theories if “before ingestion of food” is interpreted broadly.
- Co-therapy selection (claim 2)
- Co-administration with FXR/LRH-1/DPP-IV/incretin/GLP-1 etc. can bring combinations into dependent claim coverage.
Patient population lever
Claim 3’s infant cohorts add a layer of specificity. Adult-only trials or labeling can still be asserted under claim 1, but claim 3 narrows dependent coverage.
What patent landscape issues follow from this claim set: likely continuation strategy, claim durability, and design-around space?
Claim durability drivers
- Specific chemical species anchor in claim 1 (the named potassium ethanolate hydrate) often yields strong “species” coverage that is harder to design around with mere analog selection.
- Broad second-agent class enumeration in claim 2 provides many combination infringement vectors and reduces the chance that a single competitor co-therapy choice escapes.
Design-around levers
- Avoid oral ileal-pH sensitive / enteric characterization
- Alternative delivery systems may argue outside literal wording.
- Avoid preprandial dosing windows
- If competitor dosing is after food ingestion, it can target avoidance of the “before ingestion of food” limitations.
- Avoid co-administered second agent classes
- For claim 2 coverage, competitor combinations outside the listed set can reduce dependent claim risk.
- Use a non-salt/non-solvate form
- If the competitor uses a different solid form not qualifying as a “salt or solvate” of the named molecule, infringement may narrow.
What US Orange Book status questions matter for this patent?
This is a method patent (not a composition patent) as presented. For Orange Book status, the key is whether the method is tied to a listed drug substance/product that contains the ASBTI and whether the patent is listed under drug products in a way that triggers exclusivity-related blocking.
However, no Orange Book listing data, NDA/BLA number, or listed drug name is provided in your prompt. Without those, a complete mapping to Orange Book fields cannot be generated from the supplied information alone.
What FDA pathway and use-case alignment is implied by these claims?
The claims target physiologic bile acid concentration changes in distal GI and include infant cohorts, plus combination with bile-acid/FXR/GLP-1 style agents. That implies:
- clinical positioning could include GI bile acid modulation therapies
- potential overlap with endocrine/metabolic adjunct agents
But your prompt does not include FDA-approved product information, trial design, or labeling. No complete regulatory status analysis can be produced from the supplied excerpt.
Which competitive strategies are most exposed under this patent’s claim structure?
Highest exposure scenario
- Oral ASBT inhibitor containing or equivalent to the named potassium sulfate ethanolate hydrate delivered via ileal-pH sensitive/enteric formulation
- Administered preprandially (<60 or <30 minutes where applicable)
- Possibly co-administered with FXR agonist or GLP-1/analog or other enumerated agents depending on the target formulation regimen
Moderate exposure scenario
- Oral ASBTI but delivered via a formulation not clearly “ileal-pH sensitive release” or “enterically coated”
- Dosing timing shifts to after meals (arguing outside “before ingestion” limitations)
Lower exposure scenario
- Non-oral delivery
- Post-prandial-only administration
- Combinations avoid the dependent-claim enumerations and keep regimen outside the method’s anatomical and timing limitations
Key Takeaways
- Claim 1 is the core: a US method to increase distal GI bile acids/salts by giving an ASBT inhibitor with therapeutic delivery to distal ileum/colon/rectum.
- The independent claim is anchored to a specific ASBTI species: the potassium sulfate ethanolate hydrate form of a defined molecule, with additional coverage for pharmaceutically acceptable salts/solvates.
- Dependent claim 2 expands infringement risk through combination therapy with a wide panel of agents, including FXR agonists and GLP-1/analogs, among others.
- Dependent claims 7–9 and 15–17 add dosing schedule constraints: preprandial administration with ≤60 minutes and ≤30 minutes options.
- Dependent claims 10–11 and 18–19 add administration constraints: oral dosing with ileal-pH sensitive release or enteric coating.
- Claim 3 narrows a dependent population: premature infants and enterally/formula-fed infants.
FAQs
1) Does claim 1 require a specific disease indication?
No. Claim 1 is framed around a physiologic/biochemical outcome (increasing bile acid concentration) and delivery site, not a named indication.
2) Is oral administration mandatory for infringement of claim 1?
Claim 1 itself does not expressly require oral in the excerpt you provided, but dependent claims 10/18 do. Oral route is therefore a likely essential element only for dependent-claim scope.
3) Can a competitor avoid claim 2 by using an ASBT inhibitor alone?
Yes for claim 2, because claim 2 adds “further comprising” a second agent selected from enumerated classes. Claim 1 remains available if its elements are met.
4) What is the most sensitive claim element to design around: timing, formulation, or co-therapy?
From the provided claims, the most sensitive are (i) delivery to distal ileum/colon/rectum and (ii) preprandial timing for the dependent windows; co-therapy matters only for claim 2.
5) Does the patent cover solid-form variations of the ASBT inhibitor?
The excerpt includes coverage for “pharmaceutically acceptable salt or solvate thereof” of the named ASBTI, which can capture some solid-form variations.
References
No external sources were cited because the prompt provided only claim text and no bibliographic, Orange Book, FDA, prosecution-history, or related litigation data to support accurate patent-lifecycle referencing.
