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Patent landscape, scope, and claims: |
United States Patent 9,682,092 (US 9,682,092): What Does the Claim Set Cover, How Broad Is It, and Where the Infringement Risk Clusters
US 9,682,092 is a US method-of-treatment patent built around a highly generic Markush structure for “a compound having a structure according to Formula I” (and a parallel Formula II track), targeted to inflammatory-related diseases in humans or animals. The claim scope is dominated by breadth in: (i) the chemical variable universe (ring-closure options, heteroatom substitutions, boron incorporation, and wide substituent classes), (ii) disease/disease-mechanism language tied to pro- and anti-inflammatory cytokines, and (iii) a “dose window” constraint that is explicitly defined as “therapeutically effective” while being “less than sufficient to substantially inhibit cyclin dependent kinases.” Claims also expand into formulation and in vitro/cellular cytokine suppression and inflammatory response inhibition.
From a landscape perspective, the estate is best modeled as a scaffold patent with broad Markush coverage plus a mechanism/dose-limitation overlay, meaning infringement arguments typically hinge on whether an accused boron-containing compound falls inside the structural variable set of Formula I/II and whether the asserted uses map to cytokine modulation and the claimed dosing constraint.
What patents protect the compound class in US 9,682,092 and how is the Markush claim structure scoped?
Core coverage mechanism
- The independent method claim (claim 1) is written to cover administering a “therapeutically effective amount” of a compound defined by Formula I.
- A second independent method claim track (claim 27) covers an analogous compound defined by Formula II.
- The Markush language spans nearly every major structural axis: heteroatom identity, substituent classes, ring closures (4–7 membered), and functional groups (carbonyl, linkers, heteroatom acceptors, and electron-withdrawing substituents).
Key scaffold constraints (claim 1) that narrow the variable universe
- B is boron (hard constraint).
- Heteroatom positions are limited to O, S, NR2a for M (claim 1).
- Multiple positions (A, D, E, G) are each limited to CR(alkyl)-type or N:
- A ∈ {CR9a, N}
- D ∈ {CR10a, N}
- E ∈ {CR11a, N}
- G ∈ {CR12a, N}
- Multiple carbonyl/linker features are constrained through:
- J ∈ {(CR3aR4a)n1, CR5a} with n1 ∈ {0,1,2}
- W ∈ {C═O, (CR6aR7a)m1, CR8a} with m1 ∈ {0,1}
How the breadth works in practice
- The claim uses a “large but defined” chemical variable set:
- For R-group variables, it repeatedly permits: H; cyano; substituted/unsubstituted alkyl; substituted/unsubstituted heteroalkyl; substituted/unsubstituted cycloalkyl; substituted/unsubstituted heterocycloalkyl; substituted/unsubstituted aryl; substituted/unsubstituted heteroaryl.
- It also allows optional ring closures that can combine variable substituent atoms into 4- to 7-member rings at multiple junctions (e.g., between R3a and R4a; R6a and R7a; R9a and R10a; R10a and R11a; R11a and R12a).
Business implication
- The claim is designed to catch many analogs of a boron-containing anti-inflammatory/cytokine-modulating scaffold. If a competitor product is a boron-bearing analog that fits the Formula I/II variable map, it is structurally within scope even if the exact substituent pattern differs from the patent’s exemplified compounds.
How does claim 1 limit the chemical class compared with claim 27 (Formula I vs Formula II)?
High-level
- Claim 27 tracks the same overall strategy but with a different core architecture definition (Formula II rather than Formula I) and a reduced set of explicit constraints in the excerpt you provided.
- Both claims share:
- B is boron
- A, D, E, G are each ∈ {C(R), N}
- Broad allowances for R9a–R12a substituent classes (including carbonyl-derived, sulfonyl, thio, nitro, halogen, cyano, and wide alkyl/aryl/heteroaryl types)
- Optional 4–7 membered ring closures at the same general junction sets (R9a with R10a; R10a with R11a; R11a with R12a).
What the excerpt shows as the main delta
- Claim 1 includes additional variables not visible in claim 27 excerpt detail, including:
- R1a, M, R2a, J, W, and the explicit (CR3aR4a)n1 and W branches.
- Claim 27 narrows to the A/D/E/G and R9a–R12a universe with boron as the fixed element, and retains ring closure options.
Business implication
- In enforcement, you typically see parallel claim tracks to cover different scaffold cores, reducing design-around opportunities at the “core template” level. A generic or follow-on chemistry that avoids Formula I’s additional constraints may still land within Formula II’s broader A/D/E/G-centered definition.
What inflammatory diseases does US 9,682,092 cover, and how does that affect enforcement breadth?
Disease list breadth (claim 17)
Claim 17 defines a wide disease set, including:
- Autoimmune/inflammatory: arthritis, rheumatoid arthritis, inflammatory bowel disease (Crohn’s disease, ulcerative colitis), lupus, Sjogren’s syndrome, uveitis, ankylosing spondylitis, dermatitis, fibromyalgia
- Neuroinflammation/neurodegeneration: Alzheimer’s disease, Parkinson disease, multiple sclerosis, cerebral malaria
- Cardiovascular inflammatory states: congestive heart failure, stroke, restenosis, aortic valve stenosis, atherosclerosis
- Pulmonary inflammatory diseases: allergic rhinitis, asthma, COPD, sarcoidosis, cystic fibrosis, chronic granulomatous inflammation
- GI/liver: pancreatitis, autoimmune hepatitis, hepatitis C, primary biliary cirrhosis, primary sclerosing cholangitis, fulminant liver failure, celiac disease, non-specific colitis
- Renal inflammatory states: kidney failure, glomerulonephritis, vasculitis
- HIV-related cachexia and other oncology/therapy complications: “chemotherapy/radiation related complication”
- Metabolic and other systemic: diabetes type I and II, anemia, allergy, HIV-related cachexia, pulmonary/renal/cardiac sublists
Mechanism tie-in
- Claim 16 and claim 22 encode a mechanistic/dosing constraint tied to:
- inhibiting pro-inflammatory cytokine expression or stimulating anti-inflammatory cytokine expression
- while staying below an amount “sufficient to substantially inhibit cyclin dependent kinases.”
Cytokine specificity (claims 19–20)
- Pro-inflammatory cytokines listed in claim 19:
- IL-1α/β, IL-2, IL-3, IL-6, IL-7, IL-9, IL-12, IL-17, IL-18, IL-23, TNF-α, LT, LIF, Oncostatin, IFN-γ (labeled “IFNc1α, β, γ” in your excerpt)
- Anti-inflammatory cytokines listed in claim 20:
- IL-4, IL-10, IL-11, W-13, TGF-β
Business implication
- The disease breadth increases the number of potential infringement narratives across indication expansions. However, the cytokine mechanism + “less than CDK substantial inhibition” constraint can become the technical battleground.
How strong is the “dose window” limitation: less than sufficient to substantially inhibit cyclin dependent kinases?
What the claim actually says
- Claim 16: “amount sufficient to treat… by inhibiting pro-inflammatory cytokine expression or by stimulating anti-inflammatory cytokine expression, but the amount is less than sufficient to substantially inhibit cyclin dependent kinases.”
- Claim 22 repeats the same limitation.
Enforcement meaning
- This creates a dual-axis boundary:
- The dose must produce the claimed cytokine effects (functional threshold).
- The dose must be below a functional CDK inhibition threshold (“substantially inhibit” is a qualitative qualifier that invites assay-based disputes in litigation).
Practical infringement risk
- If an accused dosing regimen is argued to be below the CDK inhibition threshold, the patent can still be asserted if the accused product shows cytokine modulation without substantial CDK pathway inhibition.
- If an accused regimen unintentionally achieves CDK inhibition “substantially,” it could be argued to fall outside the claim’s “less than sufficient” boundary.
Business implication
- This is not a purely chemical or purely indication claim. It is a performance-limited claim, which tends to shift litigation from chemistry-only to PK/PD and pathway biomarker disputes.
What formulation and delivery-related claims add to the patent’s coverage?
Formulation expansion
- Claim 2 adds: administering the compound as part of a pharmaceutical formulation with pharmaceutically acceptable excipient.
Practical scope
- This is a standard formulation wrapper. It typically covers at least:
- oral tablets/capsules
- injectables
- any formulation where the claimed compound is present with pharmaceutically acceptable excipients
What it does not do
- In the excerpt provided, there is no detailed release-rate, coating, particle size, or specific excipient limitation. The formulation claim therefore likely remains broad, but it does not create strong protection for specific drug-product manufacturing methods.
How do the additional method claims target cellular and in vivo inflammatory response endpoints?
US 9,682,092 includes functional biological assays that can broaden infringement theories beyond “clinical indication” claims.
Cell-based / cytokine production claims
- Claim 24: method for inhibiting production of an inflammatory cytokine protein by cells, comprising combining cells with a therapeutic amount of the compound, where production is inhibited.
- Claim 25: therapeutic amount sufficient to inhibit cytokine production between about 50% and about 99%.
- This adds a quantifiable functional threshold.
Inflammatory response contact claim
- Claim 26: contacting a human or animal with a therapeutic amount to inhibit an inflammatory response.
Business implication
- These claims can support infringement arguments even when the end use is framed as laboratory or mechanistic testing, and can be useful in settlement leverage when the accused compound shows clear cytokine suppression in relevant assays.
Which specific compound embodiments are claimed, and what do the generic Markush examples imply?
In your excerpt, claims 3–15 and 8–15 appear to include explicit embodiment limitations (structures in subclaims 3, 4, 5, 6, 7, and enumerated compound lists in 8–15). The text you supplied omits the actual drawings/chemical formula content for those subclaims, but the pattern is clear:
- Independent Markush claims are followed by subclaims that define:
- specific R1a choices (e.g., claim 12 says R1a is H)
- specific R10a and R11a hydrogen/halogen/methyl/cyano/methoxy/hydroxymethyl/p-cyanophenyloxy patterns (claims 13–15)
- and additional structure-defined embodiments (claims 3, 4, 5, 6, 7, 8, 9, 10, 11).
How that changes the landscape
- The “embodiment” subclaims usually supply fallback claim positions: if a court finds the broad Markush definition ambiguous or not met, the narrower embodiment claims can still be asserted if an accused compound matches the specific enumerated substituent combinations.
What generic entry risks exist for products competing with US 9,682,092’s compound class?
Primary generic entry risk vector
- If a generic/follow-on compound is a boron-containing analog that falls within Formula I or Formula II variable scope, it can infringe on method claims if it is labeled or used for the claimed cytokine-related inflammatory indications and dose range.
Secondary risk vector: “dose window”
- A risk for challengers is that dose regimens can be hard to align with the “less than sufficient to substantially inhibit CDKs” qualifier. If comparative PK/PD studies show CDK inhibition above the threshold, the “design around” could weaken.
Tertiary risk vector: cellular assay claims
- Even without a clinical label, broad functional assays (claims 24–25) can be used to argue infringement if the product is used in or results in the claimed cytokine suppression effects in relevant cell systems.
Business implication
- The highest litigation probability occurs when a follow-on applicant targets the same inflammatory indications and dose range while using or causing cytokine modulation without CDK inhibition claims. Patent defenses often become fact-intensive around pathway inhibition and biomarker readouts.
How likely is overlap with other patent families: what claim elements invite cross-family mapping?
Without the full bibliographic record (priority dates, assignee, family members, and cited art), only claim-elements can be mapped to typical portfolio structures.
Claim elements that typically overlap across families
- Boron-containing heterocycle scaffolds often have multiple generations of claims around:
- core scaffold variants (Formula I vs II)
- substituent permutations (R1a, R10a, R11a, aromatic substituents)
- dosing for cytokine modulation (pro- vs anti-inflammatory cytokines)
- The specific “cytokine expression modulation” framing (IL-1, IL-6, TNF-α, IL-17, IL-23, TGF-β, IL-10, etc.) tends to map to:
- broad therapeutic use patents
- method-of-use patents
- and sometimes biomarkers-driven patents.
Business implication
- Expect layered protection: scaffold + use + dose-window + functional assay claims. Design-around generally requires structural escape from Formula I/II or a pathway-effect escape (avoiding cytokine modulation or staying outside the CDK inhibition threshold).
US 9,682,092 litigation and Orange Book status: what is known from your inputs?
No data provided
- Your prompt provides the claim text but does not provide:
- the listed FDA application/Orange Book drug identity
- any litigation docket numbers
- assignments or continuation history
- settlement agreements
- or expiration dates.
Under the operating constraints, this response cannot responsibly assert any litigation or Orange Book status for US 9,682,092.
Key Takeaways
- US 9,682,092 is structurally expansive: the independent claims cover boron-containing compounds defined by Formula I and Formula II with wide Markush substituent sets and multiple optional ring closures.
- The estate is functionally expansive: it covers inflammatory disease treatment plus mechanistic cytokine modulation (pro-inflammatory and anti-inflammatory cytokines) and extends into cell-based cytokine production inhibition and inflammatory response inhibition.
- The most strategically litigated qualifier is the dosing limitation: therapeutic cytokine effects must occur at an amount “less than sufficient to substantially inhibit cyclin dependent kinases.”
- Subclaims narrowing R-group selections and specific embodiments provide fallback positions for infringement if broad Markush coverage is disputed.
- Generic/follow-on risk is highest when a competitor’s compound is a boron analog within the Formula I/II variable set and is used at dosing regimens that modulate the listed cytokines without substantially inhibiting CDKs.
FAQs
1) Does US 9,682,092 claim specific boron chemistry or just “B is boron”?
The excerpt shows an explicit structural limitation: B is boron. The remaining variables are Markush-defined and widely permissive for substituents around the scaffold.
2) Can the patent be enforced without a specific branded indication label?
The claim set includes broad method-of-use language tied to disease and also includes cytokine and inflammatory response functional claims, enabling enforcement theories grounded in use and biological effect.
3) What is the biggest design-around lever: changing the scaffold or changing the pharmacology?
Changing scaffold structure can move an accused compound outside Formula I/II. Changing pharmacology can attempt to avoid the cytokine modulation endpoints or the “less than CDK substantial inhibition” constraint.
4) How do claims 24–25 affect preclinical and biomarker testing infringement risk?
They support claims tied to cell-based cytokine production inhibition with a quantified inhibition range (about 50% to about 99%), which can be used to argue infringement based on experimental outcomes.
5) Why do Formula I and Formula II both matter for competitive freedom-to-operate?
They cover parallel structural templates. A compound outside Formula I could still fall within Formula II, so clearance requires checking both independent tracks.
References
- US Patent No. 9,682,092. Claims as provided in prompt (claim 1–27 excerpt).
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