US Patent 10,561,651 scope, claim-by-claim protection, and US patent landscape for neuroblastoma protein kinase inhibitors
US Patent 10,561,651 claims methods for inhibiting deregulated protein kinase activity in neuroblastoma cells by administering one of four closely defined small-molecule kinase inhibitors (or pharmaceutically acceptable salts) as the sole active agent. The claim set is structurally narrow on target (ROS1 and TrkA/B/C) and on molecule identity, but broad on use context (neuroblastoma cells) and biochemical target coverage (four kinases via a single method claim).
What does US Patent 10,561,651 claim and what is the core protected method?
Featured-snippet answer: The patent protects a method of inhibiting deregulated ROS1/TrkA/TrkB/TrkC kinase activity in neuroblastoma cells by administering one of four enumerated compounds (or salts) as the sole active agent.
Claim 1 is the only independent claim
Claim 1 (independent):
A method of inhibiting deregulated protein kinase activity in a neuroblastoma cell, where the deregulated activity is one or more of:
The method comprises administering an effective amount of a compound as the sole active agent, selected from four specific chemical entities (listed in your prompt) or pharmaceutically acceptable salts.
Key scope levers in Claim 1
- Disease biology constraint: “in a neuroblastoma cell” limits infringement to settings involving neuroblastoma cells (including ex vivo assays, translational models, or clinical use if construed broadly for “cell”).
- Target constraint: the kinase activity must be “deregulated” and must fall within ROS1 and/or TrkA/TrkB/TrkC.
- Agent constraint: the method requires the compound to be the sole active agent. Co-administration with other active agents is a potential design-around lever.
- Molecule identity constraint: Claim 1 is limited to four specific structures (or salts). Substitution outside these exact members is typically outside literal coverage.
Which exact compounds are covered by claim 1 of US 10,561,651?
Featured-snippet answer: Claim 1 covers four enumerated small-molecules and their pharmaceutically acceptable salts.
Claim 1’s “sole active agent” selection set consists of:
- N-[5-(3,5-difluorobenzyl)-1H-indazol-3-yl]-4-(piperazin-1-yl)-2-(tetrahydro-2H-pyran-4-ylamino) benzamide
- N-[5-(3,5-difluorobenzyl)-1H-indazol-3-yl]-4-(4-methyl-piperazin-1-yl)-2-(tetrahydro-2H-pyran-4-ylamino) benzamide
- N-[5-(3,5-difluoro-benzenesulfonyl)-1H-indazol-3-yl]-2-((R)-2-methoxy-1-methyl-ethylamino)-4-(4-methyl-piperazin-1-yl)benzamide
- N-[5-(3,5-difluoro -benzenesulfonyl)-1H-indazol-3-yl]-2-((R)-2-methoxy-1-methyl-ethylamino)-4-(4-methyl -piperazin-1-yl)benzamide
(Your recitation shows the third and fourth species with a formatting difference; if these are truly distinct, the scope includes both. If they are the same, the claim set still covers that molecule once.)
Salt coverage
Claim 1 explicitly includes “pharmaceutically acceptable salt thereof.” That is a typical expansion that can capture multiple crystalline/ionic forms of the same active entity.
Are dependent claims 2–4 only narrowing selections or do they change infringement theory?
Featured-snippet answer: Claims 2–4 are narrow “species” dependents that lock Claim 1 to a specific one of the four molecules.
- Claim 2: species 1 only (or salt)
- Claim 3: species 2 only (or salt)
- Claim 4: species 3 (or salt)
- The claim text in your prompt shows extra spacing/formatting (e.g., “difluoro -benzenesulfonyl” and “4-methyl -piperazin”). That does not change substantive meaning if it is merely typographical.
Practical infringement impact
- If a product uses one of the listed compounds, infringement risk is assessed against Claim 1 and the relevant dependent species claims.
- If a product uses a compound not listed, literal claim coverage typically drops sharply, because Claim 1 does not use Markush “including” language for analogs. The molecule identity is enumerated.
What do dependent claims 5–8 cover about kinase targets?
Featured-snippet answer: Claims 5–8 provide target-specific dependent coverage for ROS1 or TrkA, TrkB, or TrkC as the deregulated kinase activity.
- Claim 5: deregulated activity is ROS1
- Claim 6: deregulated activity is TrkA
- Claim 7: deregulated activity is TrkB
- Claim 8: deregulated activity is TrkC
Target mapping and claim strength
Claim 1 already covers “one or more of” ROS1 and TrkA/B/C. Dependent claims mainly:
- support multiple infringement theories (depending on which kinase is demonstrably “deregulated” in the accused context)
- strengthen validity posture by showing alternative claim constructions are contemplated within the same claim family concept.
How broad is US 10,561,651 in neuroblastoma and kinase inhibition use?
Featured-snippet answer: Broad on the cell-type context (neuroblastoma cells) and on the kinase set (ROS1 + TrkA/B/C), narrow on the drug identity (4 enumerated molecules) and combination element (sole active agent).
What “deregulated” likely requires for enforcement
The patent language ties infringement to a state where kinase activity is deregulated. In litigation, that typically translates to an evidentiary requirement that the neuroblastoma cell line, tumor, or clinical setting exhibits ROS1/TrkA/B/C activity driving the disease phenotype.
“Sole active agent” changes combination therapy risk
If a regimen includes additional pharmacologically active agents, an accused method may argue it fails “sole active agent.” That creates:
- higher enforcement burden for combination regimens
- a potential product development design-around by co-administering a second active with the patented compound
What are likely claim construction hotspots for US 10,561,651?
Featured-snippet answer: The highest-friction terms are “neuroblastoma cell,” “deregulated protein kinase activity,” “one or more of,” and “sole active agent.”
Neuroblastoma cell
- Could be interpreted broadly as any cell derived from neuroblastoma or clinically relevant models.
- Narrow interpretation would still cover patient-derived cells and xenograft-derived contexts where methodology is tied to neuroblastoma cell populations.
“deregulated protein kinase activity”
- A “deregulated” state may be satisfied by overexpression, mutation-driven activation, autocrine/paracrine signaling, or pathway activation readouts.
- If the accused regimen inhibits kinase activity but the cell’s ROS1/Trk pathway is not “deregulated,” defendants can press non-infringement.
“one or more of”
- Claim 1 contemplates mixed kinase involvement. A single-pathway target (e.g., only ROS1) still lands within Claim 1.
“sole active agent”
- This term is a common litigation lever.
- It can become binary: if the accused treatment includes another drug with pharmacological activity, the literal “sole” requirement may not be met.
How does US 10,561,651 compare to broader Trk/ROS1 method-of-use patents?
Featured-snippet answer: Compared with broader platform patents covering generic “inhibiting ROS1 or TrkA/B/C in cancers,” US 10,561,651 is narrower because it requires four specific compounds and neuroblastoma cells.
Likely positioning in an estate
This kind of claim often functions as a use patent anchored to specific chemical matter. It tends to:
- follow earlier chemical composition claims (if any)
- add method coverage that can persist even when some formulations or dosing regimens change, as long as the “sole active agent” and enumerated compound requirements are met.
Orange Book status and FDA regulatory linkage for US 10,561,651?
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No Orange Book listing, NDA/BLA number, approved dosage form, or regulatory reference was provided, so the US FDA regulatory status cannot be tied to this patent without fabricating links.
Patent expiration timing: when does the protection end?
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No application filing date, priority date, or patent term adjustment data was provided. Expiration timing requires those inputs and cannot be computed reliably from the patent number alone within the constraints here.
How many US claims are there beyond the eight you provided, and what other claim types exist?
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Only claims 1–8 were provided. A complete landscape needs the full claim set (including compositions, intermediates, manufacturing methods, or additional method claims) to assess true breadth and redundancy.
Paragraph IV, biosimilar, and generic entry risk for US 10,561,651?
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No drug product identity (active ingredient), market authorization, or exclusivity regime was provided, so generic/biosimilar risk for this specific patent cannot be mapped to the correct regulatory pathway or submission types.
What design-around strategies are suggested by the claim language of US 10,561,651?
Featured-snippet answer: The claim language supports design-arounds focused on (1) changing the active agent identity, or (2) breaking “sole active agent,” or (3) disputing “neuroblastoma cell” and “deregulated kinase” premises.
1) Active-agent substitution
- Any compound outside the enumerated four (or salts) avoids literal infringement.
- In litigation, claim equivalents may still be argued, but the species-locked structure set lowers equivalence capture relative to Markush-style breadth.
2) Combination regimens
- If the accused method administers the patented compound alongside another active agent, defendants can argue “not the sole active agent.”
- This is a direct claim-element lever.
3) Target dispute
- If evidence supports that the relevant neuroblastoma cells do not exhibit “deregulated” ROS1/TrkA/B/C activity, the method may not meet the infringement premise even if kinase inhibition occurs.
What jurisdictions are covered by the US patent number 10,561,651?
Featured-snippet answer: The protection is US-only as a granted US patent. International equivalents may exist, but none are identifiable from the provided record.
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No family members, PCT/EP/WO or other jurisdictional filings were provided.
Key Takeaways
- US 10,561,651 protects a method for inhibiting ROS1 and/or TrkA/TrkB/TrkC kinase activity in neuroblastoma cells by administering one of four enumerated compounds (or pharmaceutically acceptable salts) as the sole active agent.
- The claim set is narrow on chemistry (exact molecule identity) and narrow on regimen composition (“sole active agent”), while broad on target set (ROS1 plus TrkA/B/C) and method context (neuroblastoma cells).
- Dependent claims 2–4 lock compound species; claims 5–8 lock kinase target specificity, providing multiple infringement pathways depending on which kinase activity is evidenced as deregulated.
FAQs
1) Does US 10,561,651 cover combination therapy with another anticancer drug?
The claim requires the kinase inhibitor compound to be the sole active agent, so the presence of another active agent creates a direct literal infringement challenge.
2) If the therapy targets only ROS1, is it still covered?
Yes. Claim 1 covers “one or more” of ROS1/TrkA/B/C, and Claim 5 specifically covers ROS1.
3) If a product uses a close analog of the enumerated compounds, does it infringe?
Not on the face of Claim 1, because it enumerates specific compounds by identity rather than broad Markush categories.
4) What evidence is needed to show “deregulated” kinase activity for infringement?
The asserted neuroblastoma cell context must show ROS1 and/or TrkA/TrkB/TrkC activity is deregulated, typically via pathway or activity readouts tied to the accused method context.
5) Are salts protected even if the free base is not marketed?
Yes. The claims include pharmaceutically acceptable salts of the listed compounds.
References
- United States Patent No. 10,561,651 (claims 1–8 text as provided by user).
