Patent: 10,160,747

Summary for Patent: 10,160,747

Title:	Compounds and methods for kinase modulation, and indications therefor
Abstract:	Disclosed are compounds of Formula I(b): ##STR00001## or a pharmaceutically acceptable salt, a solvate, a tautomer, an isomer or a deuterated analog thereof, wherein Ring A, Ring HD, J, each T, R.sup.3, R.sup.4, R.sup.5, each R.sup.7, and m are as described in any of the embodiments described in this disclosure; compositions thereof; and uses thereof.
Inventor(s):	Lin; Jack (Hercules, CA), Ibrahim; Prabha N. (Mountain View, CA), Albers; Aaron (San Francisco, CA), Buell; John (San Francisco, CA), Guo; Zuojun (Pasadena, CA), Pham; Phuongly (San Francisco, CA), Powers; Hannah (San Francisco, CA), Shi; Songyuan (Fremont, CA), Spevak; Wayne (Berkeley, CA), Wu; Guoxian (Foster City, CA), Zhang; Jiazhong (Foster City, CA), Zhang; Ying (Fremont, CA), Wu; Jeffrey (Berkeley, CA)
Assignee:	Plexxikon Inc. (Berkeley, CA)
Application Number:	15/460,095
Patent Claims:	see list of patent claims

US Patent 10,160,747: What the claims actually cover and how the US patent landscape stacks up

What is US 10,160,747 claiming?

US 10,160,747 is structured around a broad “Formula II(a)/II(b)” compound genus, dependent sub-genuses (Formula III(a), III(b), III(c)), and a stack of downstream claims: specific embodiments, pharmaceutical compositions, combination regimens, and methods of treatment tied to targets FLT3, CSF1R, and c-kit. The independent claim 1 is the center of gravity: it attempts to claim essentially the entire chemical design space defined by the formula variables.

Claim 1: the chemical genus

Claim 1 covers:

• Compound class: compounds of Formula II(a) or II(b), including
  • pharmaceutically acceptable salts
  • solvates
  • tautomers
  • stereoisomers
  • deuterated analogs
• Core ring logic:
  • Ring A is phenyl, pyridyl, pyrimidinyl, or pyridazinyl
  • Y is N or CR⁹
  • R⁹ is hydrogen, halo, amino, or alkyl optionally substituted with typical medicinal chemistry substituents (alkoxy/hydroxy/haloalkyl/alkoxy patterns are allowed)
• Linkage / double-bond vs single-bond variation:
  • (i) or (ii) selection defines multiple allowable connectivity patterns through Z¹, Z², Z³ (single bond vs double bond; N/C combinations)
• R² definition:
  • R² is an extensive group involving “Ring B” and substituent sets Q, Q¹, Q³, Q⁴
  • Ring B is a 5- or 6-membered saturated or unsaturated ring with 0 to 3 heteroatoms selected from O, N, S
  • Each Q / Q¹ / Q³ / Q⁴ has wide independent substitution permissions: H, alkyl, halo, cyano, haloalkyl, alkoxy, cycloalkyl, heterocycloalkyl, and multiple functional handles like oxo-containing and sulfoxide-like moieties (S(O)ₜR²² patterns)
  • q variable a is 0 to 3, and t is 0, 1, or 2, expanding the scaffold further
• Additional substitution tolerances across R³, R⁶, R⁷, R¹¹, R¹⁰, R¹², R¹³ include:
  • halo/alkyl/alkoxy patterns
  • fused/heteroaryl options
  • oxo/spiro closures under R¹²/R¹²a and R¹³/R¹³a (spirocycloalkyl or oxo)
  • flexible “alkynyl optionally substituted with R¹⁰” endings

Claim 2 through 15: narrowing but still broad

These dependent claims constrain parts of the formula but keep the overall breadth large:

• Claim 2: limits R³, R⁶ to a small halogen/methoxy set, and sets m to 1 or 2.
• Claims 3-4: Formula III(a), III(b), III(c) with R⁶a = hydrogen or fluoro (a small constraint, not a closure).
• Claims 5 and 12-15: constrain Ring A and specify allowable sets for R⁶, R¹², R¹³. Even here, the option sets remain wide (phenyl/pyridyl/heteroaryl, ethynyl substituted with multiple groups, and many substituent allowances for R¹³).

Claim 16: a large “compound selection” list

Claim 16 is a “pick list” covering many numbered structures (P-0001 through at least P-0274 and P-0271/P-0273 appears too, plus P-0135/P-0270 etc.). Practically, this does two things:

• It provides literal support for enforcement against specific members inside the genus, not just the genus itself.
• It also signals that the applicant had a substantial internal library of compounds already identified as plausible actives.

Because the text you provided does not reproduce the actual chemical structures for the P-xxxx entries, the analytical value here is structural rather than enumerative: Claim 16 converts chemical breadth into enforceable, named exemplars.

Claim 17-19: composition and combination

• Claim 17: pharmaceutical composition comprising a claim 1 compound plus carrier.
• Claim 18-19: composition further comprising a second agent. Claim 19 is extremely expansive: it lists multiple classes of chemotherapies, kinase inhibitors, antibodies, hormones, IDO inhibitors, and more. It does not narrow to one disease area. It is written to capture combination therapy broadly.

Claims 20-25: methods tied to FLT3/CSF1R/c-kit

• Claim 20: treatment for disease modulated by FLT3, CSF1R, or c-kit, including inflammatory/autoimmune/cancer settings.
• Claim 21-22: expanded disease list, including acute myeloid leukemia, neuroinflammatory and neurodegenerative indications, eye diseases, many solid tumors, and hematologic cancers.
• Claims 23-25: focus on mutated FLT3, specifically FLT3-ITD and additional mutations (D835, F691L, and D835Y).

Net effect: the claims target both oncology kinase biology and myeloid/neuroinflammatory macrophage biology (CSF1R) while also covering stem cell ablation/prep contexts and a long tail of conditions.

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How broad is the claim coverage in practice?

Claim 1 is a genus with multi-dimensional freedom across:

• aromatic selection (Ring A)
• heteroatom choice (Y)
• substitution freedom (R⁹, plus many other R variables)
• bond/connectivity choices (single vs double bond with Z¹/Z²/Z³ permutations)
• a ring system R² with a heteroatom-rich Ring B plus multi-site substitution (Q/Q¹/Q³/Q⁴; plus a and t knobs)
• two major substituent “end-cap” variables R¹² and R¹³ (each with multiple aromatic/aliphatic possibilities, and even spiro and oxo closure options)

This is typical of patents intended to survive early “design arounds.” The claim language anticipates substitution variation while still keeping a tether to a functional target class via broad method-of-treatment claims.

Critical point

A genus as large as this usually creates a patent validity risk unless the spec supports the breadth with:

• credible medicinal chemistry guidance linking formula features to activity against FLT3/CSF1R/c-kit, and
• adequate examples across the breadth, or
• a clear, narrow “inventive concept” that correlates with the full claimed space.

The claims you provided do not include the specification or the claim construction record needed to assess enablement and written description in a legal sense, but the breadth signal is clear: this is not a narrow analog set.

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Where does the claimed target biology sit in the landscape?

Claim 20-25 tie use to FLT3, CSF1R, and c-kit and, in dependent claims, to FLT3-ITD and specific secondary mutation patterns.

What that implies for infringement and validity

• Infringement leverage often comes from clinical or preclinical testing that shows the drug inhibits these targets or treats these conditions. The method claims are written broadly enough to cover any compound of claim 1 administered for these target-modulated diseases.
• Validity leverage usually comes from prior art kinase inhibitor scaffolds that were known to target FLT3 (and in some cases CSF1R/c-kit), and from “obvious to try” modifications reaching the same chemistry.

Given the claim’s breadth, a landscape review typically focuses on: 1) earlier patents that disclose similar chemical cores for FLT3/CSF1R/c-kit inhibition, 2) earlier patents that disclose similar terminal groups and heteroaryl patterns, and 3) whether earlier patents already covered genus-like formula definitions.

Your prompt does not supply the patent’s bibliographic metadata, assignee, filing date, or jurisdictional family. Without that, a precise priority-date-based novelty analysis cannot be completed.

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Patent landscape risks: what would most likely attack claims like these?

Because your text includes only the claims, not the patent family or prosecution history, the critical analysis must focus on claim form and typical attack surfaces.

1) Genus breadth vs disclosure adequacy

Claim 1 is expansive through dozens of substituent options. The common failure modes for such claims are:

• written description: does the specification show possession of the full breadth, not just a few embodiments?
• enablement: can a skilled person make and test the entire breadth without undue experimentation?

The risk increases with:

• multiple ring systems and substitution sites,
• spiro/oxo options,
• broad Q/Q¹/Q³/Q⁴ permutations.

2) Prior art overlap with known FLT3 inhibitors

FLT3 inhibitor chemistry is a crowded space historically (FLT3-ITD in AML drove a large patent wave). If prior art includes similar:

• core scaffold class,
• aromatic substitution patterns (Ring A),
• heteroatom-directed connectivity (Y and Z¹/Z²/Z³ patterns),
• and similar terminal motifs (R¹²/R¹³ as aryl/alkynyl/heteroaryl with halogen and heteroatom substitutions),

then the novelty may collapse, pushing the case into obviousness.

3) Method claims anchored to target labels

Method claims 20-25 are broad and target-driven. They can be vulnerable if:

• the compound class is already known as kinase inhibitors for FLT3 (and/or CSF1R/c-kit),
• and the use for AML, inflammatory disease, or neuroinflammation is already taught for that class.

If a prior patent discloses the same compounds or obvious structural variants, the method claims often fail on obviousness.

4) Combination claim overreach

Claim 18-19 lists many agents. Overbreadth here can create:

• indefiniteness or lack of support issues in some jurisdictions,
• validity vulnerability if the combination framing is generic and not supported by specific data showing synergy or even non-trivial benefit for the claimed compound class.

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How the claim architecture affects enforceability

Enforcement is likely to be pursued on two levels

1) Genus claim 1 for settlement leverage (broad chemical scope). 2) Specific members via Claim 16’s P-xxxx embodiments, enabling practical infringement analyses for real products.

Dependent narrowing is present but not decisive

Claims 2-15 narrow certain variables, yet because many substituent options remain, they still risk being attacked as “still broad.”

Method claims extend potential damages theories

If a product is marketed for any indication within the enumerated disease list and can be shown to be a compound within Claim 1, method claims can become a leverage point even when chemical structure comparisons are disputed.

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What business decisions should be made from this claim set

1) Treat Claim 1 as a bargaining chip, not a guaranteed clean right. The breadth is extreme, which often invites validity challenges. 2) Use Claim 16 as the practical infringement map. If the candidate product’s structure matches one of the P-xxxx structures (or closely aligns with those specific exemplars), enforcement becomes concrete. 3) Target indication screening matters. The method claims cover both oncology and inflammatory/neuroinflammatory contexts; product label and trial history can drive claim relevance. 4) Combination territory is broad. If the portfolio includes combo regimens, Claim 18-19 could support product-level infringement theories, but the same breadth raises defensibility concerns.

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Key Takeaways

• US 10,160,747 is built around an extremely broad chemical genus (Claim 1) with large combinatorial freedom across aromatic and heterocycle substitution patterns, and includes salts/solvates/tautomers/stereoisomers/deuterated analogs.
• The patent then translates breadth into enforceability via Claim 16’s large list of specific compounds (P-xxxx), plus composition and combination claims (Claims 17-19).
• Method-of-treatment claims (Claims 20-25) are target-labeled for FLT3, CSF1R, and c-kit, with explicit focus on FLT3-ITD and secondary mutations (D835, F691L, D835Y).
• The principal validity risk is the common one for genus-scale claims: breadth vs written description/enablement plus prior art overlap in FLT3 inhibitor chemistry and asserted therapeutic uses.
• For an actionable landscape assessment, the most defensible enforcement path would typically track Claim 16 exemplars and indication-specific method claims, while expecting validity attacks aimed at the full-genus scope.

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FAQs

1) Does Claim 1 cover salts and solvates, or only the free base?

It covers pharmaceutically acceptable salts and also solvates, tautomers, stereoisomers, and deuterated analogs alongside the Formula II(a)/II(b) compounds.

2) Are the biology claims only for FLT3-positive cancer?

No. Claims include diseases modulated by FLT3, CSF1R, or c-kit, and the disease list includes inflammatory and autoimmune settings as well as cancer.

3) What FLT3 mutations are explicitly called out?

The dependent method claims specify FLT3-ITD and additional D835 and/or F691L, including D835Y patterns.

4) What makes Claim 16 important for enforcement?

Claim 16 lists many numbered compound structures (P-xxxx), turning a broad genus into specific, testable targets for infringement comparisons.

5) Is the combination claim limited to one partner therapy?

No. Claim 18-19 lists a very large set of potential second agents across chemotherapy, antibody therapy, hormones, kinase inhibitors, and more.

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References

1. US Patent 10,160,747. Claims text provided in prompt.

Details for Patent 10,160,747

Applicant	Tradename	Biologic Ingredient	Dosage Form	BLA	Approval Date	Patent No.	Expiredate
Recordati Rare Diseases, Inc.	ELSPAR	asparaginase	For Injection	101063	January 10, 1978		2037-03-15
Genentech, Inc.	RITUXAN	rituximab	Injection	103705	November 26, 1997		2037-03-15
Genentech, Inc.	HERCEPTIN	trastuzumab	For Injection	103792	September 25, 1998		2037-03-15
Genentech, Inc.	HERCEPTIN	trastuzumab	For Injection	103792	February 10, 2017		2037-03-15