Scope, claims, and US patent landscape for US Drug Patent 9,820,985
US Patent 9,820,985 is a method-of-use patent centered on a single defined chemical entity (and a small set of close structural variants under a broader genus claim) for treating breast cancer with a mechanistic patient-selection scaffold tied to homologous recombination (HR) deficiency and HR/BRCA pathway defects. The claim set is built to capture both (i) monotherapy administration and (ii) combination regimens (radiation and/or selected chemotherapeutics), while maintaining a strong “right compound” anchor through a narrow structural definition in the independent claim.
What does the patent claim (scope headline)?
The core scope is:
- Drug: the stereochemically defined compound (8S,9R)-5-fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-8,9-dihydro-2H-pyrido[4,3,2-de]phthalazin-3(7H)-one (or a pharmaceutically acceptable salt/solvate).
- Indication: treating breast cancer.
- Patient population: cancers and/or subjects deficient in HR-dependent DNA double strand break (DSB) repair, including BRCA1/BRCA2 deficiency and additional HR-pathway protein deficiencies; also includes subjects who are heterozygous for relevant HR-pathway gene mutations.
- Treatment format: includes administration alone and in combination with ionizing radiation and/or chemotherapeutic agents from enumerated sets.
This structure is consistent across independent claims and the dependent layers: the patent uses broad mechanistic language (HR deficiency, BRCA phenotype) but ties enforceability to the specific drug scaffold (and a defined structural genus in a second independent method).
What are the independent claims and how do they define infringement risk?
Claim 1 (independent): single-compound breast cancer treatment
Claim 1 recites a method:
- treating breast cancer in a subject by administering a therapeutically effective amount of:
(8S,9R)-5-fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-8,9-dihydro-2H-pyrido[4,3,2-de]phthalazin-3(7H)-one (or salt/solvate).
Scope implication: infringement is tightly linked to use of that exact compound (or salts/solvates) for breast cancer treatment, regardless of whether the regimen includes radiation/chemo and regardless of the HR-deficiency status of the cancer, unless later dependent claims narrow the population.
Claim 5 (independent): broader structural genus, still breast cancer treatment
Claim 5 recites a second method:
- treating breast cancer in a subject by administering a therapeutically effective amount of a compound having the depicted core structure with variable substituents defined by a detailed definition of Y, Z, A, B, R6, R2, RA, RB, and ring-forming options for RA/RB.
It still requires:
- Y and Z to be aryl or heteroaryl with substitution patterns,
- explicit constraints like B is not OH,
- lists of permissible substituents for R6 (very broad chemical space),
- and permitted stereochemical variants implied by the genus framework.
Scope implication: this independent claim can cover a family of analogs that share the pyrido[4,3,2-de]phthalazin-3(7H)-one scaffold and conform to the substituent constraints, rather than only the single stereodefined drug of Claim 1. If Claim 5’s genus is supported in the specification, it can materially widen competitive freedom constraining “drug-analog” entrants.
How do the dependent claims expand use cases (radiation and combination chemotherapy)?
Radiation and chemo combinations (Claims 2 and 25)
- Claim 2: administration of the compound of Claim 1 in combination with ionizing radiation and/or one or more chemotherapeutic agents.
- Claim 25: mirrors Claim 2 for the method platform of Claim 5.
Practical scope effect: a competitor cannot avoid infringement by choosing combination regimens if the patient is treated with the patented compound and the regimen fits the dependent claim language (radiation and/or enumerated chemo). A “radio-not-chemo” or “chemo-not-radiation” strategy may still fall in Claim 2 because the language is disjunctive (“and/or”).
Chemotherapeutic agent lists (Claims 3, 4, 26, 27)
Broad enumerated chemo list (Claims 3 and 26)
Each chemotherapeutic agent is independently one of the following:
- methyl methanesulfonate
- temozolomide
- dacarbazine (DTIC)
- topoisomerase-1 inhibitors, including:
- Topotecan
- Irinotecan
- Rubitecan
- Exatecan
- Lurtotecan
- Gimetecan
- Diflomotecan
- homocamptothecin
- doxorubicin
- platinum based antineoplastic agent
- 7-substituted non-silatecan
- 7-silyl camptothecin
- paclitaxel
- cetuximab
- daunorubicin
- methotrexate
- hormone
- antiestrogen
- antiandrogen
- gonadotropin releasing hormone analog
- interferon, alpha interferon
- tyrosine kinase inhibitor, including:
- gemtuzumab
- BNP 1350
Scope implication: this is a wide basket. It is not limited to breast-cancer-only agents, which matters for real-world regimen design.
Narrow enumerated chemo list (Claims 4 and 27)
Each chemotherapeutic agent is independently one of:
- irinotecan
- cisplatin
- carboplatin
- paclitaxel
- temozolomide
Scope implication: even if a competitor uses only this smaller set, they can still fall within narrower dependent coverage.
What patient-selection and biomarker scope is locked in?
A large portion of dependent claims focus on HR deficiency and HR gene defects.
HR deficiency framework (Claims 7-8, 16-17, and parallel 20-21)
- Claim 7: breast cancer is deficient in the HR-dependent DNA DSB repair pathway.
- Claim 8: cancer comprises cancer cells with reduced or abrogated ability to repair DNA DSB by HR vs normal cells.
- Claim 16-17: identical structure tied to Claim 1 baseline.
- Claim 20-21: further specifies HR-protein deficiency.
BRCA1/BRCA2 deficiency (Claims 9-10, 18-19, and parallel)
- Claim 9: cancer cells have a BRCA1 or BRCA2 deficient phenotype.
- Claim 10: cancer cells are deficient in BRCA1 or BRCA2.
- Claims 18-19 mirror these for the HR-deficiency dependent layer.
Expanded HR-pathway proteins (Claims 11-12, 20-21)
- Claim 11: cancer cells are deficient in proteins involved in HR DNA DSB repair.
- Claim 12: specifies deficiency in one or more of:
- ATM
- Rad51
- Rad52
- Rad54
- Rad50
- MRE11
- NBS1
- XRCC2
- XRCC3
- cABL
- RPA
- CtIP
- MBC
Scope implication: the claim enumerates core HR components spanning sensing/signaling (ATM), recombinase machinery (Rad51/Rad52/Rad54/Rad50), MRN complex (MRE11/NBS1), replication protein A (RPA), end resection (CtIP), and additional HR factors (XRCC2/XRCC3). This supports broad patient coverage within HR-deficient tumors, not only BRCA.
Subject genotype inclusion (Claims 13-14 and 22-23)
- Claim 13: subject is heterozygous for mutation in a gene encoding a component of HR pathway.
- Claim 14: heterozygous for mutation in BRCA1 and/or BRCA2.
- Claim 22-23: same but framed as dependent on Claim 1.
Scope implication: by including heterozygous germline mutation status, the patent can cover a broad “biomarker-positive” population even where tumor HR phenotype may be argued from germline risk.
Cancer stage/setting (Claim 15 and 24)
- Claim 15 / 24: breast cancer is locally advanced or metastatic, or advanced ovarian cancer (worded across the independent claim families).
Scope implication: this supports enforcement in late-line clinical settings where biomarker testing is common.
What is the concrete chemical scope across Claims 6 (specific embodiments)?
Claim 6 lists multiple specific stereochemical or near-stereochemical exemplars that qualify under the genus framework of Claim 5. The enumerated structures include:
- (8S,9R)-5-fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-8,9-dihydro-2H-pyrido[4,3,2-de]phthalazin-3(7H)-one
- (8S,9R)-8-(4-fluorophenyl)-9-(1-methyl-1H-imidazol-2-yl)-8,9-dihydro-2H-pyrido[4,3,2-de]phthalazin-3(7H)-one
- (8S,9R)-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-8,9-dihydro-2H-pyrido[4,3,2-de]phthalazin-3(7H)-one
- (8S,9R)-5-fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-imidazol-2-yl)-8,9-dihydro-2H-pyrido[4,3,2-de]phthalazin-3(7H)-one
- (8S,9R)-5-fluoro-9-(1-methyl-1H-imidazol-2-yl)-8-phenyl-8,9-dihydro-2H-pyrido[4,3,2-de]phthalazin-3(7H)-one
- (8S,9R)-8-(4-(azetidin-1-ylmethyl)phenyl)-9-(4-fluorophenyl)-8,9-dihydro-2H-pyrido[4,3,2-de]phthalazin-3(7H)-one
- (8S,9R)-8-(4-((dimethylamino)methyl)phenyl)-5-fluoro-9-(1-methyl-1H-1,2,4-triazol-5-yl)-8,9-dihydro-2H-pyrido[4,3,2-de]phthalazin-3(7H)-one
Scope implication: Claim 6 gives concrete “anchor points” inside the genus, which can help in infringement mapping. It also suggests the patent family was drafted with multiple heteroaryl and substituent permutations in mind.
How does the claims architecture shape enforceability?
Layering design
- Independent layer 1 (Claim 1): single compound, breast cancer, administration method.
- Independent layer 2 (Claim 5): broader genus, breast cancer, administration method.
- Combination layer: radiation and chemo (Claims 2-4 and 25-27).
- Biomarker layer: HR deficiency and HR-pathway defects (Claims 7-14 and 16-23).
- Stage layer: locally advanced/metastatic or advanced ovarian cancer (Claims 15 and 24).
Enforcement levers
- To establish infringement for Claim 1, the accused regimen must involve administration of the exact single compound (or salt/solvate) for breast cancer treatment.
- To challenge analogs, Claim 5 can capture structural relatives if their substituent set falls within the defined parameters for Y/Z/A/B/R6/R2/RA/RB and the depicted core.
- The HR-deficiency and BRCA/HR-protein claims are dependent. That means they typically matter most when asserting tighter clinical populations (biomarker-defined trials) rather than broad “any breast cancer” use.
Patent landscape implications in the US (what the claim set signals about competitive freedom)
Even without family identifiers here, the claim language itself indicates how this patent will be attacked or leveraged in US practice:
1) Likely strong hold on “same compound, any regimen”
Because Claim 1 is a straightforward method of treating breast cancer with a defined drug, any competitor using that drug in breast cancer contexts will face baseline exposure. Dependent claims increase coverage for:
- radiation combinations,
- and many common chemo and targeted agents.
2) Genus claim can constrain “next analog” strategies
Claim 5’s genus language plus Claim 6’s enumerated exemplars increases risk for companies pursuing “closely related structures” as follow-on candidates. If the chemical modifications sit inside the permitted R6, Y/Z/A/B, and ring-closure constraints, infringement can be asserted against method-of-use even when the drug is not identical to Claim 1’s compound.
3) Biomarker dependence reduces overbreadth defenses but does not eliminate them
HR-deficiency framing narrows the patient population when dependent claims are asserted. That can:
- align better with clinical development focused on HR/BRCA deficiency,
- but also create avenues for design-around by targeting populations without HR deficiency and by using alternative therapeutic mechanisms (still risking Claim 1 if the main drug is used in breast cancer broadly).
4) Combination lists reduce avoidance via regimen substitution
The chemo lists are broad in Claims 3 and 26 and narrower in Claims 4 and 27, but both are inclusive of major breast cancer regimens (e.g., paclitaxel) and DNA damage repair pathway agents (e.g., temozolomide, irinotecan, platinum agents). A competitor cannot easily avoid the patent by swapping among a wide range of conventional agents.
Key takeaways
- US 9,820,985 is built around a method-of-treatment approach for breast cancer anchored to a defined (8S,9R) pyrido[4,3,2-de]phthalazin-3(7H)-one drug scaffold (Claim 1) and a substituent-defined genus (Claim 5).
- The patent captures monotherapy administration and expands to ionizing radiation and broad enumerated combination chemotherapies/targeted agents via dependent claims.
- Patient selection is supported by a dense HR-deficiency framework, including BRCA1/BRCA2 deficient phenotype and a long list of HR pathway proteins plus heterozygous germline mutations.
- The practical enforceability risk is highest where competitors use the same drug (Claim 1) in breast cancer settings, and secondarily where they use structurally compliant analogs (Claim 5) in biomarker-enriched HR-deficient populations.
FAQs
1) Does the patent cover breast cancer treatment without requiring HR deficiency?
Yes. Claim 1 requires treating breast cancer by administering the defined drug, with no HR deficiency limitation in the independent statement. HR deficiency is introduced in dependent claims (Claims 7-14 and 16-23).
2) Can combination regimens avoid the patent?
Not if they still fall within the dependent combination claims. Claims 2 and 25 include radiation and/or chemotherapy. Claims 3-4 and 26-27 enumerate chemotherapy agents, including paclitaxel and multiple DNA damage agents.
3) Is the chemical scope limited to one compound?
No. Claim 5 is a genus defined by variable substituent constraints, and Claim 6 lists specific example embodiments within that genus, widening scope beyond Claim 1’s single compound.
4) What biomarkers are explicitly listed?
BRCA1/BRCA2 (phenotype and deficiency) and multiple HR pathway proteins: ATM, Rad51, Rad52, Rad54, Rad50, MRE11, NBS1, XRCC2, XRCC3, cABL, RPA, CtIP, and MBC.
5) Does the patent address subject genotype?
Yes. Several dependent claims require the subject is heterozygous for HR-pathway gene mutations, including heterozygosity for BRCA1 and/or BRCA2.
References
- United States Patent and Trademark Office. US Patent 9,820,985 (claims provided in prompt).
