Details for Patent: 11,879,013

Which drugs does patent 11,879,013 protect, and when does it expire?

Patent 11,879,013 protects LAZCLUZE and is included in one NDA.

This patent has seventeen patent family members in sixteen countries.

Summary for Patent: 11,879,013

Title:	Combination therapies with bispecific anti-EGFR/c-Met antibodies and third generation EGFR tyrosine kinase inhibitors
Abstract:	The present invention relates to combination therapies with bispecific anti-EGFR/c-Met antibodies and 3rd generation EGFR tyrosine kinase inhibitors.
Inventor(s):	Sylvie Laquerre, Matthew Lorenzi, Sheri Moores
Assignee:	Janssen Biotech Inc
Application Number:	US15/931,726
Patent Litigation and PTAB cases:	See patent lawsuits and PTAB cases for patent 11,879,013
Patent Claim Types: see list of patent claims	Use;

Scope and patent landscape for US Drug Patent 11,879,013 (bispecific anti-EGFR/c-Met plus Formula (I) combination method)

US Drug Patent 11,879,013 claims a US method-of-treatment combining (i) an isolated bispecific anti-EGFR/c-Met antibody with (ii) a small-molecule “compound of formula (I)” (including specific salt/solvate/hydrate/tautomer forms), for EGFR or c-Met expressing cancers under defined molecular subtypes, prior-treatment status, dosing regimens, and disease indications. The claim set is broad at the level of “combination therapy” but is narrowed through specific antibody CDR sequences (SEQ ID NOs) and specific small-molecule identity (example corresponds to a defined N-(… ) acrylamide-like structure) and then broadened again via numerous patient, biomarker, and cancer-type enumerations.

Below is a structured, litigation-grade assessment of claim scope, attack surfaces (invalidity/design-around), and a practical US patent landscape framing around the likely patent cohorts that cover: the bispecific antibody, the small molecule, and the combination dosing and responder populations.

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What is claimed in US Drug Patent 11,879,013 and what is the effective scope of the combination?

Core independent claim (Claim 1) covers:

• A method of treating a subject with EGFR or c-Met expressing cancer
• by administering a combination therapy consisting of:
  1. an isolated bispecific anti-EGFR/c-Met antibody, and
  2. a compound of formula (I) (including solvate/hydrate/tautomer or pharmaceutically acceptable salts)

Functional requirement: “therapeutically effective amount” for both components.

Practical consequence: infringement focus is on the act of treating (method use), not on manufacturing. For Paragraph IV-type disputes, “likely infringement” turns on whether a generic or competitor’s product label or proposed clinical use falls within the claimed dosing, populations, and combination timing.

What parts are structurally fixed vs. variable in Claim 1?

• Fixed / identity-defining

  • the bispecific antibody is not just “any” EGFR/c-Met bispecific; it is tied to dependent claims with specific CDRs/variable regions (Claims 2-6, and implied identity in Claims 2-5).
  • the small molecule is tied to formula (I) and the dependent “represented by formula (II)” plus an explicit named structure (Claims 7-8).

• Variable / expanded

  • cancer type: Claim 23 lists many cancers (including NSCLC, multiple epithelial cancers, and others).
  • EGFR/c-Met status: Claim 9 and its dependents enumerate EGFR mutation/amplification patterns; Claim 12 adds a c-Met mutation type; Claim 13 adds KRAS substitutions.
  • clinical context: Claims 14-22 define diagnosis stage and prior EGFR TKI exposure and specific EGFR TKIs.
  • dosing timing and schedule: weekly/biweekly antibody cycles and daily small molecule dosing are specified in Claims 25-39 and sequencing in Claims 40-42.

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How specific are the antibody requirements in US 11,879,013? (CDR/sequence-defined bispecific scope)

What CDR sequences define the bispecific antibody in the claim set?

Dependent Claims 2-3 lock the antibody to specific CDRs and variable regions:

• EGFR-binding domain:
  • HCDR1 = SEQ ID NO: 1
  • HCDR2 = SEQ ID NO: 2
  • HCDR3 = SEQ ID NO: 3
  • LCDR1 = SEQ ID NO: 4
  • LCDR2 = SEQ ID NO: 5
  • LCDR3 = SEQ ID NO: 6
• c-Met-binding domain:
  • HCDR1 = SEQ ID NO: 7
  • HCDR2 = SEQ ID NO: 8
  • HCDR3 = SEQ ID NO: 9
  • LCDR1 = SEQ ID NO: 10
  • LCDR2 = SEQ ID NO: 11
  • LCDR3 = SEQ ID NO: 12

Then Claim 3 adds variable region examples:

• EGFR VH = SEQ ID NO: 13, VL = SEQ ID NO: 14
• c-Met VH = SEQ ID NO: 15, VL = SEQ ID NO: 16

Claim 5 further nails down heavy and light chain components:

• HC1 = SEQ ID NO: 17, LC1 = SEQ ID NO: 18
• HC2 = SEQ ID NO: 19, LC2 = SEQ ID NO: 20

Claim 4 specifies IgG1 isotype.

What glycoform feature is included?

Claim 6 limits the bispecific antibody to a biantennary glycan with fucose content of ~1% to ~15%.

Infringement implication: a competitor could attempt to argue non-infringement if they use an antibody with different CDRs/variable regions or non-matching glycosylation profile, but they risk capturing equivalent designs if the patent’s interpretation treats “fucose content” and “biantennary” as not limiting, or if claim construction favors a functional reading. The claim language, however, is sequence and glycan content specific.

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What is “compound of formula (I)” in US 11,879,013 and how tightly is it defined?

How the small-molecule scope is structured

• Claim 7: “compound of formula (I) … represented by a compound of formula (II)”
• Claim 8: the compound is specified by an explicit chemical name:
  • “N-(5-(4-(4-((dimethylamino)methyl)-3phenyl-1H-pyrazol-1-methoxy-2-morpholinophenyl)acrylamide …” (truncated in the user-provided text but clearly identifying a single defined structure)

Infringement implication: for method claims, any substitution that is not within formula (I)/(II) (including permitted salt/tautomer/solvate scope) is outside the literal claim.

Design-around pressure points

• Reformulation or different hydrate/solvate form is still within scope if expressly included (Claims 1, 7).
• A structurally different analog (even close pharmacophore) is outside the formula-defined boundary unless equivalency arguments succeed in a post-claim-construction framework.

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Which cancers and biomarkers are explicitly covered? (EGFR/c-Met mutation and KRAS co-biomarker scope)

Broad cancer basket

Claim 23 enumerates a wide set of malignancies, including:

• NSCLC
• epithelial cancers across multiple organs
• breast, ovarian, lung squamous/adenocarcinoma
• small cell lung
• colorectal, anal, prostate
• kidney/bladder/head and neck/pharynx/nose/pancreatic/skin/oral/tongue/esophageal/vaginal/cervical/spleen/testicular
• gastric/thymus/colon/thyroid/liver/HCC
• sporadic or hereditary papillary renal cell carcinoma (PRCC)

Claim 24 makes NSCLC a specific dependent target.

EGFR/c-Met biomarker categories

Claim 9 covers:

• wild-type EGFR or EGFR mutation
• EGFR gene amplification
• increased circulating HGF
• wild-type c-Met or c-Met mutation
• c-Met gene amplification
• mutant KRAS

Claim 10 expands EGFR mutations with extensive lists, including:

• exon 19 deletions (delE746-A, delE746_T751InsKV, many insertions/deletions)
• exon 20 indel families
• L858R
• many other listed point mutations (e.g., T790M, L858P/L858R)
• the recurring “X is any amino acids” framing for insertion/deletion variants.

Claim 11 narrows Claim 10 to exon 19 deletions and/or L858R.

Claim 12: c-Met mutation example is exon 14 skipping mutation.

Claim 13: mutant KRAS examples include G12V, G12C, G12A.

Infringement implication: the claim set does not require both EGFR and c-Met alterations. It is sufficient that the subject has EGFR or c-Met expressing cancer, with specific genetic/biomarker subsets described as dependent limitations. A clinician’s treatment decision that is aligned with any dependent set can be positioned as within those narrower sub-claims.

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When does the method apply based on diagnosis timing and prior EGFR TKI exposure?

Diagnosis status

• Claim 14: diagnosis of EGFR mutation prior to administration
• Claim 15: newly diagnosed EGFR or c-Met expressing cancer

Prior treatment exposure

Claim 16: EGFR TKI treatment naïve

Claim 17-18: resistant/relapsed to first-generation EGFR TKIs, including:

• erlotinib or gefitinib

Claim 19-20: resistant/relapsed to second-generation EGFR TKIs:

• afatinib

Claim 21-22: resistant/relapsed to third-generation EGFR TKIs:

• osimertinib

Infringement implication: if a competitor’s proposed label or study enrollment targets only one line of therapy outside these defined categories, it may avoid narrower dependent claims. Claim 1 itself is not limited to line-of-therapy, but the dependent claim layering gives litigation multiple strata.

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What dosing, schedule, and sequencing limitations are claimed?

Antibody dose and dosing interval

• Claim 25: 200 mg to 2000 mg
• Claim 26: 350 mg to 1400 mg
• Claim 27: about 350, 700, 1050, 1400 mg
• Claim 28: once weekly
• Claim 29: once every two weeks

Four-week loading then maintenance pattern:

• Claim 33: weekly for four weeks then once in two weeks thereafter, plus daily small molecule
• Claim 34-39: specific antibody dose examples (700/1050/1400 mg weekly) paired with small molecule 160 mg or 240 mg daily.

Small-molecule dose and interval

• Claim 30: 20 mg to 320 mg
• Claim 31: about 160 mg or 240 mg
• Claim 32: once a day

Combination administration timing

• Claim 40: antibody administered after compound
• Claim 41: one or more times after administering the compound
• Claim 42: antibody administered two to ten or more times after compound administration

Infringement implication: if the competitor uses a different combination timing (e.g., co-administration or first administering antibody then compound), they may avoid dependent claims 40-42. The independent claim still requires combination therapy; but timing clauses can matter in claim construction and proof.

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How does US 11,879,013 interact with “third therapy” add-ons?

Claim 43 adds further administering a third anti-cancer therapy.

Claim 44 identifies examples:

• chemotherapy
• targeted anti-cancer therapy
• kinase inhibitor

Infringement implication: this language reduces avoidance arguments that “combination” must be only dual therapy. If the competitor uses the bispecific plus Formula (I) while also adding chemotherapy or a kinase inhibitor, Claim 43 supports infringement unless the third therapy somehow forces the regimen outside the antibody and small molecule dosing/sequence limitations.

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How strong is the patent estate likely to be, given the claim structure?

Even without filing history, the claim design suggests a multi-layer defensive architecture typical of combination assets:

1. Antibody IP anchor via sequence-defined CDRs/variable regions and glycosylation constraints (dependent claim chain).
2. Small molecule IP anchor via formula boundary plus explicit named structure.
3. Combination IP anchor via method-of-treatment claims that tie both elements together for specific patient subsets and regimens.

Litigation-grade observation: the claims are built to support both:

• Direct method infringement in clinical settings using the exact antibody and small molecule; and
• Infringement-by-inducement theories where product labeling and clinical protocols are aligned with those claimed schedules.

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What patents are most likely to be “near neighbors” around US 11,879,013?

This patent’s claims indicate three dense IP clusters in the US patent landscape:

1) Bispecific antibody family

Look for US applications/patents covering:

• EGFR/c-Met bispecific architectures
• specific CDR/variable-region sequences matching SEQ IDs
• IgG1 formatting
• glycoengineering including fucose content targets

These often appear as:

• claims on antibody constructs (sequence claims, binding assays, and scaffold-specific claims)
• claims on glycosylation control and production methods
• claims on pharmaceutical compositions comprising the antibody

2) Formula (I) small-molecule family

Look for:

• composition and crystalline/solid-state form patents (hydrates/solvates/tautomers)
• salts and polymorph coverage
• synthesis and intermediate patents

3) Combination method family

Look for:

• method-of-use claims in oncology cohorts defined by EGFR and c-Met biomarkers
• combination schedule/loading paradigms (weekly antibody cycles + daily small molecule)
• sequencing clauses (antibody after compound)
• add-on therapy clauses (chemotherapy or additional kinase inhibitor)

In disputes, courts typically treat:

• antibody identity and binding parameters as central to validity/infringement;
• small-molecule definition as central to product substitution;
• scheduling and sequencing as central to whether a competitor’s protocol is within the claimed method.

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What are the main infringement and validity attack surfaces for US 11,879,013?

Infringement attack surfaces (design/label/protocol)

• Use a different bispecific antibody whose CDRs/variable regions do not match the claimed SEQ ID-defined set.
• Use an antibody with different glycosylation that falls outside the “biantennary glycan” plus “fucose 1% to 15%” limitation (if those limitations are construed as binding).
• Use a small molecule outside formula (I)/(II) scope even if it has similar target engagement.
• Change regimen to avoid the specific dose ranges and loading/maintenance schedule (Claims 25-39).
• Change administration sequence (avoid antibody “after” compound) to reduce fit within Claims 40-42.
• Avoid the enumerated patient subsets in dependent claims if those are the only relevant literal fit in a case strategy (e.g., restrict to treatment-naïve outside certain prior-exposure categories).

Validity attack surfaces

Common high-probability grounds in combination method patents include:

• Obviousness from prior art combining EGFR TKIs with EGFR/c-Met targeted biologics or c-Met/EGFR dual engagement.
• Antibody enablement and definiteness concerns if the specification does not support the claimed CDR combinations with sufficient breadth or if antibody/glyco limitations create unpredictable production scope.
• Written description and enablement for wide enumerations of cancers, mutations, and dosing schedules.

The breadth of Claim 23’s cancer list and Claim 10’s long mutation enumeration can be a double-edged sword: it helps commercial reach but increases potential enablement/WD scrutiny.

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Which competitive scenarios are most at risk under this patent?

Scenario A: exact dual therapy in EGFR-mutant/OS disruption after osimertinib

Claims 17-22 + 10-12 + 24 create a direct runway for treating:

• EGFR-mutated NSCLC
• post-osimertinib resistance/relapse
• with KRAS codriver subsets
• using the precise bispecific plus formula (I) daily dosing

Scenario B: first- or second-line EGFR TKI naïve or relapse

Claims 16 and 18-20 broaden exposure to:

• TKI-naïve patients
• post-erlotinib/gefitinib or post-afatinib settings

Scenario C: broader tumor boards beyond lung

Claim 23 expands the method to many epithelial malignancies with EGFR/c-Met expression or HGF-driven signaling. This enlarges the commercial perimeter beyond NSCLC.

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Timeline and exclusivity: what can be concluded from claim text alone?

No patent grant date, priority date, or expiration details are provided in the prompt. Without those inputs, a legally useful US exclusivity timeline cannot be computed, and no accurate claim can be made about:

• patent term expiration
• PTA/adjusted expiration
• Orange Book listing status (if any)
• whether Hatch-Waxman Paragraph IV challenges exist

Because the request requires litigation-grade precision, those fields are not filled here.

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Key takeaways

• US 11,879,013 is a method-of-treatment patent for EGFR/c-Met expressing cancers using a specific sequence-defined EGFR/c-Met bispecific antibody plus a formula-bounded small molecule (Formula (I)/(II)).
• The claim scope is wide on oncology indications and biomarker variants (many cancers; extensive EGFR indel/point mutation lists; c-Met exon 14 skipping; KRAS G12 substitutions), but narrow on the drug identities via CDR/variable region SEQ IDs, IgG1, and fucosylation content.
• Dosing and regimen are structured into weekly then biweekly antibody schedules and daily small-molecule dosing, with sequence clauses (antibody after compound) that create identifiable protocol-based design-around options.
• Competitive risk is highest for programs that use the same bispecific construct and same formula (I) and follow the claimed loading/maintenance schedules for EGFR/c-Met positive patients, especially in NSCLC and post-generation EGFR TKI settings.

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FAQs

1) Does US 11,879,013 require NSCLC specifically?
No. NSCLC is a dependent narrowing (Claim 24), but Claim 23 lists many additional cancer types.

2) Can a different antibody scaffold avoid infringement?
Yes, in principle, if it does not meet the CDR/variable region SEQ ID-defined requirements (Claims 2-5) and, if treated as limiting, the IgG1 + fucose content constraints (Claims 4-6).

3) Are different hydrates/solvates of the small molecule outside scope?
No, the claims include solvates, hydrates, tautomers, and pharmaceutically acceptable salts of the formula (I) compound.

4) Is the regimen required to follow a “compound first, antibody later” sequence?
Only the dependent sequencing claims require antibody after compound (Claims 40-42). The base independent claim requires a combination therapy but does not, by itself, impose sequencing.

5) Can chemotherapy or additional kinase inhibitors be added without leaving the claim?
The patent expressly includes “further administering a third anti-cancer therapy” including chemotherapy, targeted therapy, or kinase inhibitors (Claims 43-44).

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References

1. US Patent 11,879,013 (claim set provided in prompt).

Drugs Protected by US Patent 11,879,013

Applicant	Tradename	Generic Name	Dosage	NDA	Approval Date	TE	Type	RLD	RS	Patent No.	Patent Expiration	Product	Substance	Delist Req.	Patented / Exclusive Use	Submissiondate
Janssen Biotech	LAZCLUZE	lazertinib mesylate	TABLET;ORAL	219008-001	Aug 19, 2024		RX	Yes	No						FIRST-LINE TREATMENT OF ADULTS WITH LOCALLY ADVANCED OR METASTATIC NON-SMALL CELL LUNG CANCER (NSCLC) WITH EGFR EXON 19 DELETIONS OR EXON 21 L858R SUBSTITUTION MUTATIONS, IN COMBINATION WITH AMIVANTAMAB
Janssen Biotech	LAZCLUZE	lazertinib mesylate	TABLET;ORAL	219008-002	Aug 19, 2024		RX	Yes	Yes						FIRST-LINE TREATMENT OF ADULTS WITH LOCALLY ADVANCED OR METASTATIC NON-SMALL CELL LUNG CANCER (NSCLC) WITH EGFR EXON 19 DELETIONS OR EXON 21 L858R SUBSTITUTION MUTATIONS, IN COMBINATION WITH AMIVANTAMAB

International Family Members for US Patent 11,879,013

Country	Patent Number	Estimated Expiration	Supplementary Protection Certificate	SPC Country	SPC Expiration
Australia	2020275272
Brazil	112021022828
Canada	3140360
China	113840601
Eurasian Patent Organization	202193117
European Patent Office	3968985
Israel	287962