When do biologic drug patents expire and when will biosimilars launch?

Executive summary
US Patent 10,093,732 claims treatment of hypercoagulation using an IL-6 antibody (or fragment) defined by specific VL and VH CDR sequences (SEQ ID NOs 87-89 and 90-92, corresponding to VL SEQ ID NO 85 and VH SEQ ID NO 86). Dependent claims broaden the patient population (including cancer), clinical biomarkers (D-dimer, CRP), and regimen scope (statins and anticoagulants; chemotherapy/oncology combinations; adjunct drug labels are explicitly enumerated). The patent’s enforceability and commercial coverage hinge on (1) whether accused products practice the claim’s CDR-defined antibody, (2) whether “improved or restored” coagulation is evidenced by measurable endpoints, and (3) whether claim scope is vulnerable to obviousness/anticipation over earlier IL‑6/cytokine blockade and known hypercoagulation indications.

Critical point: the independent claim is not “any anti-IL‑6 antibody.” It is constrained to a particular CDR set and mapped to specific parent VL/VH sequences. That can sharply narrow validity and infringement risk versus a broad “tocilizumab-like” narrative. At the same time, dependent claims add functional and therapeutic breadth that can raise enablement and obviousness scrutiny if the specification does not provide robust support across the long, enumerated disease lists (especially the expanded oncology tumor taxonomy).

H1: US Patent 10,093,732 claims landscape for IL-6 antibody treatment of hypercoagulation (CDR-defined VL/VH, cancer, D-dimer/CRP, statin-anticoagulant regimens)

What is US 10,093,732 actually claiming: method-of-treatment using CDR-defined anti-IL‑6 antibodies?

Short answer: It claims a clinical method for patients with hypercoagulation, where the therapeutic agent is an IL‑6 antibody or fragment that includes specific VL and VH CDRs defined by SEQ ID NOs 87-89 (VL) and 90-92 (VH), corresponding to VL SEQ ID NO 85 and VH SEQ ID NO 86.

Independent claim 1 structure and claim construction pressure points

Claim 1 requires all of:

Patient with a disease “associated with hypercoagulation.”
Administer an IL‑6 antibody or fragment.
Coagulation profile is “improved or restored to normal.”
Antibody comprises:
- VL polypeptide with CDRs of SEQ ID NO 87, 88, 89 corresponding to VL CDRs of VL chain sequence SEQ ID NO 85.
- VH polypeptide with CDRs of SEQ ID NO 90, 91, 92 corresponding to VH CDRs of VH sequence SEQ ID NO 86.

Construction levers likely to matter in litigation

CDR literalism: CDR-defined antibodies often lead courts to focus on sequence identity/functional equivalents at the CDR level, not just overall similarity. Any accused antibody must match at least the CDR requirements (or infringe under equivalence arguments if available under the governing circuit).
“Normal” coagulation profile: requires a definition in the patent record. If “normal” is not tightly anchored to assay ranges (PT/INR, D-dimer thresholds, fibrin degradation products, etc.), the term can become a practical evidentiary battleground.
Causation: method claims typically require that the IL‑6 antibody administration results in profile improvement. That can be contested as correlation versus causal effect.

Which anti‑IL‑6 antibodies could fall within the literal scope of claim 1?

Short answer: Only IL‑6 antibodies whose VL/VH CDRs match the claimed CDR sets (SEQ IDs 87-89 and 90-92 mapped to SEQ IDs 85 and 86) would fall within literal claim 1. Dependent claims further specify aglycosylation, Fc modifications, human/humanized/SCF/chimeric forms, heavy/light constant regions, and sequence identity thresholds (90%).

Dependent claims that narrow the antibody identity

Claim 6 (aglycosylated): narrows to glycoform-lacking Fc or engineered aglycosylated constructs, depending on how the claim is supported.
Claim 7 (heavy/light constant regions in SEQ ID NO:588 and 586): ties to specific constant region sequences, restricting to particular heavy/light constant frameworks.
Claim 8 (Fc region modified): requires Fc engineering altering effector function, half-life, proteolysis, and/or glycosylation.
Claim 9 (human/humanized/scF/chimeric): excludes fully murine formats.
Claim 13 (≥90% identity to SEQ ID NOs 86 and 85): provides an alternate route to capture variants of the parent VH/VL sequences via identity thresholds, even if not exact CDR match is argued.

Key risk: how “CDR-defined” scope interacts with product engineering

If an IL‑6 program uses CDR grafting, framework swaps, or changes to constant regions/Fc effector properties, infringement turns on which elements are changed:

Changing frameworks but preserving CDRs can still infringe if CDRs remain identical and the antibody falls within the constant-region/identity limitations.
Changing CDRs to alter antigen binding likely avoids literal scope, but equivalence arguments can still be litigated.

When does US 10,093,732 expire in the US, and what exclusivity cliffs matter for generic entry?

Short answer: Patent term and any pediatric extension depend on the application filing and any PTA/PTE calculations embedded in the USPTO record. Without the patent’s filing date, priority chain, and any PTA/PTE, a precise expiration date cannot be stated here.

What patents or prior art could attack validity: do earlier IL‑6 blockers anticipate these hypercoagulation method claims?

Short answer: Earlier IL‑6 pathway therapeutics (historically including tocilizumab and other anti‑IL‑6/IL‑6R biologics) create strong obviousness pressure for “IL‑6 blockade improves inflammation-driven coagulation,” but US 10,093,732’s independent claim is antibody-sequence constrained. That means the strongest validity challenges would likely combine:

prior disclosure of IL‑6 blockade for thromboinflammatory states, with
prior disclosure or suggestion of the specific antibody CDR sequences or near-identity variants, or
antibody engineering that yields predictable CDR-framework/function combinations.

Anticipation vs obviousness likely to track different claim elements

Disease/condition + hypercoagulation: prior art in sepsis, DIC, thrombosis, COVID-associated coagulopathy (if in the record), and malignancy-associated thrombosis can support the “method for hypercoagulation” portion.
IL‑6 antibody use: tocilizumab-style therapeutics likely anticipate the general concept of IL‑6 blockade for inflammatory conditions that correlate with coagulation.
CDR-defined antibodies: anticipatory references must disclose the exact antibody sequences or the CDR sets mapped to the stated SEQ IDs. This is less common in broad prior art. Obviousness can still win if the art provides a clear path to engineer or select those CDRs from known scaffolds.
“Improved or restored to normal coagulation profile”: prior art must disclose measurable improvements in coagulation parameters, not just reduced inflammatory markers.

What formulations are protected: antibody structure claims vs administration regimen claims

Short answer: The patent protects a method of treatment whose therapeutic ingredient is a specific IL‑6 antibody (or fragment) with defined VL/VH CDRs, plus dependent claims covering aglycosylation and Fc engineering, and method-of-treatment regimens that include anticoagulants and statins.

Fc engineering and effector-function scope

Claim 8 explicitly requires Fc modifications affecting effector function/half-life/proteolysis/glycosylation.
Claim 12 ties to Fc derived from particular IgG subclasses (IgG1-4).
These elements can matter for whether an accused IL‑6 antibody with altered Fc (for example, altered ADCC) lands inside or outside the narrower dependent claims.

Aglycosylation

Claim 6 is a high-specificity limitation. Many market IL‑6 biologics are glycosylated, so aglycosylation capture is likely limited to specially engineered products.

How broad is the patient population: what diseases are named or covered by the “hypercoagulation-associated” definition?

Short answer: Claim 1 covers any disease “associated with hypercoagulation,” and dependent claim 18 enumerates thrombotic and bleeding-related coagulopathies and clinical contexts: venous thrombosis, pulmonary embolism, pregnancy thrombosis, DIC (acute/chronic), postoperative clot formation, immobility, HIT/HITT, atrial fibrillation, valve implantation, genetic thrombophilias (Factor V Leiden, prothrombin mutation, MTHFR), and trauma.

Oncology expansion

Claim 10 adds a cancer patient requirement.
Claim 11 lists an extremely broad set of cancers, effectively asserting the method across a wide tumor taxonomy.

Critical validity pressure point: such breadth invites scrutiny for whether the specification provides enabling guidance for hypercoagulation management across the oncology list, especially if the examples are concentrated in a subset of cancers or in general “cancer-associated thrombosis” contexts.

What biomarker endpoints are recited: D-dimer and CRP

Short answer: Claim 2 ties treatment to elevated serum D-dimer and/or elevated CRP levels prior to treatment.

Claim 19 adds coagulation measurement methods

Claim 19 recites assessment approaches:

Serum levels: D-dimer, Factor II, Factor V, Factor VIII, Factor IX, Factor XI, Factor XII, fibrin degradation products, thrombin-antithrombin III complex, fibrinogen, plasminogen, prothrombin, von Willebrand factor.
Functional assays: PT, prothrombin ratio (PR), INR.

This provides litigation-friendly hooks because assay-based endpoints can be compared across clinical protocols, even if “normal” ranges vary by lab.

What drug-combination space is covered: statins and anticoagulants

Short answer: Claim 3 and claim 4 add optional co-administration with at least one statin and/or at least one anticoagulant selected from a long explicit list.

Anticoagulant coverage (examples are exhaustive in the claim)

Claim 4 enumerates classes and named actives including:

Antiplatelet agents: aspirin, clopidogrel, ticlopidine, dipyridamole.
Direct inhibitors/anticoagulants: argatroban, bivalirudin, desirudin, lepirudin, tirofiban, eptifibatide.
Heparins: heparin, low molecular weight heparin.
Factor Xa inhibitors: fondaparinux.
Vitamin K antagonists: warfarin, acenocoumarol, phenindione, phenprocoumon.
Direct thrombin inhibitors: dabigatran and dabigatran etexilate.
Additional agents: ximelagatran/xemelagatran (as listed).

Statin coverage

Claim 4 enumerates atorvastatin, cerivastatin, fluvastatin, lovastatin, mevastatin, pitavastatin, pravastatin, rosuvastatin, simvastatin.

Practical infringement impact

Many hypercoagulation regimens already use anticoagulants/statins. Claim dependence can create a situation where infringement requires that the accused regimen includes the specifically recited classes and that IL‑6 therapy is combined with them in the patented manner.

Does the patent cover cancer regimens with chemotherapy and targeted agents?

Short answer: Yes. Claim 15-16 expand the regimen to include chemotherapy agents or other therapeutic compounds, enumerating a wide set including VEGF antagonists (e.g., bevacizumab), EGFR antagonists (cetuximab), platin/taxanes, irinotecan, 5‑fluorouracil, gemcitabine, steroids, cyclophosphamide, melphalan, vinca alkaloids, mustines (listed), tyrosine kinase inhibitors, radiotherapy, sex hormone modulators (SERMs/SARMs), PDGF antagonists, TNF antagonists, IL‑1 antagonists, IL‑12R antagonists, and “toxin conjugated monoclonal antibodies” and tumor antigen monoclonals.

Claim mechanics

Claim 15 requires the anti‑IL‑6 antibody is part of a regimen including a chemotherapy agent or another therapeutic compound.
Claim 16 enumerates categories and examples; this can help enforce across combination trial protocols, but it also broadens potential invalidity attack based on lack of specific support across all listed oncology drugs.

What kinds of antibody formats are included: humanized, single-chain, chimeric, fragments

Short answer: Claim 9 includes “human, humanized, single chain or chimeric” formats. That means the patent can cover fragments if they retain the required VL/VH CDR mapping.

Fragment pathway
If an accused product is an antibody fragment, infringement depends on whether the fragment still has the required CDR sequences and retains relevant structural features required by dependent claims (e.g., Fc, aglycosylation).

What generic or biosimilar entry risks exist if an IL‑6 antibody is the commercial product?

Short answer: If US 10,093,732 is asserted against a marketed IL‑6 antibody product, biosimilar makers face risk if their candidates retain the claimed VL/VH CDRs or identity-threshold equivalents. If the patented CDRs map to a proprietary biologic, competitors can often design around by CDR changes.

Critical nuance: the patent is not limited by “IL‑6 receptor” vs “IL‑6 ligand.” It reads on “IL‑6 antibody,” which could include IL‑6 ligand binders or potentially IL‑6R antagonists depending on patent’s own definitions. That matters for the competitive set.

How strong is the patent estate for this IL‑6 hypercoagulation concept beyond 10,093,732?

Short answer: Strength cannot be scored without the related family members, continuations, priority documents, and cited references. The independent claim’s sequence constraints suggest that other family patents may be needed to establish coverage around alternate CDR variants, Fc formats, and additional indications.

What patent litigation has affected or could affect US 10,093,732?

Short answer: Litigation and settlements depend on docket-level facts (parties, asserted claims, claim constructions, and stay/termination outcomes). Those facts are not provided here.

What is the Orange Book status of US 10,093,732 relevant to biosimilar/generic pathways?

Short answer: US 10,093,732 concerns an antibody method-of-treatment claim. Such protection typically tracks with biologics licensing and biosimilar exclusivity frameworks, not standard small-molecule Orange Book generic substitution. Exact Orange Book listings require the underlying approved product and patent linkage records, which are not included here.

Timeline: where this claim set sits relative to typical biologic exclusivity and patent enforcement

A defensible enforcement timeline requires:

priority date
issue date and any PTA/PTE
any related method claims in the family
regulatory approval date of the covered product(s)
any biosimilar reference product exclusivities

These inputs are not included in the prompt, so a specific calendar timeline cannot be produced.

Risk matrix: claim element-by-element vulnerability and infringement leverage

Claim element	Scope effect	Infringement leverage (accused product)	Validity leverage (prior art)
IL‑6 antibody with VL CDRs SEQ ID 87-89	narrows biologic to specific CDR set	product must match CDRs or meet identity variant requirements	anticipatory prior art must disclose exact CDRs; otherwise obviousness strategy needed
IL‑6 antibody with VH CDRs SEQ ID 90-92	narrows further	similarly CDR match required	same as above
“Improved or restored to normal” coagulation profile	introduces functional clinical requirement	defendants challenge proof and endpoints	prior art must show coagulation improvement, not just biomarker shift
D-dimer/CRP elevated prior to treatment (dep. claim 2)	defines patient selection	requires regimen targeting those biomarkers	prior art may show D-dimer/CRP are associated but must tie to method outcomes
Statin/anticoagulant add-on regimen (dep. claims 3-4)	adds combination requirement	defendants can attempt regimen non-inclusion	prior art can show standard-of-care anticoagulation; combination might be obvious
Cancer + broad tumor list (claims 10-11)	expands indication	accused use outside oncology reduces risk	breadth increases enablement/obviousness risk if support is thin across all tumors
Aglycosylation (dep. claim 6) and Fc modifications (dep. claims 8,12)	format-limited	many marketed IL‑6 antibodies may not be aglycosylated	prior art antibody engineering may be cited for obviousness
Identity threshold ≥90% (dep. claim 13)	captures variants	partial sequence changes may still infringe	prior art may include near-identical antibodies; requires comparison of sequences

Key Takeaways

US 10,093,732 is a CDR-defined antibody method-of-treatment patent: independent claim 1 is constrained to specific VL and VH CDRs (SEQ ID NOs 87-89 and 90-92 mapped to SEQ ID NOs 85 and 86).
Dependent claims materially expand clinical coverage through: biomarker-based selection (D-dimer/CRP), combination regimens (statins and extensive anticoagulant lists), and broad oncology applicability (including extensive tumor taxonomy).
Litigation focus typically concentrates on CDR/sequence match, the clinical proof needed to show coagulation improvement to “normal,” and whether the broad dependent indication lists are sufficiently supported to withstand enablement/obviousness scrutiny.
Competitive design-around is primarily a CDR engineering problem. Format-dependent dependent claims (aglycosylation, Fc modifications) further narrow what products could plausibly be asserted.

FAQs

1) How can a competitor assess infringement risk for US 10,093,732 without matching the full antibody sequence?
By mapping candidate antibodies’ VL/VH CDR sequences to the claimed CDR sets (SEQ ID NOs 87-89 and 90-92) and then testing whether the candidate meets the dependent identity threshold (≥90% identity to SEQ ID NOs 85 and 86) and any Fc/aglycosylation limitations for relevant dependent claims.

2) Do the listed anticoagulants in claim 4 expand infringement beyond standard thrombosis care?
They expand coverage only where the accused method includes the claimed add-on regimen using at least one of the enumerated anticoagulants and the IL‑6 antibody defined by the independent claim.

3) Does the cancer tumor list in claim 11 create a validity weakness from overbreadth?
It can, because the list is extremely broad. Courts often scrutinize whether the specification supports applying the method to the entire enumerated scope, especially if examples or data are concentrated in narrower cancer subsets.

4) What coagulation endpoints are most litigation-relevant under claim 19?
D-dimer and fibrin degradation products for serum panels, and PT/INR/PR for functional clotting assays are anchored directly in the claim, enabling cross-trial comparisons of what constitutes “improved” coagulation profile.

5) Can a biosimilar avoid infringement if it preserves IL‑6 binding but changes CDRs?
Changing CDRs to avoid the specific VL/VH CDR sets (and the linked identity/sequence constraints) is the most direct route to avoid literal infringement. The risk then shifts to whether equivalence theories apply for the relevant jurisdiction and claim limitations asserted.

References (APA)

No cited sources were provided in the prompt, and no patent record, litigation docket, or FDA/Orange Book linkage documents were included.

Applicant	Tradename	Biologic Ingredient	Dosage Form	BLA	Approval Date	Patent No.	Expiredate
Bausch Health Us, Llc	IPRIVASK	desirudin	For Injection	021271	April 04, 2003	10,093,732	2035-11-05
Janssen Biotech, Inc.	REOPRO	abciximab	Injection	103575	December 22, 1994	10,093,732	2035-11-05
Genentech, Inc.	RITUXAN	rituximab	Injection	103705	November 26, 1997	10,093,732	2035-11-05
Idec Pharmaceuticals Corp.	RITUXAN	rituximab	Injection	103737	February 19, 2002	10,093,732	2035-11-05
>Applicant	>Tradename	>Biologic Ingredient	>Dosage Form	>BLA	>Approval Date	>Patent No.	>Expiredate

Patent: 10,093,732

Summary for Patent: 10,093,732