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

US Patent 10,787,507 (IL-6 Antibody) Claims & US Patent Landscape for Hypercoagulation in Transplant Recipients

Executive summary: US Patent 10,787,507 claims US methods for treating hypercoagulation in transplant recipients by administering an IL-6 antibody/fragment defined by specific CDR sequence sets (SEQ ID NOs) and monitoring coagulation profiles (e.g., D-dimer, CRP and multiple coagulation factors). The claim set is broad on: (i) patient population (“transplant recipient”), (ii) IL-6 antibody format (human, humanized, chimeric, single-chain; modified Fc; fragment), and (iii) combination regimens (statins and a wide menu of anticoagulants). The most legally meaningful constraints are the specific CDR-defined antibody identity and the transplant + hypercoagulation + coagulation-monitoring treatment workflow. Practically, enforcement in the US depends on whether competing IL-6 antibodies and antibody fragments either (a) fall outside the CDR-defined structural boundaries, or (b) are still found to “contain” the claimed CDR sets despite sequence variation elsewhere.

What is US Patent 10,787,507 and what treatment does it claim?

Core claim logic (Claim 1):
A method of treating a patient with a disease/condition associated with hypercoagulation where the patient is a transplant recipient, comprising:

Administering an IL-6 antibody or antibody fragment that “contains”

variable light chain CDRs of SEQ ID NO: 4, 5 and 6
variable heavy chain CDRs of SEQ ID NO: 7, 8 or 120, and 9

Improving or restoring coagulation profile to normal
Monitoring the patient to assess coagulation profile

What the claim covers in plain terms:

A targeted immunotherapy approach: neutralizing IL-6 (or binding via antibody fragments)
A transplant context: hypercoagulation is treated in transplant recipients
A measurable clinical endpoint: coagulation markers are monitored and improved/restored

How the claim is operationalized (dependent claims):

Claim 2 narrows the “hypercoagulation-associated condition” to aberrant levels of multiple markers: D-dimer; Factor II, V, VIII, IX, XI, XII; fibrinogen; plasminogen; prothrombin; von Willebrand factor; TAT complex; fibrin degradation products.
Claim 3 makes monitoring via measurement of those serum markers explicit, pre- or post-treatment.
Claim 4 adds marker triggers: elevated D-dimer and/or CRP prior to treatment.
Claim 5 allows add-on therapies: at least one statin or anti-coagulant.
Claims 6-10 broaden or refine the antibody format and Fc features:
- Fc derived from IgG1/2/3/4 (Claim 6)
- Modified Fc for effector function/half-life/proteolysis/glycosylation (Claim 8)
- Human/humanized/single-chain/chimeric (Claim 9)
- VH/VL sequence identity thresholds to listed SEQ ID NOs (Claim 10)
Claim 12 is a long regimen list that includes classic oncology biologics and small molecules and supportive modalities, indicating the patent attempts to capture transplant-associated hypercoagulation in oncology-style treatment contexts.
Claim 13 narrows monitoring to serum D-dimer measurement.

Which antibodies fall within the IL-6 CDR boundaries of US Patent 10,787,507?

What matters legally: the claim uses CDR sequence sets. Competitors can design around by changing CDR sequences so they do not “contain” SEQ ID NO: 4-6 and 7, 8 or 120, and 9.

Key structural constraints embedded in the claims:

The antibody is defined by CDR identity, not by target epitopes, isotype, or generic IL-6-binding.
The claim allows multiple antibody scaffolds if the required CDRs are present.
Claim 10 further layers identity thresholds using VH and VL polypeptide sequence identity to SEQ ID NOs (≥90% identity) which creates an additional route for infringement arguments: even if CDRs are met, VH/VL sequence identity can be tested.

H3: Are “CDR swaps” a likely design-around path?

Yes. If an accused antibody’s CDRs do not match the required SEQ ID NOs exactly (or are argued not to “contain” them), the method claim should not read on it. The practical litigation issue becomes whether the accused antibody includes the claimed CDRs in the same arrangement and whether sequence “near-misses” still satisfy claim interpretation.

H3: How does modified Fc (Claim 8) affect infringement?

Modified Fc language can reduce design-around leverage based solely on isotype or Fc engineering. If the antibody still has the claimed CDRs, Fc modifications may not avoid infringement.

What is the scope of “transplant recipients” for US Patent 10,787,507?

Claim 1 restricts the method to “transplant recipient.” The patent text you provided does not define specific transplant types (organ, hematopoietic stem cell transplant, etc.). The legal consequence is that the claim can be argued to apply broadly to any transplant recipient population where hypercoagulation is present.

Risk to generics/biosimilar competitors:
The method claim is not tied to specific dosing regimens. It is workflow-based: administer the IL-6 antibody meeting the claimed structural definition and monitor coagulation outcomes.

What hypercoagulation markers are claimed and how does that impact clinical use?

The patent claims a monitoring framework for coagulation and thrombosis-relevant biomarkers.

H3: Which biomarkers are enumerated

D-dimer
Factor II, V, VIII, IX, XI, XII
Fibrin degradation products
Thrombin-antithrombin (TAT) III complex
Fibrinogen
Plasminogen
Prothrombin
von Willebrand factor
CRP (explicitly in Claim 4)

H3: What claim coverage looks like in practice

Broad monitoring approach: Claim 2 + 3 enumerates multiple markers and allows pre- or post-treatment assessment.
Narrow monitoring shortcut: Claim 13 makes D-dimer sufficient for assessing coagulation profile. That increases infringement likelihood because D-dimer is commonly measured clinically in thrombosis/hypercoagulation contexts.

How strong are US Patent 10,787,507 claims against IL-6 pathway competitors?

H3: General IL-6 biologics vs CDR-defined antibodies

The patent is not a generic “IL-6 blockade for hypercoagulation” claim. It is tied to specific CDR sets. Strength in enforcement depends on whether a competitor’s IL-6 antibody:

uses different CDRs (good for defense), or
shares the exact CDR sequences (bad for defense), or
can be shown to “contain” the claimed CDR sequences through sequence identity/claim construction.

H3: Biosimilar and interchangeability risk

If a biosimilar is highly similar to a reference antibody but does not preserve the exact required CDR sequences at issue, it may fall outside claim scope. If CDRs are preserved, method claims can still create exposure even when the biosimilar is approved and labeled for IL-6 indications.

What does the add-on therapy language in Claims 5-12 do to enforceability?

Claim 5 expands method scope to patients receiving statins or anticoagulants.
Claim 7 includes a very wide list of anticoagulants and statins.

H3: Why this matters

It reduces the ability of a defendant to argue “the method wasn’t followed because the patient wasn’t co-treated with anticoagulants/statins.” Many transplant/hypercoagulation protocols include anticoagulation or lipid-lowering strategies; the claim anticipates that.

H3: Does Claim 12 broaden beyond hypercoagulation?

Claim 12 lists multiple anti-cancer therapies, targeted biologics, chemo agents, immunotherapies, and radiotherapy. The legal use of that list typically supports argument that the IL-6 antibody is administered as part of a broader regimen, likely aimed at transplant-oncology workflows.

When does US Patent 10,787,507 lose exclusivity?

This section cannot be completed from the information provided. The claims alone do not supply:

earliest effective filing date,
prosecution history,
patent term adjustment or extension,
maintenance status.

No exclusivity timeline is included here.

How many other US patents typically surround a CDR-defined IL-6 hypercoagulation transplant claim?

This section cannot be completed from the information provided. A meaningful “how many” requires:

assignee/owner identification,
publication family search,
citation mapping,
related continuation/divisional/grant documents.

No count is included here.

What patent litigation risks attach to this claim set (method claims + CDR definition)?

H3: Likely infringement theories

Literal infringement based on CDR content: comparing the accused antibody’s VH/VL CDR sequences and identity thresholds to the patent’s SEQ IDs.
Method performance in transplant patients: evidence from clinical protocols, chart review, or trial records showing IL-6 antibody administration plus coagulation monitoring.
Marker-based endpoint linkage: use of D-dimer and other coagulation markers consistent with Claims 2-4 and 13.

H3: Likely validity challenges

Even without the spec text, typical US validity pressure points for this kind of claim include:

anticipation/obviousness based on IL-6 blockade in thrombosis, inflammation-associated coagulation, or transplant settings,
indefiniteness or enablement if the antibody definition relies on sequence details not fully supported in the disclosure, and
written description issues for broad antibody format language (Fc modifications, chimeric/humanized/single-chain) tethered to specific CDRs.

No case-specific litigation timeline or docketing is included here because it requires bibliographic and legal-record inputs not present in the prompt.

What is the Orange Book status of US Patent 10,787,507?

This section cannot be completed from the information provided. Orange Book status depends on:

which product(s) cite this patent,
NDA/BLA listing data.

No Orange Book mapping is included here.

How does this patent compare with other IL-6 IL-6R programs for hypercoagulation?

A meaningful comparison requires identifying the IL-6 antibody product(s) and their patent families. The prompt provides no drug name, assignee, or bibliographic identifiers beyond the patent number.

No product-by-product comparison is included here.

Commercial exposure: what revenue is at risk under this method claim?

Revenue exposure depends on:

which IL-6 antibodies are used in transplant recipients for hypercoagulation,
uptake patterns,
trial outcomes,
label status and off-label use,
payer mix and guideline adherence.

The prompt provides none of these commercialization facts.

No revenue exposure estimate is included here.

Key Takeaways

US Patent 10,787,507 is a CDR-defined IL-6 antibody method-of-treatment for hypercoagulation in transplant recipients, coupled to coagulation-profile monitoring.
The most enforcement-relevant constraint is the requirement that the IL-6 antibody contains specific light-chain and heavy-chain CDRs (SEQ ID NO sets), with additional ≥90% identity language for certain VH/VL sequences.
Claims 2-4 and 13 focus on clinically familiar markers, especially D-dimer and CRP, increasing the factual record relevance for clinical documentation.
Claims 5-7 and 12 broaden the regimen context so co-administration with anticoagulants/statins is within claim scope.
Exclusivity timelines, Orange Book listing, and litigation/patent-family landscape cannot be derived from the provided claim text alone.

FAQs

Can a competitor avoid US Patent 10,787,507 by using a different IL-6 antibody isotype or Fc engineering?
If the antibody’s CDR sequences still meet the claimed SEQ ID-defined requirements, Fc engineering alone may not avoid infringement.
Does monitoring only D-dimer satisfy the monitoring limitation?
Claim 13 states coagulation-profile assessment by serum D-dimer measurement.
Is co-administration of warfarin or heparin required for infringement?
No. Claims 5-7 are dependent; infringement of Claim 1 does not require co-treatment with anticoagulants/statins.
Does the claim cover antibody fragments and single-chain formats?
Yes. The claims include IL-6 antibody or antibody fragment and cover human/humanized/single-chain/chimeric antibodies.
Does the patent apply only to transplant patients with elevated D-dimer?
Not under Claim 1. D-dimer elevation is specified in dependent Claim 4; Claim 1 covers any disease/condition associated with hypercoagulation in transplant recipients, with monitoring required.

References

No external sources were cited because the prompt did not include bibliographic or family-identifying information required to support accurate patent-landscape citations.

Title:	Antagonists of IL-6 to prevent or treat thrombosis
Abstract:	The present invention is directed to therapeutic methods using IL-6 antagonists such as antibodies and fragments thereof having binding specificity for IL-6 to prevent or treat thrombosis in diseases associated with abnormal blood coagulation or fibrinolysis. In preferred embodiments these patients will comprise those exhibiting elevated D-dimer or other cogulation cascade related proteins and optionally will further exhibit elevated C reactive protein prior to treatment. The subject therapies also may include the administration of other actives such as chemotherapeutics, anti-coagulants, statins, et al.
Inventor(s):	Smith; Jeffrey T. L. (Dublin, GB)
Assignee:	VITAERIS INC. (Vancouver, BC, unknown)
Application Number:	15/902,041
Patent Claims:	see list of patent claims
Patent landscape, scope, and claims summary:	US Patent 10,787,507 (IL-6 Antibody) Claims & US Patent Landscape for Hypercoagulation in Transplant Recipients Executive summary: US Patent 10,787,507 claims US methods for treating hypercoagulation in transplant recipients by administering an IL-6 antibody/fragment defined by specific CDR sequence sets (SEQ ID NOs) and monitoring coagulation profiles (e.g., D-dimer, CRP and multiple coagulation factors). The claim set is broad on: (i) patient population (“transplant recipient”), (ii) IL-6 antibody format (human, humanized, chimeric, single-chain; modified Fc; fragment), and (iii) combination regimens (statins and a wide menu of anticoagulants). The most legally meaningful constraints are the specific CDR-defined antibody identity and the transplant + hypercoagulation + coagulation-monitoring treatment workflow. Practically, enforcement in the US depends on whether competing IL-6 antibodies and antibody fragments either (a) fall outside the CDR-defined structural boundaries, or (b) are still found to “contain” the claimed CDR sets despite sequence variation elsewhere. What is US Patent 10,787,507 and what treatment does it claim? Core claim logic (Claim 1): A method of treating a patient with a disease/condition associated with hypercoagulation where the patient is a transplant recipient, comprising: Administering an IL-6 antibody or antibody fragment that “contains” variable light chain CDRs of SEQ ID NO: 4, 5 and 6 variable heavy chain CDRs of SEQ ID NO: 7, 8 or 120, and 9 Improving or restoring coagulation profile to normal Monitoring the patient to assess coagulation profile What the claim covers in plain terms: A targeted immunotherapy approach: neutralizing IL-6 (or binding via antibody fragments) A transplant context: hypercoagulation is treated in transplant recipients A measurable clinical endpoint: coagulation markers are monitored and improved/restored How the claim is operationalized (dependent claims): Claim 2 narrows the “hypercoagulation-associated condition” to aberrant levels of multiple markers: D-dimer; Factor II, V, VIII, IX, XI, XII; fibrinogen; plasminogen; prothrombin; von Willebrand factor; TAT complex; fibrin degradation products. Claim 3 makes monitoring via measurement of those serum markers explicit, pre- or post-treatment. Claim 4 adds marker triggers: elevated D-dimer and/or CRP prior to treatment. Claim 5 allows add-on therapies: at least one statin or anti-coagulant. Claims 6-10 broaden or refine the antibody format and Fc features: Fc derived from IgG1/2/3/4 (Claim 6) Modified Fc for effector function/half-life/proteolysis/glycosylation (Claim 8) Human/humanized/single-chain/chimeric (Claim 9) VH/VL sequence identity thresholds to listed SEQ ID NOs (Claim 10) Claim 12 is a long regimen list that includes classic oncology biologics and small molecules and supportive modalities, indicating the patent attempts to capture transplant-associated hypercoagulation in oncology-style treatment contexts. Claim 13 narrows monitoring to serum D-dimer measurement. Which antibodies fall within the IL-6 CDR boundaries of US Patent 10,787,507? What matters legally: the claim uses CDR sequence sets. Competitors can design around by changing CDR sequences so they do not “contain” SEQ ID NO: 4-6 and 7, 8 or 120, and 9. Key structural constraints embedded in the claims: The antibody is defined by CDR identity, not by target epitopes, isotype, or generic IL-6-binding. The claim allows multiple antibody scaffolds if the required CDRs are present. Claim 10 further layers identity thresholds using VH and VL polypeptide sequence identity to SEQ ID NOs (≥90% identity) which creates an additional route for infringement arguments: even if CDRs are met, VH/VL sequence identity can be tested. H3: Are “CDR swaps” a likely design-around path? Yes. If an accused antibody’s CDRs do not match the required SEQ ID NOs exactly (or are argued not to “contain” them), the method claim should not read on it. The practical litigation issue becomes whether the accused antibody includes the claimed CDRs in the same arrangement and whether sequence “near-misses” still satisfy claim interpretation. H3: How does modified Fc (Claim 8) affect infringement? Modified Fc language can reduce design-around leverage based solely on isotype or Fc engineering. If the antibody still has the claimed CDRs, Fc modifications may not avoid infringement. What is the scope of “transplant recipients” for US Patent 10,787,507? Claim 1 restricts the method to “transplant recipient.” The patent text you provided does not define specific transplant types (organ, hematopoietic stem cell transplant, etc.). The legal consequence is that the claim can be argued to apply broadly to any transplant recipient population where hypercoagulation is present. Risk to generics/biosimilar competitors: The method claim is not tied to specific dosing regimens. It is workflow-based: administer the IL-6 antibody meeting the claimed structural definition and monitor coagulation outcomes. What hypercoagulation markers are claimed and how does that impact clinical use? The patent claims a monitoring framework for coagulation and thrombosis-relevant biomarkers. H3: Which biomarkers are enumerated D-dimer Factor II, V, VIII, IX, XI, XII Fibrin degradation products Thrombin-antithrombin (TAT) III complex Fibrinogen Plasminogen Prothrombin von Willebrand factor CRP (explicitly in Claim 4) H3: What claim coverage looks like in practice Broad monitoring approach: Claim 2 + 3 enumerates multiple markers and allows pre- or post-treatment assessment. Narrow monitoring shortcut: Claim 13 makes D-dimer sufficient for assessing coagulation profile. That increases infringement likelihood because D-dimer is commonly measured clinically in thrombosis/hypercoagulation contexts. How strong are US Patent 10,787,507 claims against IL-6 pathway competitors? H3: General IL-6 biologics vs CDR-defined antibodies The patent is not a generic “IL-6 blockade for hypercoagulation” claim. It is tied to specific CDR sets. Strength in enforcement depends on whether a competitor’s IL-6 antibody: uses different CDRs (good for defense), or shares the exact CDR sequences (bad for defense), or can be shown to “contain” the claimed CDR sequences through sequence identity/claim construction. H3: Biosimilar and interchangeability risk If a biosimilar is highly similar to a reference antibody but does not preserve the exact required CDR sequences at issue, it may fall outside claim scope. If CDRs are preserved, method claims can still create exposure even when the biosimilar is approved and labeled for IL-6 indications. What does the add-on therapy language in Claims 5-12 do to enforceability? Claim 5 expands method scope to patients receiving statins or anticoagulants. Claim 7 includes a very wide list of anticoagulants and statins. H3: Why this matters It reduces the ability of a defendant to argue “the method wasn’t followed because the patient wasn’t co-treated with anticoagulants/statins.” Many transplant/hypercoagulation protocols include anticoagulation or lipid-lowering strategies; the claim anticipates that. H3: Does Claim 12 broaden beyond hypercoagulation? Claim 12 lists multiple anti-cancer therapies, targeted biologics, chemo agents, immunotherapies, and radiotherapy. The legal use of that list typically supports argument that the IL-6 antibody is administered as part of a broader regimen, likely aimed at transplant-oncology workflows. When does US Patent 10,787,507 lose exclusivity? This section cannot be completed from the information provided. The claims alone do not supply: earliest effective filing date, prosecution history, patent term adjustment or extension, maintenance status. No exclusivity timeline is included here. How many other US patents typically surround a CDR-defined IL-6 hypercoagulation transplant claim? This section cannot be completed from the information provided. A meaningful “how many” requires: assignee/owner identification, publication family search, citation mapping, related continuation/divisional/grant documents. No count is included here. What patent litigation risks attach to this claim set (method claims + CDR definition)? H3: Likely infringement theories Literal infringement based on CDR content: comparing the accused antibody’s VH/VL CDR sequences and identity thresholds to the patent’s SEQ IDs. Method performance in transplant patients: evidence from clinical protocols, chart review, or trial records showing IL-6 antibody administration plus coagulation monitoring. Marker-based endpoint linkage: use of D-dimer and other coagulation markers consistent with Claims 2-4 and 13. H3: Likely validity challenges Even without the spec text, typical US validity pressure points for this kind of claim include: anticipation/obviousness based on IL-6 blockade in thrombosis, inflammation-associated coagulation, or transplant settings, indefiniteness or enablement if the antibody definition relies on sequence details not fully supported in the disclosure, and written description issues for broad antibody format language (Fc modifications, chimeric/humanized/single-chain) tethered to specific CDRs. No case-specific litigation timeline or docketing is included here because it requires bibliographic and legal-record inputs not present in the prompt. What is the Orange Book status of US Patent 10,787,507? This section cannot be completed from the information provided. Orange Book status depends on: which product(s) cite this patent, NDA/BLA listing data. No Orange Book mapping is included here. How does this patent compare with other IL-6 IL-6R programs for hypercoagulation? A meaningful comparison requires identifying the IL-6 antibody product(s) and their patent families. The prompt provides no drug name, assignee, or bibliographic identifiers beyond the patent number. No product-by-product comparison is included here. Commercial exposure: what revenue is at risk under this method claim? Revenue exposure depends on: which IL-6 antibodies are used in transplant recipients for hypercoagulation, uptake patterns, trial outcomes, label status and off-label use, payer mix and guideline adherence. The prompt provides none of these commercialization facts. No revenue exposure estimate is included here. Key Takeaways US Patent 10,787,507 is a CDR-defined IL-6 antibody method-of-treatment for hypercoagulation in transplant recipients, coupled to coagulation-profile monitoring. The most enforcement-relevant constraint is the requirement that the IL-6 antibody contains specific light-chain and heavy-chain CDRs (SEQ ID NO sets), with additional ≥90% identity language for certain VH/VL sequences. Claims 2-4 and 13 focus on clinically familiar markers, especially D-dimer and CRP, increasing the factual record relevance for clinical documentation. Claims 5-7 and 12 broaden the regimen context so co-administration with anticoagulants/statins is within claim scope. Exclusivity timelines, Orange Book listing, and litigation/patent-family landscape cannot be derived from the provided claim text alone. FAQs Can a competitor avoid US Patent 10,787,507 by using a different IL-6 antibody isotype or Fc engineering? If the antibody’s CDR sequences still meet the claimed SEQ ID-defined requirements, Fc engineering alone may not avoid infringement. Does monitoring only D-dimer satisfy the monitoring limitation? Claim 13 states coagulation-profile assessment by serum D-dimer measurement. Is co-administration of warfarin or heparin required for infringement? No. Claims 5-7 are dependent; infringement of Claim 1 does not require co-treatment with anticoagulants/statins. Does the claim cover antibody fragments and single-chain formats? Yes. The claims include IL-6 antibody or antibody fragment and cover human/humanized/single-chain/chimeric antibodies. Does the patent apply only to transplant patients with elevated D-dimer? Not under Claim 1. D-dimer elevation is specified in dependent Claim 4; Claim 1 covers any disease/condition associated with hypercoagulation in transplant recipients, with monitoring required. References No external sources were cited because the prompt did not include bibliographic or family-identifying information required to support accurate patent-landscape citations. More… ↓ ⤷ Start Trial

Applicant	Tradename	Biologic Ingredient	Dosage Form	BLA	Approval Date	Patent No.	Expiredate
Bausch Health Us, Llc	IPRIVASK	desirudin	For Injection	021271	April 04, 2003	10,787,507	2038-02-22
Janssen Biotech, Inc.	REOPRO	abciximab	Injection	103575	December 22, 1994	10,787,507	2038-02-22
Genentech, Inc.	RITUXAN	rituximab	Injection	103705	November 26, 1997	10,787,507	2038-02-22
>Applicant	>Tradename	>Biologic Ingredient	>Dosage Form	>BLA	>Approval Date	>Patent No.	>Expiredate

Patent: 10,787,507

Summary for Patent: 10,787,507