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

Comprehensive patent-landscape analysis for US Patent 10,106,605 (EPO-binding antibody for macular edema)
US Patent 10,106,605 claims methods of treating macular edema by administering an EPO-binding antibody (or antigen-binding fragment) defined by specific CDR sequences (HCDR1-3 and LCDR1-3) and optional sequence-identity fallbacks. The independent claim is narrow at the antigen-binding level (EPO binder plus multiple CDR sets selected from four enumerated embodiments). Dependent claims broaden use combinations (VEGF/anti-VEGF add-on regimens) but stay anchored to the same EPO-binding antibody definition.

Result for freedom-to-operate and challenge strategy: the critical infringement hook is not “an anti-EPO antibody,” but an antibody whose variable-region CDRs match one of the four specific CDR triplets (SEQ ID NO sets). Competitive risk concentrates in licenses or design-around work that preserves those CDRs while swapping framework or Fc.

Key takeaways (high-level):

Claim scope is defined by CDR sequence selection (four specific CDR sets) plus 90% identity fallbacks (claims 2 and 3).
Co-therapy claims (VEGF/ranibizumab/etc.) do not create a second active ingredient risk unless the EPO binder matches the CDR definition.
The enforceability analysis hinges on whether the asserted EPO-binding antibodies are functionally and structurally within the CDR-defined bounds, and whether prior art already disclosed those EPO-binder CDRs for ophthalmic edema.

What does US Patent 10,106,605 claim for treating macular edema with an EPO-binding antibody?

Core claim 1 (independent): a method of treating macular edema by administering an effective amount of a composition comprising an antibody (or antigen-binding fragment) that:

Binds EPO; and
Contains specific CDR sequences in the heavy and light chains, chosen from four enumerated CDR sets:
- Option (a): heavy CDRs SEQ ID NOs: 1,2,3 and light CDRs 4,5,6
- Option (b): heavy CDRs 21,22,23 and light CDRs 24,25,26
- Option (c): heavy CDRs 41,42,43 and light CDRs 44,45,46
- Option (d): heavy CDRs 61,62,63 and light CDRs 64,65,66

Important structural consequence: claim 1 is not satisfied by any generic anti-EPO antibody. It is satisfied only if the administered antibody’s CDRs match one of the four defined CDR triplet combinations (or fall within the later identity-based dependent claims).

What do the dependent claims broaden versus narrow?

Claim 2: at least 90% identity to SEQ ID NOs: 13 and 14 (heavy and light variable sequences), plus corresponding alternative identity pairs for 33/34, 53/54, 73/74.
Claim 3: at least 90% identity to variable sequences 15/16, 35/36, 55/56, 75/76.

Claim 4: antibody format flexibility (human/chimeric, mAb, single chain, Fab/Fab’/F(ab’)2/Fv/scFv).
Claim 5: IgG isotype.

Claim 6: method effect limitations tied to outcomes in the eye: decreasing retinal vein dilation, decreasing vascular leakage, and/or increasing blood flow. This is a functional limitation that can matter at litigation if the accused product’s clinical/PK-PD evidence is contested.

Claims 7-9: co-administration with anti-VEGF antibodies or receptors and optionally ranibizumab.

Claim 7: “further comprises administering an anti-VEGF antibody or anti-VEGF receptor antibody.”
Claim 8: optional addition of a second composition selected from ranibizumab, bevacizumab, pegaptanib, aflibercept, pazopanib, sorafenib, sunitinib, and rapamycin.
Claim 9: the second composition comprises ranibizumab.

Claims 10-14: additional embodiment-specific anchoring to particular CDR/identity sets, including explicit recurrence of the 21/22/23 + 24/25/26 CDR combination and identity to 33/34 and 35/36.

What is the legal “shape” of the infringement test?

The enforcement lever is likely to be a variable-region / CDR mapping infringement analysis:

If the accused antibody is an EPO binder but has different CDRs, claim 1 likely does not read.
If the accused antibody matches one of the four CDR-defined embodiments (or is within the dependent 90% identity fallbacks), then the method claim can potentially be asserted even if the antibody is presented in a different format (subject to the specific definition in the claim).

Which antibodies are implicated by the CDR-based structure in US 10,106,605?

The claims point to a tightly defined EPO-binding antibody family characterized by multiple explicit SEQ ID NO CDR definitions. Without the patent’s specification text and the actual amino-acid sequences, the analysis here focuses on landscape mechanics rather than exact identification of a commercial antibody product.

What can be concluded from claim structure:

The patent is written like an antibody patent with several defined CDR combinations, rather than a broad “anti-EPO for ocular edema” method patent.
The presence of both CDR-specific embodiments and sequence-identity backups indicates that the patentee anticipated near-variant designs and sought to capture them under identity.

How does the 90% identity language change design-around risk?

Identity-based dependent claims (claims 2 and 3) can capture antibodies that do not exactly match the named sequences but have high similarity in the defined variable-region sequences.
For design-around, it is typically easier to alter CDRs substantially than to keep them at the same functional level while reducing identity below the claimed threshold.

How many independent claim “entry points” exist in US 10,106,605?

Even though only claim 1 is independent, claim 1 itself contains four alternative CDR sets (a)-(d). That matters for both novelty defenses and claim charting.

Entry points inside claim 1:

(a) CDRs 1-3 and 4-6
(b) CDRs 21-23 and 24-26
(c) CDRs 41-43 and 44-46
(d) CDRs 61-63 and 64-66

Downstream broadening:

Claims 2-3 add sequence-identity variants tied to additional SEQ ID NO sets (13/14, 33/34, 53/54, 73/74 and 15/16, 35/36, 55/56, 75/76).
Claims 4-6 and 7-9 expand format and co-therapy scope, but do not materially change the core antibody identity requirement.

What patent landscape surrounds US 10,106,605 for EPO-binding antibodies and ocular edema?

Landscape segmentation that matters for litigation and licensing:

Antibody domain patents: CDR-defined EPO-binding antibodies (the most direct competitive zone).
Ophthalmic edema therapeutic patents: methods for macular edema, retinal vein dilation, vascular leakage, ocular blood flow.
Combination therapy patents: EPO-pathway modulators with anti-VEGF agents or standard anti-VEGF regimens.
Manufacturing and formulation patents: if the claim at issue includes only “composition comprising an antibody,” additional formulation/device barriers may arise outside this patent.

Critical limitation in this patent: it is not enough that an antibody binds EPO. It must bind EPO and have one of the defined CDR sets, making the key prior art and competitive risk primarily CDR-defined EPO antibodies, not just general EPO antagonists or EPO receptor ligands.

What prior art theories would most directly attack US 10,106,605?

Given the CDR specificity, the highest-probability validity attack uses anticipation or obviousness based on EPO-binding antibodies with matching CDRs or high-identity variable regions.

Most relevant validity hooks

Anticipation (35 USC 102): a single reference discloses an EPO-binding antibody with the same heavy and light CDR triplets (or identical/fully defined variable sequences) plus ocular/macuar edema treatment.
Obviousness (35 USC 103): multiple references combine to show that the specific CDR-defined antibody (or 90% identity variant) would have been obvious, and that applying it to macular edema would have been obvious.
Enablement/description arguments typically require showing the patent does not teach how to make and use the claimed EPO binder embodiments.

Why claim 6’s functional outcomes can matter

If litigation is evidence-driven, claim 6’s limitations can allow argument about whether a competitor’s antibody achieves retinal vein and vascular leakage effects in the accused setting.

When does US 10,106,605 expire and what exclusivity timeline matters for generics or biosimilars?

US 10,106,605 is a U.S. utility patent. The exclusivity timeline for competition is generally governed by:

Patent expiration under U.S. utility terms (typically 20 years from earliest effective non-provisional filing date), adjusted for patent term adjustments.
If the claimed subject matter is tied to a biologic, the regulatory exclusivity framework (BLA/IND pathways) can add layers, but the patent rights at issue here are method-of-use or method treatment claims anchored to antibody identity.

No expiration dates are computable from the claim text alone, because the filing date, priority chain, and any terminal disclaimers or PTA adjustments are not provided.

What is the Orange Book status of US 10,106,605?

This patent is directed to an antibody composition used for macular edema, implying it would be listed, if at all, under the Orange Book only if it is associated with an FDA-approved drug product with an NDA (not typical for most antibody biologics, which are often under BLA and listed in the Purple Book, not Orange Book).

No Orange Book listing identifiers are present in the claim text, so a verified Orange Book status cannot be extracted here.

Which FDA pathway issues affect enforcement of US 10,106,605?

The claim is a method of treating macular edema with an EPO-binding antibody. Enforcement typically depends on whether the accused product:

Is an antibody that binds EPO with the claimed CDRs (or 90% identity variable regions in dependent claims).
Is used in the U.S. in a way that corresponds to the claimed method.

If an accused product is marketed with labeling that encourages the claimed method, indirect infringement theories can be central in U.S. litigation.

However, FDA labeling and pathway specifics are not provided in the prompt, so a product-level pathway mapping cannot be stated.

What generic entry risks exist for macular edema EPO-binding antibody methods?

For antibodies, “generic” usually means biosimilar (under the BPCIA framework). Method-of-use claims can still restrict biosimilar entry if the biosimilar applicant seeks approval with labeling that infringes the protected method.

Risk mechanics:

If the biosimilar applicant must propose labeling carve-outs (“skinny label”) to avoid the claimed method, it can trigger litigation risk similar to Orange Book/§271(e)(2) scenarios.
If the claims are narrow to CDR-defined antibodies, biosimilar makers may argue their molecules’ CDRs do not fall within the claim scope.

But again, without knowing the actual antibodies/biologics covered by the patent, and without listing numbers and Orange/Purple Book entries, a quantitative risk ranking across products is not possible from the claim text alone.

What patent litigation affects US 10,106,605?

The claim text provides no parties, case numbers, or asserted patents. Without docket-level facts, litigation status cannot be stated.

Key Takeaways

US 10,106,605 is CDR-defined: infringement turns on whether the administered EPO-binding antibody contains one of four enumerated heavy/light CDR set combinations (SEQ ID NO sets within claim 1).
Dependent claims add 90% identity fallbacks to specific variable-region sequences, reducing the design-around space for near variants.
VEGF co-therapy language broadens regimen combinations but does not remove the requirement for the claimed EPO-binding antibody identity.
Method effect limitations (retinal vein dilation, vascular leakage, blood flow) may support evidence arguments at enforcement, but the decisive element remains antibody sequence mapping to the CDR definitions.

FAQs

Do claims in US 10,106,605 cover any anti-EPO antibody for macular edema?
No. Claim 1 requires EPO-binding plus specific CDR sequence triplets selected from four enumerated SEQ ID NO combinations.
Can a competitor avoid infringement by using a different antibody scaffold or Fc region?
Yes in principle, but only if the heavy/light CDRs (or the claimed 90% identity variable regions in dependent claims) fall outside the defined ranges. The claim language concentrates on variable-region CDRs, not Fc.
Does adding ranibizumab change infringement risk under this patent?
Not by itself. Ranibizumab appears as an optional co-therapy in dependent claims, but the EPO-binding antibody still must satisfy claim 1’s CDR-defined requirements.
Are “functional outcomes” like reduced vascular leakage part of infringement proof?
Claim 6 includes functional outcomes in the claimed method. If asserted, proof may require evidence that administration decreases retinal vein dilation and/or vascular leakage and/or increases blood flow.
What matters most for designing around US 10,106,605?
Substantial divergence in heavy and light chain CDR sequences away from the enumerated SEQ ID NO sets, and avoiding the dependent 90% identity bands for the defined variable sequences.

References (APA)

United States Patent No. 10,106,605. (Claims text provided in prompt).

Title:	Compositions and methods for antibodies targeting Epo
Abstract:	The present invention relates to compositions and methods for the inhibition of EPO. The invention provides antibodies and antigen binding fragments thereof that bind to EPO and are able to inhibit EPO-dependent cell proliferation and/or EPO-dependent cell signaling.
Inventor(s):	Ghosh; Joy (Brookline, MA), Rutz; Mark Anthony (Munich, DE), Tissot-Daguette; Kathrin Ulrike (Neuried, DE), Splawski; Igor (Cambridge, MA), Roguska; Michael (Cambridge, MA)
Assignee:	NOVARTIS AG (Basel, CH)
Application Number:	15/180,879
Patent Claims:	see list of patent claims
Patent landscape, scope, and claims summary:	Comprehensive patent-landscape analysis for US Patent 10,106,605 (EPO-binding antibody for macular edema) US Patent 10,106,605 claims methods of treating macular edema by administering an EPO-binding antibody (or antigen-binding fragment) defined by specific CDR sequences (HCDR1-3 and LCDR1-3) and optional sequence-identity fallbacks. The independent claim is narrow at the antigen-binding level (EPO binder plus multiple CDR sets selected from four enumerated embodiments). Dependent claims broaden use combinations (VEGF/anti-VEGF add-on regimens) but stay anchored to the same EPO-binding antibody definition. Result for freedom-to-operate and challenge strategy: the critical infringement hook is not “an anti-EPO antibody,” but an antibody whose variable-region CDRs match one of the four specific CDR triplets (SEQ ID NO sets). Competitive risk concentrates in licenses or design-around work that preserves those CDRs while swapping framework or Fc. Key takeaways (high-level): Claim scope is defined by CDR sequence selection (four specific CDR sets) plus 90% identity fallbacks (claims 2 and 3). Co-therapy claims (VEGF/ranibizumab/etc.) do not create a second active ingredient risk unless the EPO binder matches the CDR definition. The enforceability analysis hinges on whether the asserted EPO-binding antibodies are functionally and structurally within the CDR-defined bounds, and whether prior art already disclosed those EPO-binder CDRs for ophthalmic edema. What does US Patent 10,106,605 claim for treating macular edema with an EPO-binding antibody? Core claim 1 (independent): a method of treating macular edema by administering an effective amount of a composition comprising an antibody (or antigen-binding fragment) that: Binds EPO; and Contains specific CDR sequences in the heavy and light chains, chosen from four enumerated CDR sets: Option (a): heavy CDRs SEQ ID NOs: 1,2,3 and light CDRs 4,5,6 Option (b): heavy CDRs 21,22,23 and light CDRs 24,25,26 Option (c): heavy CDRs 41,42,43 and light CDRs 44,45,46 Option (d): heavy CDRs 61,62,63 and light CDRs 64,65,66 Important structural consequence: claim 1 is not satisfied by any generic anti-EPO antibody. It is satisfied only if the administered antibody’s CDRs match one of the four defined CDR triplet combinations (or fall within the later identity-based dependent claims). What do the dependent claims broaden versus narrow? Claim 2: at least 90% identity to SEQ ID NOs: 13 and 14 (heavy and light variable sequences), plus corresponding alternative identity pairs for 33/34, 53/54, 73/74. Claim 3: at least 90% identity to variable sequences 15/16, 35/36, 55/56, 75/76. Claim 4: antibody format flexibility (human/chimeric, mAb, single chain, Fab/Fab’/F(ab’)2/Fv/scFv). Claim 5: IgG isotype. Claim 6: method effect limitations tied to outcomes in the eye: decreasing retinal vein dilation, decreasing vascular leakage, and/or increasing blood flow. This is a functional limitation that can matter at litigation if the accused product’s clinical/PK-PD evidence is contested. Claims 7-9: co-administration with anti-VEGF antibodies or receptors and optionally ranibizumab. Claim 7: “further comprises administering an anti-VEGF antibody or anti-VEGF receptor antibody.” Claim 8: optional addition of a second composition selected from ranibizumab, bevacizumab, pegaptanib, aflibercept, pazopanib, sorafenib, sunitinib, and rapamycin. Claim 9: the second composition comprises ranibizumab. Claims 10-14: additional embodiment-specific anchoring to particular CDR/identity sets, including explicit recurrence of the 21/22/23 + 24/25/26 CDR combination and identity to 33/34 and 35/36. What is the legal “shape” of the infringement test? The enforcement lever is likely to be a variable-region / CDR mapping infringement analysis: If the accused antibody is an EPO binder but has different CDRs, claim 1 likely does not read. If the accused antibody matches one of the four CDR-defined embodiments (or is within the dependent 90% identity fallbacks), then the method claim can potentially be asserted even if the antibody is presented in a different format (subject to the specific definition in the claim). Which antibodies are implicated by the CDR-based structure in US 10,106,605? The claims point to a tightly defined EPO-binding antibody family characterized by multiple explicit SEQ ID NO CDR definitions. Without the patent’s specification text and the actual amino-acid sequences, the analysis here focuses on landscape mechanics rather than exact identification of a commercial antibody product. What can be concluded from claim structure: The patent is written like an antibody patent with several defined CDR combinations, rather than a broad “anti-EPO for ocular edema” method patent. The presence of both CDR-specific embodiments and sequence-identity backups indicates that the patentee anticipated near-variant designs and sought to capture them under identity. How does the 90% identity language change design-around risk? Identity-based dependent claims (claims 2 and 3) can capture antibodies that do not exactly match the named sequences but have high similarity in the defined variable-region sequences. For design-around, it is typically easier to alter CDRs substantially than to keep them at the same functional level while reducing identity below the claimed threshold. How many independent claim “entry points” exist in US 10,106,605? Even though only claim 1 is independent, claim 1 itself contains four alternative CDR sets (a)-(d). That matters for both novelty defenses and claim charting. Entry points inside claim 1: (a) CDRs 1-3 and 4-6 (b) CDRs 21-23 and 24-26 (c) CDRs 41-43 and 44-46 (d) CDRs 61-63 and 64-66 Downstream broadening: Claims 2-3 add sequence-identity variants tied to additional SEQ ID NO sets (13/14, 33/34, 53/54, 73/74 and 15/16, 35/36, 55/56, 75/76). Claims 4-6 and 7-9 expand format and co-therapy scope, but do not materially change the core antibody identity requirement. What patent landscape surrounds US 10,106,605 for EPO-binding antibodies and ocular edema? Landscape segmentation that matters for litigation and licensing: Antibody domain patents: CDR-defined EPO-binding antibodies (the most direct competitive zone). Ophthalmic edema therapeutic patents: methods for macular edema, retinal vein dilation, vascular leakage, ocular blood flow. Combination therapy patents: EPO-pathway modulators with anti-VEGF agents or standard anti-VEGF regimens. Manufacturing and formulation patents: if the claim at issue includes only “composition comprising an antibody,” additional formulation/device barriers may arise outside this patent. Critical limitation in this patent: it is not enough that an antibody binds EPO. It must bind EPO and have one of the defined CDR sets, making the key prior art and competitive risk primarily CDR-defined EPO antibodies, not just general EPO antagonists or EPO receptor ligands. What prior art theories would most directly attack US 10,106,605? Given the CDR specificity, the highest-probability validity attack uses anticipation or obviousness based on EPO-binding antibodies with matching CDRs or high-identity variable regions. Most relevant validity hooks Anticipation (35 USC 102): a single reference discloses an EPO-binding antibody with the same heavy and light CDR triplets (or identical/fully defined variable sequences) plus ocular/macuar edema treatment. Obviousness (35 USC 103): multiple references combine to show that the specific CDR-defined antibody (or 90% identity variant) would have been obvious, and that applying it to macular edema would have been obvious. Enablement/description arguments typically require showing the patent does not teach how to make and use the claimed EPO binder embodiments. Why claim 6’s functional outcomes can matter If litigation is evidence-driven, claim 6’s limitations can allow argument about whether a competitor’s antibody achieves retinal vein and vascular leakage effects in the accused setting. When does US 10,106,605 expire and what exclusivity timeline matters for generics or biosimilars? US 10,106,605 is a U.S. utility patent. The exclusivity timeline for competition is generally governed by: Patent expiration under U.S. utility terms (typically 20 years from earliest effective non-provisional filing date), adjusted for patent term adjustments. If the claimed subject matter is tied to a biologic, the regulatory exclusivity framework (BLA/IND pathways) can add layers, but the patent rights at issue here are method-of-use or method treatment claims anchored to antibody identity. No expiration dates are computable from the claim text alone, because the filing date, priority chain, and any terminal disclaimers or PTA adjustments are not provided. What is the Orange Book status of US 10,106,605? This patent is directed to an antibody composition used for macular edema, implying it would be listed, if at all, under the Orange Book only if it is associated with an FDA-approved drug product with an NDA (not typical for most antibody biologics, which are often under BLA and listed in the Purple Book, not Orange Book). No Orange Book listing identifiers are present in the claim text, so a verified Orange Book status cannot be extracted here. Which FDA pathway issues affect enforcement of US 10,106,605? The claim is a method of treating macular edema with an EPO-binding antibody. Enforcement typically depends on whether the accused product: Is an antibody that binds EPO with the claimed CDRs (or 90% identity variable regions in dependent claims). Is used in the U.S. in a way that corresponds to the claimed method. If an accused product is marketed with labeling that encourages the claimed method, indirect infringement theories can be central in U.S. litigation. However, FDA labeling and pathway specifics are not provided in the prompt, so a product-level pathway mapping cannot be stated. What generic entry risks exist for macular edema EPO-binding antibody methods? For antibodies, “generic” usually means biosimilar (under the BPCIA framework). Method-of-use claims can still restrict biosimilar entry if the biosimilar applicant seeks approval with labeling that infringes the protected method. Risk mechanics: If the biosimilar applicant must propose labeling carve-outs (“skinny label”) to avoid the claimed method, it can trigger litigation risk similar to Orange Book/§271(e)(2) scenarios. If the claims are narrow to CDR-defined antibodies, biosimilar makers may argue their molecules’ CDRs do not fall within the claim scope. But again, without knowing the actual antibodies/biologics covered by the patent, and without listing numbers and Orange/Purple Book entries, a quantitative risk ranking across products is not possible from the claim text alone. What patent litigation affects US 10,106,605? The claim text provides no parties, case numbers, or asserted patents. Without docket-level facts, litigation status cannot be stated. Key Takeaways US 10,106,605 is CDR-defined: infringement turns on whether the administered EPO-binding antibody contains one of four enumerated heavy/light CDR set combinations (SEQ ID NO sets within claim 1). Dependent claims add 90% identity fallbacks to specific variable-region sequences, reducing the design-around space for near variants. VEGF co-therapy language broadens regimen combinations but does not remove the requirement for the claimed EPO-binding antibody identity. Method effect limitations (retinal vein dilation, vascular leakage, blood flow) may support evidence arguments at enforcement, but the decisive element remains antibody sequence mapping to the CDR definitions. FAQs Do claims in US 10,106,605 cover any anti-EPO antibody for macular edema? No. Claim 1 requires EPO-binding plus specific CDR sequence triplets selected from four enumerated SEQ ID NO combinations. Can a competitor avoid infringement by using a different antibody scaffold or Fc region? Yes in principle, but only if the heavy/light CDRs (or the claimed 90% identity variable regions in dependent claims) fall outside the defined ranges. The claim language concentrates on variable-region CDRs, not Fc. Does adding ranibizumab change infringement risk under this patent? Not by itself. Ranibizumab appears as an optional co-therapy in dependent claims, but the EPO-binding antibody still must satisfy claim 1’s CDR-defined requirements. Are “functional outcomes” like reduced vascular leakage part of infringement proof? Claim 6 includes functional outcomes in the claimed method. If asserted, proof may require evidence that administration decreases retinal vein dilation and/or vascular leakage and/or increases blood flow. What matters most for designing around US 10,106,605? Substantial divergence in heavy and light chain CDR sequences away from the enumerated SEQ ID NO sets, and avoiding the dependent 90% identity bands for the defined variable sequences. References (APA) United States Patent No. 10,106,605. (Claims text provided in prompt). More… ↓ ⤷ Start Trial

Applicant	Tradename	Biologic Ingredient	Dosage Form	BLA	Approval Date	Patent No.	Expiredate
Genentech, Inc.	AVASTIN	bevacizumab	Injection	125085	February 26, 2004	10,106,605	2036-06-13
Genentech, Inc.	LUCENTIS	ranibizumab	Injection	125156	June 30, 2006	10,106,605	2036-06-13
Genentech, Inc.	LUCENTIS	ranibizumab	Injection	125156	August 10, 2012	10,106,605	2036-06-13
Genentech, Inc.	LUCENTIS	ranibizumab	Injection	125156	October 13, 2016	10,106,605	2036-06-13
Genentech, Inc.	LUCENTIS	ranibizumab	Injection	125156	March 20, 2018	10,106,605	2036-06-13
Regeneron Pharmaceuticals, Inc.	EYLEA	aflibercept	Injection	125387	November 18, 2011	10,106,605	2036-06-13
>Applicant	>Tradename	>Biologic Ingredient	>Dosage Form	>BLA	>Approval Date	>Patent No.	>Expiredate

Patent: 10,106,605

Summary for Patent: 10,106,605