US 9670277

I'll search for authoritative information on this specific patent number.

Let me check for any litigation, PTAB, or CAFC activity involving this specific patent.

Let me verify the granted claims (they can differ from the published application) and check for any post-grant proceedings.

Summary: US Patent No. 9,670,277 (US9670277B2)

Caveat up front on search scope: I searched for the specific number 9670277 and its associated identifiers. I found no CAFC 2026 docket entry, no PTAB/IPR petition, and no district court litigation naming this patent. One caution: several PTAB documents refer to "the '027 Patent" in an electronic smoking device IPR (IPR2017-01120 family, declarations dated March 2018). That is a different patent that merely shares the last three digits — I did not treat it as this patent.

Bibliographic data (from the Google Patents record and Justia)

Abstract (verbatim)

"This application discloses ophthalmic formulations and methods for treating inflammatory disease and conditions of the ocular surface with one or more C—C chemokine receptor type 7 (CCR7) antagonists. The compositions may be formulated for subconjunctival or topical administration to the eye and are effective in the treatment of inflammatory disease and conditions of the ocular surface."

Plain-language overview of the independent claims

The claims I can verify come from the pre-grant publication (US 2014/0147449 A1), which lists 20 claims. Two independent claims are visible:

Claim 1 — Method of treatment. A method for treating an inflammatory condition of the ocular surface by administering to the eye of a patient an ophthalmic formulation containing an effective amount of one or more CCR7 antagonists. Plainly: use a CCR7-blocking agent as eye medicine to treat ocular-surface inflammation. Dependent claims narrow it to (2) an anti-CCR7 antibody; (3) an N-terminal truncation mutant of CCL19; (4) an N-terminal truncation mutant of CCL21; (5) a concentration of 0.10%–2.0% (w/v); (6) an allergic ocular-surface condition; (7) a specific conjunctivitis list (hay fever, allergic, perennial, seasonal, atopic, vernal, kerato-, atopic kerato-, vernal kerato-, allergic rhinoconjunctivitis, giant papillary); (8) a broader inflammation list (uveitis, scleritis, keratitis, retinitis, iritis, uveoretinitis, uveoscleritis, episcleritis, optic neuritis, retrobulbar neuritis, blepharitis, Mooren's ulcer, etc.); (9) a tear substitute; (10) an ophthalmic lubricant; (11) human subject.

Claim 12 — Composition. An ophthalmic formulation comprising one or more CCR7 antagonists, suitable for administration to a subject's eye. Plainly: the eyedrop/ophthalmic product itself, defined by its CCR7-antagonist content and its suitability for ocular use. Dependent claims narrow it to (13) subconjunctival administration; (14) topical administration; (15) pH 5.5–7; (16) aqueous; (17) single-dose unit; (18) plus a tear substitute; (19) plus an ophthalmic lubricant.

Uncertainty: The claim listing I retrieved is from the published application, and the text of claim 20 was truncated in the source. I cannot confirm from authoritative sources whether the granted patent's claim set is identical to the published application's, or whether claim 20 is a third independent claim. For a legally operative claim set, the granted patent's printed claims should be checked directly (USPTO Patent Public Search / PatentCenter for US 14/001,594).

Technical substance (for context)

The specification argues that existing AC therapies (antihistamines, mast-cell stabilizers, NSAIDs) act downstream on histamine/IgE mediators but do not target the upstream step where dendritic cells (DCs) stimulate Th2 lymphocytes. The inventors used an ovalbumin (OVA)-induced murine allergic conjunctivitis model with adoptively transferred OVA/Alum-primed T cells and subconjunctivally (SCJ) injected bone-marrow-derived DCs:

• Wild-type DCs augmented clinical AC signs, conjunctival mast-cell/eosinophil infiltration, Th2 cytokines (IL-4, IL-13), and OVA-specific IgE.
• CCR7⁻/⁻ DCs failed to do so, and CCR7⁻/⁻ hosts injected with WT DCs still mounted responses — supporting a DC-intrinsic CCR7 requirement for allergen-laden DC mobilization to the draining lymph node.
• Topical 1% anti-CCR7 antibody significantly reduced clinical scores in actively immunized mice at 20 min, 6 h, and 24 h post-challenge (days 3 and 4, p<0.05) relative to isotype control.

The patent cites specific reagents and sequences: mouse CCR7 (NCBI NP_031745.2, GI:116268121); human CCR7 (Gene ID 1236; NM_001838.3; NP_001829.1); rat IgG2A clone #4B12 (R&D Systems MAB3477); mouse IgG2A clone #150503 (R&D Systems MAB197). It also cites U.S. Pat. Nos. 8,066,996; 7,691,856; 7,678,798; and U.S. Pub. 2011/0014128 as sources of CCR7 antagonists.

Related family members (not the same patent)

• WO 2012/148547 A1 (PCT publication)
• US 2015/0307619 A1 — "Use of C-C Chemokine Receptor Type 7 (CCR7) Inhibitors," a later Schepens application covering CCR7 blockade for dry eye disease (DED), including topical anti-CCR7 antibody data.

Explicit uncertainty statements

1. I found no appellate (CAFC 2026), PTAB, or ITC activity for US 9,670,277; absence of results in a web search is not proof of absence.
2. The justia/Google Patents assignee string contains a typo ("Reasearch"); I have reproduced it literally rather than correcting it.
3. The granted claim set may differ from the published application's claims; treat the claim summaries above as indicative of the published application, not as an authoritative reproduction of the granted claims.

I'll research litigation involving US patent 9670277. Let me search multiple sources.

The initial searches returned many false positives (other patents ending in "027"). Let me refine with more targeted searches.

Let me check the Unified Patents litigation portal and other litigation databases directly.

Let me do a couple more targeted searches on litigation-specific databases.

I'll verify the structured "no proceedings on file" result against public sources before writing up.

Let me run a few more targeted checks on patent-owner-level and subject-matter-level PTAB activity.

One more pass to close out the obvious false-positive channels.

PTAB / AIA Trial Proceedings — US 9,670,277 B2

Search date: 2026-09-21. Canonical source: the structured "PTAB proceedings on file" block (USPTO Open Data Portal ingest) supplied in this prompt, which returns zero AIA trial proceedings. I attempted to corroborate that with targeted web searches (patent number + "IPR," owner name + petitioner, application number, and subject matter × "inter partes review"). No proceeding naming this patent surfaced. Note that the searches did turn up two recurring false positives, discussed under "Strategic summary," that I explicitly did not treat as this patent.

Proceedings overview

Total AIA trial proceedings on US 9,670,277: 0 — none active, none where claims were invalidated, none where claims were sustained, none settled, none with institution denied. The defensive posture this gives a defendant is not "hardened patent" so much as "uncontested but commercially abandoned": no petitioner has ever taken a shot at these claims at the Board, so the claims have never been tested on the merits in an adversarial forum — but the patent is recorded as Expired – Fee Related (adjusted expiration 2032-03-07), which is a separate and often more decisive piece of leverage. The absence of PTAB activity here is not evidence of validity; it is evidence that no one has had a reason to spend $300K–$500K invalidating a patent nobody appears to be asserting.

Proceedings

None to report. Because there are no proceedings on file, the per-proceeding template (type, filed date, status, panel, grounds, institution decision, FWD at claim-level granularity, settlement, appeal, defensive value) cannot be populated for any AIA trial. I decline to manufacture proceeding numbers, panels, or dispositions. To verify independently:

• USPTO Patent Trial and Appeal Board End-to-End (PTAB E2E) / PTAB Center case search: https://ptab.uspto.gov
• USPTO Open Data Portal (the source of the canonical block): https://data.uspto.gov
• Federal Circuit docket / opinions and CourtListener for any § 319 appeal: https://courtlistener.com

Strategic summary

Claim status: every claim of US 9,670,277 is UNTESTED at the PTAB. No claim has been canceled, disclaimed in response to an instituted trial, canceled by statutory disclaimer, or held unpatentable in an FWD. Equally, no claim has been affirmed patentable by the Board. If a demand letter cites claims 1–20, the correct characterization is "untested in an adversarial validity forum," not "surviving" and not "dead." Two independent caveats from the prior analysis carry forward unchanged: (i) the claim listing available in public sources is from the pre-grant publication US 2014/0147449 A1, and the granted printed claims should be pulled from PatentCenter for US 14/001,594 before relying on any particular claim number; and (ii) the earlier sections flagged that claim 20's text was truncated in the source I had.

Estoppel landscape: none. § 315(e)(2) estoppel is inapplicable because no IPR has been instituted. This matters in both directions. There is no petitioner estopped from re-litigating art. But there is also no prior petitioner whose search was deemed "reasonable" — meaning the field of available grounds is wide open: patents, printed publications, and (unlike IPR) § 112 and § 101 grounds. If a defendant needs to knock this patent down, the PTAB is not the only door and, given zero prior filings, not a particularly crowded one:

• 35 U.S.C. § 101 may be a live angle. The claims are directed to administering a known class of agent (an anti-CCR7 antibody or CCL19/CCL21 truncation mutant) to treat a known inflammatory disease — a therapeutic-administration method whose eligibility depends heavily on whether the specification's finding (DC-intrinsic CCR7 is required for allergen-laden DC mobilization to the draining LN) supplies an inventive concept. That question is addressable in the district court, where it is cheaper and earlier than an IPR.
• 35 U.S.C. § 112 (written description/enablement) is likewise unavailable in IPR and available in litigation. The prior-art landscape around CCR7 antagonists was already crowded at the 2011 priority date — the specification itself cites U.S. Pat. Nos. 7,691,856 (thiadiazoledioxides), 7,678,798 (piperazinylpiperidine derivatives), 8,066,996 (anti-CCR7 antibodies), and U.S. Pub. 2011/0014128 — so the claims' breadth relative to the disclosed support is a fair target.
• Ex parte reexamination under 35 U.S.C. § 302 remains available to anyone at any time on patents/printed publications, carries no estoppel, and is not implicated by the absence of an IPR.
• A § 315(b) one-year bar has never begun to run for anyone, since it runs from service of a complaint alleging infringement. If you have been served, the clock is now yours.

Pattern signals are all negative. There is no repeat petitioner, no joinder, no defensive aggregator (no Unified Patents, RPX, or similar) in the chain, no Patent Owner Preliminary Response activity, no Director Review request, and no § 319 appeal — because there is no proceeding. A single unasserted patent owned by a nonprofit research institute, with no litigation docket behind it, is exactly the profile that never generates PTAB paper.

Two false positives I explicitly excluded (flagging because they will trip up automated docket screening):

1. U.S. Patent 9,074,027 (Ansell Healthcare / Reckitt Benckiser, synthetic polyisoprene articles) is routinely cited as "the '027 Patent" in PTAB filings, e.g. IPR2017-00063. Different patent, different art, different owner.
2. U.S. Patent 7,151,027 (Spansion / Macronix, memory fabrication) appears as "the '027 Patent" in IPR2014-00898 and IPR2014-00108. Also unrelated.

A third near-miss worth naming: search results for the string "'594 patent" frequently point to U.S. 9,340,594 (Regeneron, aflibercept, asserted in the Celltrion / Formycon litigations). That number collides visually with this patent's application number 14/001,594 but is an entirely different patent. Do not conflate them.

Recommended next steps

1. If you are a defendant: Do not budget for an IPR on the assumption that prior IPRs exist to piggyback on — there are none. The § 315(b) clock, if you have been served, is your primary timing constraint, and any IPR you file would be the first ever on this patent, with no § 325(d)/Advanced Bionics baggage from earlier Office consideration to overcome.
2. Lead with the status question. The Google Patents record lists Legal status: Expired – Fee Related — but the same record describes that status as "an assumption and not a legal conclusion." Confirm the maintenance-fee history for US 14/001,594 in PatentCenter before doing anything expensive. If the patent lapsed for non-payment of a maintenance fee and the § 1.378 reinstatement window has closed, lapse is a complete defense and the invalidity analysis is academic. If it lapsed within the window, a petition for unintentional delay could revive it, so confirm the relevant deadlines rather than assuming finality. Even if revived, an expired term caps exposure to the six-year damages lookback under 35 U.S.C. § 286.
3. Confirm the operative claim set. Before quoting any claim number at a counterparty, pull the granted claims from USPTO Patent Public Search / PatentCenter for application 14/001,594. The prior sections correctly flagged that the publicly available listing is the pre-grant publication's, and that the granted claims may differ.
4. If you want to preserve PTAB options: with no IPR on file, you are not estopped, but you also get no benefit from anyone else's work. Note the current institution regime — as of 2025-10-16, Director Squires's memorandum shifts institution decisions to the Director (with a "summary notice") rather than the merits panel, and proposed rules would bar IPRs against patents that previously survived a validity challenge and require § 102/§ 103 stipulations. None of that changes the analysis for a patent with a clean zero-IPR history, but it does raise the cost of a denied institution.
5. State the position plainly to your client: "No PTAB proceedings exist for US 9,670,277. No claim has been canceled, and none has been confirmed. The patent's recorded status is expired for fee non-payment. The absence of IPR activity is a signal that the patent has not been assertively monetized — not that it is strong."

I'll reconstruct the assignment record for US 9,670,277. Let me run targeted searches against the assignment indexes and cross-reference sources.

Let me pull the assignment/legal-events record directly and cross-reference the assignee's current status.

Let me try to retrieve the specific reel/frame and the Google Patents "Legal Events" panel for this patent.

Assignment-chain reconstruction — US 9,670,277 B2

⚠️ Scope/verification caveat (read first)

I was able to retrieve the Google Patents legal-events record for US 9,670,277 (provided as authoritative in the source text) and cross-reference the assignee's corporate history. I was NOT able to retrieve a USPTO-reel/frame-level record from the Patent Assignment Center in this session — the assignment-search searches either returned unrelated patents ending in "027" or were cut off. So the table below reports the event as Google Patents records it, and I explicitly flag where the reel/frame and correspondent are unknown rather than guessed. Per your constraints, I am not fabricating reel numbers.

The Google Patents record contains exactly one post-filing assignment event:

"2014-02-11 — Assigned to THE SCHEPENS EYE RESEARCH INSTITUTE, INC. — reassignment — THE SCHEPENS EYE RESEARCH INSTITUTE, INC. ASSIGNMENT OF ASSIGNORS INTEREST (SEE DOCUMENT FOR DETAILS). Assignors: SABAN, Daniel; DANA, Reza"

Inventors

Unusual-pattern assessment: One of two inventors (Saban) left the Schepens/Harvard orbit. On its own this is not the classic "all inventors departed within 12 months of filing → fire-sale" tell, because (a) Dana remained at the assignee institution for years afterward, and (b) the assignee is a nonprofit research institute whose standard practice is assignment of inventions, not inventor-held portfolios. Flag as not present / not a meaningful signal.

Original assignee

• Entity on the issued patent: Schepens Eye Research Institute, Inc. (assignment record spelling: "The Schepens Eye Reasearch Institute, Inc." — typo as recorded; flagged in the earlier summary and reproduced literally).
• Primary line of business: Nonprofit academic vision-research institute, Boston, MA; affiliated with Harvard Medical School's Department of Ophthalmology.
• Status / corporate history: In 2011 Schepens unified with / was acquired by the Massachusetts Eye and Ear Infirmary (widely reported as forming "the world's largest private ophthalmology research enterprise"; one Mass. Eye and Ear annual report describes the Foundation's "acquisition of the Schepens Eye Research Institute"). Mass. Eye and Ear is a member of Mass General Brigham (formerly Partners HealthCare). So the ultimate parent today is Mass General Brigham / Mass Eye and Ear; Schepens operates as the "Schepens Eye Research Institute of Massachusetts Eye and Ear."
• Product embodying the claims: No commercial ophthalmic product is on the market under this patent. Schepens is a research institution; the disclosure is preclinical (murine OVA AC model, topical anti-CCR7 antibody). No FDA-approved product maps to the claims. Licensing/industry collaborations exist but there is no evidence of a marketed CCR7-antagonist eyedrop traceable to this patent.
• Current status: Operating (as an affiliate of Mass General Brigham). Not dissolved, not in bankruptcy.

Assignment timeline

1. ~2012-02-24 (PCT filing) / 2014-02-11 (recorded) — Reel/Frame not retrievable in this session (see caveat)

   • Conveyance: Assignment of Assignors' Interest (inventor → institution)
   • Assignor: DANA, Reza; SABAN, Daniel
   • Assignee: THE SCHEPENS EYE RESEARCH INSTITUTE, INC.
   • Correspondent: Not determinable from the sources retrieved. (Unable to confirm the attorney/firm of record; not guessed.)
   • Context: Standard academic employment/invention assignment — inventors conveying rights to their research institution. Routine, pre-commercial.

2. 2017-06-06 — no assignment; patent granted. (This is a grant event, not a transfer.)

No further assignments are recorded. After the 2014 inventor→institute conveyance, the Google Patents chain shows no sale, license recordation, security agreement, or subsequent transfer. The patent sat with the original nonprofit assignee until it went abandoned for non-payment of maintenance fees (status: Expired – Fee Related; adjusted expiration 2032-03-07).

If Assignment Center shows no records beyond the original one, that is itself the finding: a single inventor-assignment to a nonprofit research institute, with no evidence of any NPE transfer. I recommend confirming the reel/frame directly at the USPTO Assignment Center by application number 14/001,594 and patent 9,670,277.

Timeline diagram

timeline
    title Ownership of US 9670277
    2011 : Schepens unifies with Mass Eye and Ear
    2012 : PCT application filed by Schepens
    2014 : Inventors assign rights to Schepens
         : US national stage published
    2017 : Patent granted to Schepens
    2020s : Patent expires for unpaid fees

(Adjust the final year label if the exact maintenance-fee lapse date is confirmed; the recorded adjusted expiration is 2032-03-07, but the "Expired – Fee Related" status indicates fees were missed before the full term ran.)

NPE / troll-pattern signals

Verdict

Insufficient data (only the original assignment).

The entire recorded chain is a single, routine inventor→institution assignment (Dana & Saban → The Schepens Eye Research Institute, Inc.), with zero NPE-pattern indicators. The assignee is a real research nonprofit (now an affiliate of Massachusetts Eye and Ear / Mass General Brigham), not a shell; the patent was never asserted in the litigation I could find, was never commercialized, and simply lapsed for unpaid maintenance fees. Because I could not pull the reel/frame or correspondent from the USPTO Assignment Center in this session, I am withholding anything stronger than "insufficient data" rather than overstating a clean-chain conclusion — but on the evidence in hand, there is no NPE or troll signal to report.

For verification, search by application 14/001,594 or patent 9,670,277 at the USPTO Assignment Center: https://assignmentcenter.uspto.gov/ (mirror index: https://assignment.uspto.gov/patent/index.html).

Cross-check note vs. prior sections

• Consistent with the earlier Patent summary (single 2014 assignment; expired-fee status; Schepens assignee with the "Reasearch" typo).
• One correction to flag: the "Reasearch" typo in the assignee string is the assignment-record spelling; the patent-facing assignee name and the institution's legal name are "Schepens Eye Research Institute, Inc." / "The Schepens Eye Research Institute" — these are the same entity, not two different assignees.
• No contradiction with the Litigation summary; the absence of any transfer-to-asserter is consistent with the absence of NPE suits.

I'll research the prior art references cited on the face of US 9,670,277. Let me search multiple sources.

I found the granted claims and the cited-references list on Justia. Note the granted claim 1 recites "CCR7 antibodies" — not "antagonists" — which differs from the published application. Let me pull the full list of cited references and details on each.

Prior-Art Analysis for US Patent No. 9,670,277 (US 9,670,277 B2)

Analyst note / correction to the earlier section first. The previously generated summary described the claim set from the pre-grant publication (US 2014/0147449 A1), which had 20 claims including a composition claim 12 and "CCR7 antagonist" language. The granted patent's claims (as reproduced on Justia) are materially different and this changes the § 102 analysis:

• Claim 1 (granted): "A method for treating an inflammatory condition of the ocular surface, said method comprising administering to the eye of a subject in need thereof an ophthalmic formulation comprising an effective amount of one or more C—C chemokine receptor type 7 (CCR7 antibodies)."
• The granted claim set appears to run claims 1–10 only (method claims), all now limited to antibodies. The earlier summary's "Claim 12 — Composition" and the "N-terminal truncation mutant" claims (published claims 3–4) appear to have been cancelled or amended out during prosecution.

This is the single most important fact for prior-art relevance: the operative claims require an anti-CCR7 antibody administered to the eye. Prior art that discloses CCR7 antagonists generally (peptides, small molecules, fusion proteins) is only relevant as § 103 background, not as § 102 anticipation. I flag this as an explicit contradiction with the earlier Summary section.

Sourcing caveat: I reached the tool-call limit before I could independently verify the content of every foreign reference. Where I could not verify a reference's substance, I say so rather than guessing. All citations below are as listed on the face of US 9,670,277 via Justia (https://patents.justia.com/patent/9670277) and Google Patents (https://patents.google.com/patent/US9670277/en).

A. Patent references cited on the face of US 9,670,277

Notes on the substantive ones:

• US 2010/0285020 A1 (Aifantis et al.). Discloses that chemokine-receptor–driven chemotaxis (Notch-induced, involving the CCR7 axis) controls migration of dendritic/leukemic cells. It is mechanistic/biological background on CCR7-mediated DC trafficking. It does not disclose administering an anti-CCR7 antibody to the eye for ocular-surface inflammation. Relevant only as § 103 background on the DC-mobilization mechanism the patent exploits. (Confirms relationship: US 9,670,277 appears in the "Cited By" list of US 2010/0285020.)

• US 2011/0104236 A1 (Dana & Chauhan). Same-inventor family art (Reza Dana). Discloses topical ocular delivery of a therapeutic antibody (anti-IL-17) to treat ocular-surface inflammatory disorders, with dosage-form disclosure (topical drops, 0.01–50% w/v, contact lens, gel, etc.). Its relevance is to the delivery-form and ocular-surface-treatment elements of the granted claims — not to CCR7. Because the target is IL-17, not CCR7, it cannot anticipate claim 1; it is potentially useful § 103 art for the "administer to the eye an antibody formulation for ocular surface inflammation" concept.

• WO 2009/139853 A2. This is the most technically on-point patent citation: it is directed to human monoclonal antibodies against CCR7. However, it addresses anti-CCR7 antibodies as binding agents/antagonists generally — not their use in an ophthalmic formulation for ocular-surface inflammation. It therefore cannot anticipate claim 1 (which requires "administering to the eye"). Its obviousness relevance is that it supplies the "one or more CCR7 antibodies" element; a § 103 rejection would still need a teaching/suggestion to apply such an antibody topically/subconjunctivally for ocular-surface inflammation (which is where US 2011/0104236 becomes relevant).

B. Non-patent literature cited on the face of US 9,670,277

The boilerplate NPL group (Ma, Bowie, Burgess, Lazar, Bork, Aagaard, Warzocha, Guido, Vajdos, Brown) is the classic examiner citation cluster used to support § 112 written-description / § 103 positions about antibodies to a known protein and truncated peptides — not § 102 anticipatory art.

C. Bottom-line § 102 assessment

No cited reference anticipates any granted claim of US 9,670,277 under 35 U.S.C. § 102. The reason is structural: every granted claim requires the combination of (i) an anti-CCR7 antibody, (ii) administered to the eye, in (iii) an ophthalmic formulation for an (iv) inflammatory condition of the ocular surface. Each element appears only piecemeal across the cited art:

• Anti-CCR7 antibodies → WO 2009/139853.
• Ocular-surface antibody delivery → US 2011/0104236 (but for IL-17).
• CCR7 in DC mobilization → US 2010/0285020 (biology only).
• CCR7 peptide antagonists → Pilkington et al. (CCL19 truncation mutants).

Where the granted claims could still be attacked is § 103 — e.g., WO 2009/139853 (anti-CCR7 antibody) in view of US 2011/0104236 (topical ocular antibody for ocular-surface inflammation), optionally with US 2010/0285020 for the mechanism. That is an obviousness case, not § 102 anticipation.

Also note (outside the "cited references" scope you asked about): the specification's own body cites prior art that is arguably more on-point for the CCR7/allergy mechanism than anything on the front page — Yamashita et al. 2006, Grinnan et al. 2006, Hintzen et al. 2006 (allergic-airway inflammation in CCL19/CCL21-deficient plt and CCR7⁻/⁻ mice) and Jin Y et al. 2010 (tolerogenic CCR7 role in ocular surface DCs). Those are candidates for a deeper § 103/§ 102(2) attack and should be pulled in full text.

D. Explicit uncertainties

1. The foreign references (JP 2002-284777; WO 2004/033440; WO 2009/025763; WO 2009/089036) were listed on the patent face but I did not independently verify their content; I have not assigned them a § 102 position.
2. I treated the Justia "Referenced Cited" table as complete, but it may be truncated; Google Patents should be cross-checked for any additional cited references.
3. I could not complete verification of the exact granted claim count (Justia displayed claims 1–10); if any claim beyond 10 exists, confirm directly at USPTO PatentCenter for application 14/001,594.
4. Assignment-record spelling "Reasearch" is reproduced literally, not corrected.

I'll research the prior art landscape for this patent, building on the previously generated sections.

Let me dig into the specific pre-2011 references that would form the obviousness combinations.

Let me verify a few key references and check the European counterpart's search report.

Obviousness Analysis — US 9,670,277 under 35 U.S.C. § 103

Building on prior sections: This analysis takes as its starting point the claim summaries, technical substance, and family members set out in the earlier "Patent summary" section. Two caveats from that section carry forward and materially affect the analysis below:

1. The claim set I can verify is from the pre-grant publication US 2014/0147449 A1, not the granted text. The granted claims may differ. Everything below is directed to the published claim set (claim 1 method; claim 12 composition, plus dependents).
2. Because the application was filed Feb. 24, 2012 (before March 16, 2013), pre-AIA §§ 102/103 apply. The critical date is the Feb. 24, 2011 priority date; the § 102(b) one-year date is Feb. 24, 2010.

1. Legal framework

• Pre-AIA § 103 asks whether the subject matter as a whole would have been obvious to a person of ordinary skill in the art (POSITA) at the critical date, in view of the scope and content of the prior art, the differences between the art and the claims, and the level of ordinary skill. Graham v. John Deere.
• KSR Int'l v. Teleflex (2007): a combination is obvious where the elements were known, there was a known problem for which the combination supplied a predictable solution, and the POSITA had a "reasonable expectation of success." Where there are "a finite number of identified, predictable solutions," the fact that the path was obvious to try supports obviousness. A reference need not provide an express motivation; reasoned judgment and common sense suffice.
• The "teaching away" exception requires that the prior art, when considered as a whole, discourage the claimed route — an alternative that is "more attractive" is not enough. In re Fulton.

2. What the claims require (the § 103 target)

The two independent claims require the following elements:

Dependents add: anti-CCR7 antibody (2); N-terminal truncation mutants of CCL19/CCL21 (3–4); 0.10–2.0 % w/v (5); allergic/allergic-conjunctivitis sub-genuses (6–8); tear substitute / lubricant (9–10, 18–19); human (11); subconjunctival or topical route (13–14); pH 5.5–7 (15); aqueous (16); single-dose unit (17).

None of these elements is a new chemical entity, a new mechanism, or an unexpected result. Each maps onto well-known prior art, as shown below.

3. The prior-art landscape (all pre-Feb. 24, 2011)

I group the references that the record shows to exist. Dates in brackets; where I could only confirm a reference through the patent's own specification (which the earlier section already noted is authoritative), I say so.

(A) CCR7 as the master mediator of DC egress from tissue to lymph node — the core mechanism

(B) The ocular-surface-specific link — the closest art

• Jin Y et al., "The chemokine receptor CCR7 mediates corneal antigen-presenting cell trafficking," Mol Vis 2007;13:626–634 (verified via PubMed PMID 17515886; published April 27, 2007). This is the single most damaging reference. It teaches, in the eye:

  • CCR7 and its ligand CCL21 are upregulated in the inflamed cornea;
  • the CCR7⁺ cells are CD11b⁺CD11c⁺ DC-lineage cells;
  • OVA-loaded APC traffic from the cornea to the draining LN in a CCR7-dependent manner;
  • subconjunctivally injected neutralizing antibody against CCL21 significantly suppresses the flow of OVA⁺CD11c⁺ cells to the draining LN.

  That is, Jin 2007 already discloses the claimed mechanism, the claimed cell type, the claimed route (subconjunctival antibody), and the claimed functional consequence (blocking the CCR7 axis at the ocular surface reduces APC trafficking to the draining LN). Note this is a § 102(b) printed publication (published >1 year before the Feb. 24, 2011 priority date), so the fact that the senior author (Dana) is a co-inventor here does not remove it as prior art — pre-AIA § 103(c) disqualifies only § 102(e)/(f)/(g) art, not § 102(b) publications.

(C) DCs are necessary and sufficient for allergic (Th2) inflammation

• Lambrecht 2000, J Clin Invest 106:551–9 (myeloid DCs induce Th2 responses → eosinophilic airway inflammation) (cited).
• Sung 2001, J Immunol 166:1261–71 (OVA-pulsed DCs induce airway eosinophilia) (cited).
• van Rijt 2005, J Exp Med 201:981–91 (depleting CD11c⁺ DCs during challenge abrogates asthma features) (cited).
• KleinJan 2006, J Allergy Clin Immunol 118:1117–25 ("An essential role for dendritic cells in human and experimental allergic rhinitis," i.e., DCs as a novel therapeutic target in allergic mucosal disease) (cited; surfaced in search).

(D) A model of allergic conjunctivitis exists

• Ozaki A et al., Microbiol Immunol 2004;48(1):39–48 — the established murine AC model the inventors themselves used (cited in the patent; referenced in Schlereth/Saban later work).

(E) CCR7 antagonists are known and available

• Pilkington et al., J Biol Chem 2004;279(39):40276–82 — N-terminal truncation mutants of CCL19 and CCL21 act as CCR7 antagonists (expressly cited in the patent as the basis for claims 3–4).
• US 7,691,856 — thiadiazole dioxide/oxide CCR7 antagonists (cited in the patent).
• US 7,678,798 — piperazinylpiperidine CCR7 antagonists (cited in the patent).
• US 8,066,996 — anti-CCR7 antibodies and immunoassays (cited in the patent).
• US 2011/0014128 A1 — soluble CCR7 fragments (cited in the patent).
• Anti-CCR7 antibodies were commercially available (R&D Systems MAB3477 clone 4B12 for mouse; MAB197 clone 150503 for human; BD 3D12; eBioscience CCR7.6B3) — all listed in the patent itself.

(F) Chemokine-receptor antagonists expressly indicated for conjunctivitis / allergic eye disease

• US 7,700,772 (Merck Sharp & Dohme; inventors Yang/Pasternak/Mills; filed Feb. 8, 2005; granted Apr. 20, 2010) — abstract states the compounds "are modulators of chemokine receptor activity and are useful in the prevention or treatment of certain inflammatory and immunoregulatory disorders and diseases, allergic diseases, atopic conditions including allergic rhinitis, dermatitis, conjunctivitis, and asthma…" (verified via Justia's attorney-profile listing of the patent). This reference expressly names conjunctivitis as an indication for a chemokine-receptor modulator.
• US 2002/0168358 A1, "Treatment of T-cell mediated diseases" — claims/methods directed to modulating CCR7 and its ligands SLC/MIP-3β; lists allergic diseases including asthma, allergic rhinitis, atopic dermatitis among the treatable "SLC/CCR7-related disorders" (verified via Google Patents and patentimages full text).

(G) Teaching-away material (discussed in § 6)

• Yamashita 2006, JACI 117:1040–6 — CCL21/CCL19 "critical for resolution of airway inflammation."
• Grinnan 2006, JACI 118:1234–41 — plt mutant mice (impaired lymphoid CCL19/CCL21) show enhanced allergen-induced airway inflammation.
• Hintzen 2006, J Immunol 177:7346–54 — tolerance to inhaled antigen relies on CCR7-dependent DC transport.
• Jin Y et al., Invest Ophthalmol Vis Sci 2010;51(2):816–21 — per the patent's own characterization, CCR7 on ocular-surface DCs plays a "tolerogenic" role in the corneal-transplant model.

4. Primary combination rendering claim 1 obvious

Combination: Jin 2007 (B) + Lambrecht 2000 / KleinJan 2006 (C) + Ozaki 2004 (D); optionally with Sozzani/Val/Gunn/Saeki (A).

Claim-chart:

Motivation to combine (the KSR rationales):

1. Known problem in the same field. The patent's own Background concedes the need for new AC agents; allergic conjunctivitis was a known, widespread problem.
2. Known cause. (C) taught that tissue DCs that capture allergen and traffic to the draining node are necessary for Th2/eosinophilic allergic inflammation and are "a novel target for therapeutic intervention" (KleinJan 2006).
3. Known check-point. (B) taught, specifically in the eye, that the CCR7–CCL21 axis is what moves allergen-laden ocular DCs to the draining LN, and that a locally administered antibody against that axis blocks the migration (Jin 2007).
4. Predictable solution. If (i) DC migration from the eye to the node is required for allergic sensitization (A, B) and (ii) that migration is CCR7-dependent and blockable locally (B), then blocking CCR7 at the ocular surface to interrupt the allergic cascade is a direct, logical application of a known solution to a known problem — precisely the "predictable use of prior-art elements according to their established functions" that KSR makes obvious.

In other words, Jin 2007 already supplies nearly every element — ocular-surface DCs, the CCR7 axis, OVA allergen, subconjunctival antibody blockade, and suppressed trafficking to the draining node. The only step the patent adds is to apply the same blockade to the allergy setting (rather than transplant) and to read out allergic endpoints — an endpoint swap that (C) and (D) render routine.

5. Rendering the composition claim (12) and the dependents obvious

• Claim 12 (ophthalmic formulation comprising a CCR7 antagonist). Every CCR7-antagonist genus in § 3(E) (Pilkington peptides; US 7,691,856; US 7,678,798; US 8,066,996; US 2011/0014128) came with conventional pharmaceutical-composition teaching ("a pharmaceutically acceptable carrier"). Combine any of those with Jin 2007's local ocular delivery and US 7,700,772's express recitation of conjunctivitis as a chemokine-modulator indication, and an "ophthalmic formulation comprising a CCR7 antagonist" is at minimum obvious and might be argued anticipated by a CCR7-antagonist patent that expressly lists conjunctivitis/ophthalmic use. (I could not retrieve the disease lists of US 7,691,856 / US 7,678,798 to confirm anticipation — flagged as uncertain.)
• Claim 2 (anti-CCR7 antibody). Jin 2007 used an antibody against the CCR7 ligand; anti-CCR7 antibodies themselves were commercially catalogued (MAB3477, MAB197, 3D12, 6B3) and disclosed in US 8,066,996. Substituting a receptor-directed antibody for the ligand-directed antibody is an obvious, predictable variation (same target axis, same effect).
• Claims 3–4 (N-terminal truncation mutants of CCL19/CCL21). Pilkington 2004 expressly discloses these as CCR7 antagonists; using a known antagonist for its known purpose is obvious.
• Claim 5 (0.10–2.0 % w/v) and the 1 % eye-drop example. Antibody concentration in an ophthalmic drop is a routine optimization parameter (and the patent's own working example uses 1 % anti-CCR7 eye drops, squarely within the claimed range). Under In re Aller / KSR, optimizing a known concentration range to achieve a known result is obvious absent a showing of criticality — none appears in the specification.
• Claims 9–10, 18–19 (tear substitute / lubricant). Combining an active with an ophthalmic vehicle/tear substitute is routine and, indeed, the specification lists only conventional tear substitutes (HPMC, CMC, PVA, GENTEAL®, etc.).
• Claims 13–17 (subconjunctival/topical; pH 5.5–7; aqueous; single-dose unit). These are standard ophthalmic formulation parameters. Jin 2007 supplies subconjunctival administration; pH ~5.5–7 and aqueous, isotonic drops are conventional ophthalmic-formulation knowledge.

6. The strongest non-obviousness (rebuttal) arguments — and why they likely fail

A competent patentee would argue teaching away + unpredictability, built on § 3(G):

Argument. The art as a whole pointed away from blocking CCR7 to treat allergy. Yamashita 2006 said CCL19/CCL21 are needed to resolve airway inflammation; Grinnan 2006 said plt mice with impaired CCR7-ligand signaling get worse allergen-induced airway disease; Hintzen 2006 said CCR7-dependent DC transport is required for tolerance; and Jin's own ocular work (Jin 2010 IOVS) ascribed a tolerogenic role to CCR7 on ocular-surface DCs. So the POSITA would have predicted that blocking CCR7 at the ocular surface would exacerbate, not treat, allergic inflammation — i.e., the art taught away from the claim.

Why it is vulnerable.

1. Different tissue and different cell compartment. The teaching-away references concern the airway or transplant tolerance, and the plt/CCR7⁻/⁻ data implicate global CCR7 loss (lymphocytes, Tregs), not DC-intrinsic CCR7 at the ocular surface. The patent itself draws this very distinction ("a focus on the function of the CCR7-CCL19/CCL21 axis on DCs from the ocular surface"), which is an admission that the whole-animal data were of limited predictive value — a concession that cuts against non-obviousness.
2. Jin 2007 teaches the opposite direction in the eye. Whatever Jin 2010 said about transplant tolerance, Jin 2007 affirmatively taught that blocking the CCR7 axis at the ocular surface reduces APC trafficking out of the eye — the exact causal step the patent exploits. Conflicting art does not defeat obviousness; KSR permits "drawing both pro and con conclusions."
3. No unexpected result. The patent reports results that are exactly what the mechanism predicts (less DC trafficking → less Th2 cytokine → less IgE → fewer clinical signs). An outcome that follows linearly from the known mechanism is not "unexpected." The patent does not establish that CCR7 blockade treats AC better than or contrary to what the art predicted; it establishes only that the prediction was correct.
4. Finite, predictable solutions. With CCR7, CCL19 and CCL21 as the only three druggable nodes of the axis, the POSITA had a small, identified set of candidates (anti-CCR7 antibody, anti-CCL19/21 antibody, truncation-mutant peptides, small-molecule antagonists) — the classic KSR "finite number of identified, predictable solutions."

Net assessment. The teaching-away argument is genuine but probably insufficient: it rests on different-tissue data, while in-eye art (Jin 2007) points toward the claim. At best it raises a genuine fact question suitable for expert declarations; it is unlikely to survive as a matter of law.

7. Bottom line

The patent's vulnerability is structural: its independent claims recite a known mechanism (CCR7-dependent DC trafficking), a known class of agents (CCR7 antagonists), and a known disease (ocular allergy), all of which pre-date the priority date — and, critically, the closest reference (Jin 2007) is an eye-specific, subconjunctival-antibody, OVA-trafficking study by the same laboratory. The only meaningful hurdle to a § 103 rejection is the teaching-away cluster (Yamashita/Grinnan/Hintzen/Jin 2010), and that cluster is weakened by its different-tissue, whole-animal character.

8. Explicit uncertainties (do not over-read this analysis)

1. Granted claims unverified. This analysis targets the published claims (US 2014/0147449 A1). If the granted claims are narrower (e.g., limited to anti-CCR7 antibody at a specific dose, or to a specific conjunctivitis), the obviousness calculus could shift, particularly for dependent claims reciting a 1 % antibody eye-drop limitation that the patent's own example embodies.
2. Reference dates. Bilbiographic details for Sozzani/Val/Gunn/Saeki/Pilkington/Lambrecht/KleinJan/Ozaki are taken from the patent's specification citations and were not independently re-verified against the primary sources in this session; only Jin 2007 (Mol Vis 13:626) and US 7,700,772 were confirmed via external records (PubMed; Justia listing).
3. US 7,691,856 and US 7,678,798 disease lists not retrieved. I could not confirm whether these CCR7-antagonist patents expressly recite ocular/conjunctival use. If they do, claim 12 faces outright anticipation rather than mere obviousness.
4. No asserted-art record. The earlier sections found no litigation, PTAB, or CAFC activity on US 9,670,277, so there is no real-world invalidity contention (and no examiner-cited-art list from a reexam) to anchor this analysis. The combinations above are constructed by me from the references the patent itself cites plus the references surfaced in search; they are not drawn from any prosecution or litigation paper.
5. Assignee/typo caveat ("Reasearch") carried over from the prior section is immaterial to § 103 but should not be silently corrected.