Invalidity dossier
US 11548934
Means and methods for treating and diagnosing fibrosis or fibrosis-associated diseases
Current assignee: Heidelberg Biotech GmbH
Added 9/11/2026, 10:59:34 PM
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Patent summary
Title, assignee, inventors, filing/issue dates, abstract, and a plain-language overview of the claims.
I'll search for this specific patent number across USPTO and CAFC sources.
Let me pull the patent's own record pages and check for any CAFC/litigation activity.
Let me try to retrieve the actual claim text and confirm assignee/legal status.
US 11,548,934 B2 — Verification Summary
Note on scope: I searched for this exact number and did not auto-correct it. I located the patent's USPTO/Google Patents record and the Justia patent-history page. I could not retrieve the verbatim granted claim set, and I found no CAFC 2026 docket activity for this number. Details below are flagged accordingly.
1. Identification & bibliographic data
| Field | Value (as recorded) |
|---|---|
| Patent number | US 11,548,934 B2 |
| Title | Means and methods for treating and diagnosing fibrosis or fibrosis-associated diseases |
| Application no. | 15/781,028 (US national phase) |
| Pre-grant publication | US 2020/0270332 A1 (published 2020-08-27) |
| Priority date | 2015-12-03 |
| Filing date | 2016-12-05 (PCT filing date; Justia: "Filed: Dec 5, 2016") |
| Issue/grant date | 2023-01-10 |
| Adjusted expiration | 2038-07-12 |
| Legal status | Active |
| Inventors | Amir Abdollahi (Heidelberg); Kashi Javaherian (Lexington, MA); Jürgen Debus (Heidelberg); Cheng Zhou (Dossenheim) |
| Original assignee | Deutsches Krebsforschungszentrum DKFZ |
| Current assignee (Google Patents) | Heidelberg Biotech GmbH |
| Examiners | Sudhakar Katakam (primary); Zachary J Miknis (assistant) |
| US class | 424/134.1 (antibody/immunoglobulin fusion protein) |
| CPC | C07K14/78; A61K38/00; A61K45/06; A61K9/0019; A61P1/16; A61P11/00; A61P11/06; A61P13/12; A61P15/00; A61P17/00; A61P17/02; A61P19/02; A61P27/02; A61P29/00; A61P3/10; A61P35/00; A61P37/02; A61P43/00; A61P9/12 |
Assignment chain (from the Google Patents legal-events record):
- 2018-09-19 — assignment recorded to Deutsches Krebsforschungszentrum (assignors: Abdollahi, Debus, Javaherian, Zhou).
- 2026-04-30 — reassignment to Heidelberg Biotech GmbH (assignor: Prof. Dr. med. Dr. rer. nat. Amir Abdollahi).
- 2026-04-30 — reassignment to Abdollahi from Deutsches Krebsforschungszentrum.
⚠️ Two flags on this: (a) Justia's Patent History page still lists the assignee as Deutsches Krebsforschungszentrum (Heidelberg), i.e., the two databases disagree; (b) the 2026-04-30 reassignment dates post-date the "current date" of April 26, 2026 you supplied, so that entry cannot be reconciled with your stated date. I am reporting both literally rather than reconciling them.
2. Abstract
The present invention is concerned with a protein oligomer comprising (i) at least two NC-1 monomers of collagen 18 or (ii) at least two endostatin domains of collagen 18 or (iii) at least two N-terminal peptides of the collagen 18 endostatin domain, for use in treating, ameliorating or preventing fibrosis or a fibrosis-associated disease, a vascular endothelial growth factor (VEGF)-related disease or a matrix metalloproteinase (MMP)-related disease. The invention further relates to the mentioned protein oligomer for use for detecting and/or diagnosing fibrosis or a fibrosis-associated disease, a VEGF-related disease or an MMP-related disease.
This text is corroborated across IBM/Justia inventor listings and Patent Encyclopedia's rendering of US 2020/0270332 A1.
3. Independent claims — plain-language overview
Confidence caveat: I do not have the authoritative granted claim text for US 11,548,934. The full patent text supplied to me is the description/specification and is truncated mid-sentence in the sequence-listing discussion; it does not include the claims. My searches did not surface the granted claims verbatim. The following is therefore an inference from the patent's own summary, definitions, and field-of-use language, not a quotation, and the claim count, preamble wording, and exact scope are unverified.
Based on the specification, the independent claims most plausibly fall into these buckets:
Composition / oligomer claim — a protein oligomer comprising at least two NC-1 monomers of collagen 18, or at least two endostatin domains of collagen 18, or at least two N-terminal peptides of the collagen 18 endostatin domain. The specification repeatedly stresses that oligomerization (dimer/trimer) is a prerequisite for binding fibronectin, VEGF, integrin α5β1, MMP-2 and MMP-9, and that monomeric endostatin does not bind these partners (see the specification's discussion of FIGS. 9–12).
Method-of-treatment claim (fibrosis) — administering such an oligomer to treat, ameliorate or prevent fibrosis or a fibrosis-associated disease. The specification's enumerated fibrosis indications include scleroderma and other skin fibrosis, keloid/hypertrophic scar, morphea, GVHD-associated fibrosis, subepithelial fibrosis, endomyocardial fibrosis, uterine fibrosis, myelofibrosis, retroperitoneal fibrosis, nephrogenic systemic fibrosis, post-surgical scarring, asthma, cirrhosis/liver fibrosis, aberrant wound healing, glomerulonephritis, endometriosis, multifocal fibrosclerosis, and radiation-induced fibrosis (notably radiation-induced pneumonitis / lung fibrosis).
Method-of-treatment claim (VEGF-related and/or MMP-related disease) — a parallel independent claim directed to VEGF-related disease (e.g., wet macular degeneration, endometriosis, bronchial asthma, diabetes mellitus, radiation-induced vascular permeability/"radionecrosis", vaso-tonus alterations, VEGF-addicted tumors, VEGF-dependent ascites) and/or MMP-related disease (specifically MMP-2/MMP-9-related, per the specification).
Diagnostic / detection claim — use of the oligomer for detecting and/or diagnosing fibrosis or a fibrosis-associated disease, a VEGF-related disease, or an MMP-related disease. The specification contemplates labeling the oligomer (e.g., radioisotopes, DOTA chelation for ⁶⁸Ga PET imaging, with the human Superstatin peptide of SEQ ID NO: 13 as an example).
Important structural note: the specification is written throughout in EPO "for use in…" style (purpose-limited format). US practice generally requires such subject matter to be recast as method claims or composition claims. I cannot confirm how the granted US claims actually handle this, and a US patent would not ordinarily issue with "for use" Swiss-type claim language unchanged. This is an unresolved question in my summary.
Key technical content underpinning the claims (from the specification):
- "NC-1 monomer" is defined as comprising an oligomerization domain, a hinge region, and/or an endostatin domain, or fragments thereof.
- The endostatin domain of human collagen 18 is SEQ ID NO: 19; the N-terminal peptide spans roughly residues 1–132 of SEQ ID NO: 19, with narrower sub-ranges (1–115, 1–92, 1–76, 1–27, 1–25).
- Oligomerization can be native (NC-1 association domain, ~residues 10–60 of SEQ ID NO: 4), Fc-mediated, or artificial (Gln7→Cys substitution creating a disulfide).
- "Knobs-into-holes" (KiH) Fc engineering (S354C/T366W "knob"; Y349C/T366S/L368A/Y407V "hole") is described for producing defined monomers.
- SEQ ID NOs: 3, 4, 7, 9, 10, 13, 15, 18, 19, 20, 22, 27, 29 are listed as fusion proteins/oligomer components; SEQ ID NOs: 6, 24, 25, 26, 28, 30 as preferred Fc sequences.
4. CAFC / litigation check
No results. My search for CAFC 2026 docket entries, IPRs, or litigation involving "11548934" / "US 11,548,934" returned nothing. Absence of search hits is not proof of absence — CAFC dockets are not fully indexed by general web search, and a recently docketed appeal could be invisible. To confirm authoritatively you would need to query the CAFC docket system directly (and, for district court, PACER/Docket Navigator) using the patent number.
One unrelated artifact to disregard: a third-party aggregator (patentleaderboard.com) lists this patent under an "Alcatel Lucent" page for Amir Abdollahi. That appears to be an entity-matching error by the aggregator, not a recorded legal assignment. The recorded assignment parties are DKFZ, Abdollahi, and Heidelberg Biotech GmbH.
5. Explicit uncertainties
- Granted claim text not verified — the plain-language claim overview above is inferred from the specification, not read off the granted claims. Treat it as a hypothesis.
- Claim count and dependency structure unknown.
- Assignee conflict — Google Patents says Heidelberg Biotech GmbH; Justia says Deutsches Krebsforschungszentrum.
- Date anomaly — the 2026-04-30 reassignment entries post-date your stated current date of 2026-04-26.
- Related-family caution — do not conflate this patent with US 2023/0341406 A1 "Means and methods for treating angiogenesis-related diseases" (also DKFZ; a divisional of Ser. No. 14/240,273, priority 2011-08-23) or with US 11,912,755 "Endostatin fragments and variants for use in treating fibrosis." These are separate families with different priority chains.
- Sequence listings — the specification states SEQ ID NOs 1–17 are depicted in WO 2013/026913, incorporated by reference. I did not independently verify the sequence content.
Generated 9/12/2026, 12:48:12 AM
Cases on file (0)
Specific litigation cases in our database that name US patent 11548934. The free-form analysis below may also discuss cases beyond this list.
No cases on file mention this patent. Upload a CSV or add a case manually in Admin → Manage litigation cases.
Litigation summary
Past and pending lawsuits — plaintiffs, defendants, jurisdictions, outcomes, and notable rulings.
I'll search for litigation involving US patent 11548934 across the sources you specified.
Let me search more targeted litigation sources.
Summary of findings
Based on my searches of patent-litigation-focused sources (Unified Patents portal/litigation case list, CourtListener/CAFC opinions, ITC §337 notices, and general web searches keyed to the exact number), I found no litigation — district court, ITC §337, CAFC appeal, or PTAB proceeding — involving U.S. Patent No. 11,548,934.
I want to be explicit about the limits of this conclusion: I could not complete a full sweep of PACER docket data or a direct Docket Navigator / Lex Machina query within this session (my search tooling returned only general web results). So the statement "no litigation is known" reflects the evidence I was able to retrieve, not a certified negative across all federal dockets.
What the searches did and did not return
| Search target | Result |
|---|---|
| Unified Patents portal / litigation case list for "11548934" | No case entries. Unified Patents-related hits were for unrelated patents (e.g., Voice Tech Corp. v. Unified Patents, LLC, Fed. Cir. No. 22-2163, re U.S. Pat. 10,491,679). |
| ITC §337 notices mentioning a '934-style number | Only unrelated patents (e.g., U.S. Pat. Nos. 8,764,172; 9,370,934; 11,535,038; 12,240,248; 12,240,249 — the Epson ink-cartridge investigation). Note the caution here: 9,370,934 and 11,535,038 are not the same patent as 11,548,934, and I did not conflate them. |
| CAFC / CourtListener | No opinion or appeal referencing 11,548,934. |
| General infringement-complaint searches ("US 11,548,934" + complaint/defendant) | Zero relevant results. |
| Assignee-side search (Heidelberg Biotech GmbH, DKFZ, Abdollahi, endostatin/NC-1 fibrosis) | Only prosecution/assignment and family-member activity — no enforcement actions. |
Known litigation
None identified. Plaintiff(s): N/A. Defendant(s): N/A. Jurisdiction: N/A. Case number: N/A. Filing date: N/A. Outcome/status: N/A.
Context from the patent record (prosecution/ownership, not litigation)
Although there is no litigation, the patent's own bibliographic record shows activity that is often a precursor to enforcement and worth monitoring:
- Patent: U.S. 11,548,934 B2, "Means and methods for treating and diagnosing fibrosis or fibrosis-associated diseases"; application 15/781,028; filed 2016-12-05; priority 2015-12-03; granted 2023-01-10; status Active, adjusted expiration 2038-07-12.
- Original assignee: Deutsches Krebsforschungszentrum (DKFZ), with an assignment recorded 2018-09-19 (assignors: Abdollahi, Debus, Javaherian, Zhou).
- Current assignee per the record: Heidelberg Biotech GmbH, via reassignment events recorded 2026-04-30 (assignor of interest: Prof. Dr. med. Dr. rer. nat. Amir Abdollahi; and DKFZ's interest assigned to Abdollahi). This is a small-entity/startup consolidation of the portfolio, which is the type of event that precedes licensing demands or infringement suits.
- Related family members that could be asserted alongside it: e.g., US 2021/0363225 and US 2023/0382975 (Universität Heidelberg / Heidelberg Biotech NC-1-Fc and oligomer filings), and a further granted member surfaced as US 12,577,291 B2. No litigation was found on those either.
Caveats on the assignment dates
The record lists reassignment entries dated 2026-04-30, which is four days after the "current date" you gave (2026-04-26). I am reporting the identifier/dates literally as they appear in the source rather than correcting them; you may want to verify the assignment record directly via the USPTO Assignment database if the timing matters.
Recommended next steps to confirm a true negative
- PACER / CourtLink / Docket Navigator exact-string query on
11,548,934and11548934across all districts (the "no litigation" finding above is based on open web sources, which do not index every docket). - USPTO Patent Trial and Appeal Board API / PTAB Center for IPR/PGR/CBM petitions naming the '934 patent.
- USITC EDIS full-text search for
11,548,934. - Monitor Heidelberg Biotech GmbH as new assignee for any first-filed complaint or §337 complaint.
If you'd like, I can run additional targeted searches (e.g., a specific district or a named competitor such as an endostatin/anti-fibrotic developer) to look for a complaint that cites the '934 patent.
Generated 9/12/2026, 12:48:04 AM
Proceedings on file (0)
All PTAB activity →AIA trial proceedings (IPR / PGR / CBM) filed at the USPTO Patent Trial and Appeal Board against this patent. Sourced from the USPTO Open Data Portal and refreshed every six hours; each proceeding number deep-links to the PTAB E2E docket.
No PTAB proceedings on file. This patent has not been challenged via IPR, PGR, or CBM. The absence is itself a signal — well-asserted patents eventually attract IPRs. The LLM analysis below may surface filings the ODP feed hasn’t indexed yet.
PTAB challenges
AIA trial proceedings at the USPTO Patent Trial and Appeal Board — IPR, PGR, and CBM. Petitioners, judge panels, claim-level invalidation outcomes from Final Written Decisions, and Federal Circuit appeals. The single most important defensive datapoint after litigation history.
I'll verify the structured-data finding with targeted searches before writing the report.
Proceedings overview
Total AIA trial proceedings on file against U.S. 11,548,934: 0 — no IPRs, no PGRs, no CBMs, no derivation proceedings. There is nothing to break down by active / invalidated / sustained / settled / institution-denied, because there is no docket: every claim of the '934 patent that issued on 2023-01-10 remains live and untested at the Board.
The defensive posture this creates is the opposite of a hardened patent and also the opposite of a dead one:
- No claim is canceled. If you received a demand letter, you cannot respond "claims 1-5 are dead." You have no PTAB disposition, no certificate of cancellation under 35 U.S.C. § 318(b), and no Federal Circuit mandate to point to. Every claim the patent owner asserted is presumptively valid under § 282.
- You would be the first petitioner. That means the entire prior-art universe is still available to you — nothing has been consumed by a prior petitioner's ground, and no § 315(e) estoppel has attached. It also means there is no Board claim-construction record, no institution decision reasoning, and no FWD findings to mine. You would be buying the first ticket on an unlitigated patent.
- No Patent Owner track record. Heidelberg Biotech GmbH (current assignee) has never had to defend these claims in an AIA trial. Its posture, its experts, and its willingness to settle are all unknown from the public record.
This is consistent with the litigation section of this analysis, which likewise found no district court, ITC § 337, or CAFC activity. A patent that has neither been asserted nor challenged is a portfolio asset in cold storage, not a litigation weapon with a history.
Cautions on the "no proceedings" finding
- Shorthand-conflation trap. My searches repeatedly surfaced other patents colloquially called "the '934 patent" — e.g., the Electronic Scripting Products patent at issue in Valve Corp. v. Elec. Scripting Prods., IPR2019-00062/-00063/-00084, and the Koss patent at issue against Bose. These are not U.S. 11,548,934. I did not conflate them, and you should not either if you run your own searches.
- Structured data governs. The "PTAB proceedings on file" block supplied from the USPTO Open Data Portal is the canonical list and returns nothing. My web searches found no contradictory evidence, but web search is a weak instrument for PTAB coverage.
- PGR window is closed and must stay closed. U.S. 11,548,934 issued 2023-01-10 and claims priority to 2015-12-03 with a 2016-12-05 filing, so it was PGR-eligible (post-2013-03-16 filing). The 9-month PGR window under § 321(c) expired on or about 2023-10-10. Any new challenge in 2026 is IPR-only — which means § 112 grounds (enablement, written description, indefiniteness) and most § 102(a)(1) "public use / on-sale" art are off the table; you are limited to patents and printed publications under §§ 102/103 per § 311(b).
- I do not have the claim text. The authoritative patent text supplied to me for this analysis is the description/definitions body and does not include the claims. I therefore cannot state which claims are independent, what the claim count is, or which limitations carry the weight. Do not treat any claim-number statement below as claim-language verification — pull the claims from USPTO PatentCenter or Google Patents before drafting anything.
Proceedings
None. There is no proceeding number to report, and I will not invent one.
| Field | Value |
|---|---|
| Proceeding number | N/A — no AIA trial on file |
| Type | N/A |
| Filed | N/A |
| Status | N/A |
| Judge panel | N/A — no panel has ever been designated |
| Petition grounds | N/A |
| Institution decision | N/A |
| Final Written Decision | N/A |
| Settlement / termination | N/A |
| Appeal | N/A |
Strategic summary
Claim status across the patent. Because no AIA trial has ever been instituted, the claim ledger is entirely one-directional: zero canceled, zero sustained-by-FWD, all claims UNTESTED. "Untested" is not the same as "strong" or "weak" — it means the Board has never construed a single limitation. Contrast this with a patent that survived an IPR: a surviving claim carries the Board's express patentability finding on the record of the art presented, which is real defensive value. The '934 patent has none of that. It also has none of the offensive frailty that comes with a mixed or adverse FWD. If you are deciding whether to file, understand that you are not litigating against a body of PTAB precedent — you are litigating against the specification and prosecution history, which the analysis above shows is unusually dense with definitions and alternatives but which I have not been able to review at the claim level.
Estoppel landscape. There is no § 315(e)(2) estoppel against anyone. No petitioner has filed, so no petitioner or privy is barred from raising any ground in district court or before the Board. Practical consequences for a defendant today:
- If you file an IPR, you are the first mover. Every § 102/§ 103 combination built on patents and printed publications is available to you, including grounds a prior petitioner would have been expected to raise.
- If you do not file and litigate in district court, you face no adverse estoppel either — but you also forgo the § 315(b) clock dynamics, since with no complaint served there is no one-year bar running against anyone yet. (The one-year bar is petitioner-specific and complaint-triggered; § 315(b) has not begun to run on any would-be petitioner on the record I can see.)
- If the patent owner sues you, institution risk is at its methodological lowest for a first petition. There is no General Plastic follow-on problem, no § 325(d) "same or substantially the same art previously presented" problem from a prior Board record, and no Fintiv-style parallel-proceeding history to weigh — all of which are discretionary-denial vectors that a second petitioner on a well-worn patent has to fight.
Pattern signals. None of the usual patterns exist yet: no serial petitioner, no defensive aggregator (no Unified Patents or RPX-style entity appears anywhere in the chain), no Patent Owner appeal practice at the Federal Circuit, no IPR-driven amendment practice. The one monitoring signal is ownership, not litigation: the record shows the portfolio moving from Deutsches Krebsforschungszentrum DKFZ to Heidelberg Biotech GmbH (reassignment events recorded 2026-04-30), with related family filings surfaced as US 2021/0363225 and US 2023/0382975 and a further granted member reported as US 12,577,291 B2. Concentration of a research-institute portfolio into a single-purpose biotech vehicle is a classic precondition for outbound licensing or first-filed enforcement. If a complaint appears, an IPR petition clock starts running against that defendant within days.
One cross-section inconsistency to note. The litigation section flagged that the assignment records are dated 2026-04-30, four days after the "current date" given in that section (2026-04-26). Under today's date (2026-09-12) that anomaly is moot — those dates are now in the past — but the underlying records should still be verified directly against the USPTO Assignment database if the ownership chain matters to your standing or privity analysis.
Recommended next steps
- Treat this as a true negative, but verify it at the source. Confirm the empty result through the channels a PTAB practitioner would actually rely on, since my finding rests on the structured ODP block plus open-web search:
- USPTO Patent Trial and Appeal Board PTAB E2E / PTAB Center — search by patent number 11,548,934 and by application 15/781,028: https://ptab.uspto.gov/
- USPTO Open Data Portal AIA proceedings datasets (the source of the canonicity claim above): https://data.uspto.gov/
- USITC EDIS and PACER/CourtListener for any parallel assertion that would signal a petition is imminent: https://www.courtlistener.com/
- The Board's own AIA trial statistics to sanity-check that Bio/Pharma patents at this vintage are not systematically shielded from filings: https://www.uspto.gov/sites/default/files/documents/ptab_aia_fy2024__roundup.pdf
- Get the claims before doing anything else. I could not review claim language from the authoritative text supplied. Identity of the independent claims, the number of claims, and whether the claims are purpose-limited ("for use in treating…") versus composition claims will determine whether an IPR is even the right vehicle and what the § 311(b) art strategy looks like. Retrieve from PatentCenter (application 15/781,028) and re-run the prior-art analysis at the claim level.
- Because PGR is time-barred (window closed ~2023-10-10), scope your invalidity theory to § 102/§ 103 on patents and printed publications. Note this cuts against you in one specific way: § 112 written-description and enablement attacks on the very broad functional/definitional language in the specification ("protein oligomer comprising at least two NC-1 monomers… for use in treating") cannot be raised at the Board in 2026 and would have to be litigated in district court.
- If you are a defendant and no complaint has been served yet, you hold the timing initiative. A declaratory-judgment-triggered § 315(a)(1) bar is a real trap: filing a DJ action for invalidity before an IPR petition can bar that petition. Sequence the IPR petition ahead of any DJ filing, or you may forfeit the Board forum entirely.
- Monitor Heidelberg Biotech GmbH as first-mover risk. Set a watch on new complaints naming the '934 patent and its family members (US 2021/0363225, US 2023/0382975, US 12,577,291 B2). The first complaint against a competitor is the event that converts this empty PTAB docket into a populated one — and it will simultaneously start a § 315(b) one-year clock for that defendant.
Bottom line for a defendant: the demand letter's claims are all still valid and enforceable, and no PTAB proceeding has blunted them. But you would be the first challenger to an untested patent, with zero estoppel against you, the whole printed-publication prior-art space open, and institution-discretion risk at its floor. The absence of PTAB activity here is not a sign the patent is invincible — well-asserted patents eventually attract IPRs, and this one has never been asserted.
Generated 9/12/2026, 12:48:34 AM
Ownership chain (3)
Asserters network →Structured records extracted from the assignment-history narrative below. Each entity links to its full ownership-network profile.
? · recorded 2018-09-19 · Assignment
Abdollahi, Amir; Debus, Jürgen; Javaherian, Kashi; Zhou, ChengDeutsches Krebsforschungszentrum (DKFZ)
? · recorded 2026-04-30 · Assignment
Deutsches Krebsforschungszentrum (DKFZ)Abdollahi, Prof. Dr. med. Dr. rer. nat. Amir
spin-out
? · recorded 2026-04-30 · Assignment
Abdollahi, Prof. Dr. med. Dr. rer. nat. AmirHeidelberg Biotech GmbH
spin-out
Assignment history
Inventors, original assignee, and the chain of ownership recorded with the USPTO — including the correspondent attorney who recorded each assignment, since shell-LLC chains often share one repeat-player attorney even when the entity names look unrelated. Surfaces NPE / patent-troll patterns: shell-entity transfers, known asserters in the chain, repeat correspondent fingerprints, pre-litigation assignments, and bankruptcy fire-sales.
I'll research the assignment chain for US 11,548,934, starting with the assignees and correspondence of record.
Let me dig into the assignee entities and the recorded assignment events.
Ownership & Assignment Reconstruction — US 11,548,934 B2
Important scoping note up front. I could not retrieve the primary assignment records themselves. My tooling surfaced only the Google Patents Legal Events feed (reproduced in the authoritative patent text above) and secondary patent databases — not the USPTO Assignment Center record set. That means I have no reel/frame numbers, no execution dates, and no correspondent-of-record data for any link in this chain. Everything below is drawn from the legal-events feed unless stated otherwise, and the fields the task specifically asks me to capture (reel/frame, correspondent) are marked as not retrieved rather than invented. A direct query at the Assignment Center is required to complete this file.
Inventors
| Inventor | Likely employer at filing (2015–2016) | Basis |
|---|---|---|
| Amir Abdollahi | Deutsches Krebsforschungszentrum (DKFZ), Heidelberg / Heidelberg University Hospital (radiation oncology) | Named as assignor to DKFZ in the 2018-09-19 assignment; later the sole assignor into Heidelberg Biotech GmbH |
| Jürgen Debus | Heidelberg University Hospital (Radiooncology) / DKFZ affiliation | Named assignor to DKFZ, 2018-09-19 |
| Kashi Javaherian | External — historically a Harvard/Children's Hospital Boston–affiliated endostatin researcher, not a DKFZ staff scientist | Named assignor to DKFZ, 2018-09-19; his endostatin/NC-1 work long predates this filing (he is a named inventor on the Bergers/Javaherian immunofusin art cited in this family) |
| Cheng Zhou | DKFZ (junior researcher) | Named assignor to DKFZ, 2018-09-19 |
Unusual pattern flagged: the inventor list is mixed-institution — three DKFZ/Heidelberg-based inventors plus one external, US-based endostatin scientist. That is consistent with a research-collaboration invention rather than a pure in-house invention, and it is the reason the 2018 assignment needed all four signatures. I found no evidence of inventors departing the original assignee within 12 months of filing; on the contrary, Abdollahi is the pivot of the later transfer (see below). Employer attributions for Javaherian are my inference, not a documented record — treat as unclear.
Original assignee
Deutsches Krebsforschungszentrum (DKFZ) — the German Cancer Research Center, Heidelberg. This is the assignee named on the issued patent and the entity that filed the PCT/National Phase (application 15/781,028, filed 2016-12-05).
- Line of business: Germany's largest biomedical research institute; a non-profit, publicly funded (federal/state) basic-and-translational research center. It is not a product company.
- Did it ship a product embodying the claims? No. The claimed subject matter is a protein oligomer (NC-1 / endostatin-domain / N-terminal-endostatin-peptide multimers, or Fc-fusion variants) for treating fibrosis and VEGF-/MMP-related disease. The patent text is preclinical (bleomycin- and radiation-induced lung fibrosis models). No commercial embodiment from DKFZ.
- Current status: Operating as a research institute (no bankruptcy, no dissolution). But it is no longer the owner — per the legal-events record it divested its interest on 2026-04-30.
Assignment timeline
The Assignment Center record set was not retrievable in this session, so I cannot populate reel/frame or correspondent. What the Google Patents legal-events feed establishes is the following. I list the recorded events literally, with the caveat that only the recording dates and parties are known; execution dates and reel/frame are not retrieved.
Executed: unknown / recorded 2018-09-19 — Reel not retrieved
- Conveyance: Assignment of interest (recorded as "ASSIGNMENT OF ASSIGNORS INTEREST")
- Assignor: Abdollahi, Amir; Debus, Jürgen; Javaherian, Kashi; Zhou, Cheng (all four inventors)
- Assignee: Deutsches Krebsforschungszentrum (DKFZ)
- Correspondent: not retrieved — the legal-events feed does not expose this field.
- Context: Standard inventor→institute assignment perfecting DKFZ's title (obligation-to-assign for a DKFZ-led invention). Note it was recorded ~21 months after the 2016-12-05 filing.
Executed: unknown / recorded 2026-04-30 — Reel not retrieved
- Conveyance: Assignment ("ASSIGNMENT OF ASSIGNOR'S INTEREST")
- Assignor: Deutsches Krebsforschungszentrum (DKFZ)
- Assignee: Abdollahi, Prof. Dr. med. Dr. rer. nat. Amir (an individual)
- Correspondent: not retrieved
- Context: Research institute → individual inventor transfer. In context this is the first leg of a spin-out/technology-transfer recapitalization, not a fire-sale.
Executed: unknown / recorded 2026-04-30 — Reel not retrieved
- Conveyance: Assignment ("ASSIGNMENT OF ASSIGNOR'S INTEREST")
- Assignor: Abdollahi, Prof. Dr. med. Dr. rer. nat. Amir (individual)
- Assignee: Heidelberg Biotech GmbH
- Correspondent: not retrieved
- Context: Second leg of the same-day spin-out: the inventor who acquired DKFZ's rights contributes them to the commercializing company. Current assignee per the record.
Net chain: DKFZ → (Abdollahi) → Heidelberg Biotech GmbH, all recorded on a single day, 2026-04-30.
Timeline diagram
timeline
title Ownership of US 11548934
2015 : Priority date 2015-12-03
2016 : PCT filed by DKFZ
2018 : Inventors assign rights to DKFZ
2020 : US publication
2023 : Patent granted
2026 : DKFZ assigns rights to Abdollahi
: Abdollahi assigns rights to Heidelberg Biotech
NPE / troll-pattern signals
Shell-entity transfer — Not present. The transferee is Heidelberg Biotech GmbH, a German Gesellschaft mit beschränkter Haftung with a Heidelberg, Germany address (confirmed on the CN112236448B family member, which lists the patentee as "海德堡生物技术有限公司 / 德国海德堡"). It holds a genuine multinational portfolio — e.g. EP4316502A3, ES2968766T3, CN112236448B, and granted US 12,577,291 B2 — all in the same NC-1-Fc technology, which is the profile of an operating spin-out, not a single-purpose Delaware/Texas assertion vehicle. No registered-agent-service address or single-member-LLC tell surfaced.
Known asserter in the chain — Not present. No assignee in the chain (DKFZ, Abdollahi as individual, Heidelberg Biotech GmbH) matches Acacia, Marathon, Intellectual Ventures, IPNav, Wi-LAN, Mosaid/Conversant, Vringo, Pendrell, Innovatio, MPHJ, Lumen View, Round Rock, Document Generation Corp, or any Spangenberg entity. The prior litigation sweep likewise surfaced no Unified Patents / RPX high-frequency-plaintiff listing for this patent.
Repeat correspondent across the chain — Unclear / not retrievable. This is the signal I was specifically asked to capture and it is the one field the legal-events feed does not expose. No correspondent of record for any of the three recordings could be retrieved, so I cannot test for recurrence. Open item — this is the highest-value field to pull from the Assignment Center.
Cascading transfers — Not present (weak data point, see caveat). There are effectively two hops on a single day (2026-04-30), which technically satisfies "multiple consecutive assignments in <24 months." However, the intermediate is a natural person (the inventor), not a chained LLC, and the destination is an operating company. Same-day, two-step institute→inventor→spin-out sequences are a common European technology-transfer mechanic (they let the inventor transfer clean, unencumbered title). I do not score this as a cascade, but I flag it because a same-day double recording is also the shape an NPE uses to launder title — the distinguisher is the nature of the intermediate and the destination, not the timing. Unclear if the correspondent field later shows a repeat NPE-side filer.
Pre-litigation transfer — Not present. The prior litigation analysis found no infringement suit naming US 11,548,934 in any district, at the ITC, or on appeal. With no first suit to anchor against, the 6-month window test cannot be triggered. (If a first complaint were filed after 2026-10-30, the 2026-04-30 transfers would retroactively fall inside that window — worth a calendar watch.)
Bankruptcy fire-sale — Not present. DKFZ is a solvent, state- and federally funded research institute; there is no Chapter 7/11, no estate sale.
Privateering — Not present. The transfer runs in the opposite direction from the classic privateering fact pattern: a research institute divests to its own inventor, who contributes to a commercializing company that he appears to run (Abdollahi holds the equity/control role). That is a founder-led spin-out, not an operating company arming an unrelated NPE against competitors. No SEC-filing or EFF/Patent Progress coverage of a privateering arrangement was found.
Defensive aggregator — Not present. The chain does not terminate at RPX, AST, LOT Network, Unified Patents, or OIN. It terminates at a small operating biotech.
Verdict
Insufficient data.
The signal set that can be tested comes back clean — no shell-entity LLC, no listed NPE, no bankruptcy, no privateering, no defensive aggregator, and no litigation at all — and the visible chain (DKFZ → inventor → Heidelberg Biotech GmbH, all recorded 2026-04-30) is the textbook founder-led university spin-out, the inverse of an NPE pattern. But I cannot return anything stronger than Insufficient data because the two fields that decide an NPE call were not retrievable: no reel/frame numbers and no correspondent of record for any of the three recordings, so signals 3 and 4 remain untested, and the patent's own grant/publication record supplies no reel/frame either. Pull the three recordings at the USPTO Assignment Center — search by patent number at https://assignment.uspto.gov/patent/index.html (equivalently https://assignmentcenter.uspto.gov/) — capture the correspondent/attorney of record on each, and confirm whether the two 2026-04-30 entries are one transaction or two independent recordings. That single query resolves the only open questions in this file.
Cross-reference / contradiction flagged
The prior Litigation summary section states the "current date" it was given was 2026-04-26 and treated the 2026-04-30 reassignments as four days in the future. This section was prepared with the current date of 2026-09-12, so those recordings are now in the past and are reported here as historical events. The two sections agree on substance (same events, same parties); only the relative timing framing differs. No factual contradiction between sections.
Generated 9/12/2026, 12:48:39 AM
Prior art
Earlier patents, publications, and products that may anticipate or render the claims unpatentable.
I'll search for the USPTO record and the patent's cited references.
Let me try to pull the citation tables from additional sources.
Let me try to retrieve the actual cited-reference tables from FPO and Google Patents.
Scope, method, and an important limitation up front
I searched for the US 11,548,934 record and its citation apparatus (Google Patents record, FPO/Justia, and the family pages that carry the "Cited By" tables). Two things must be stated plainly before any § 102 analysis:
- I could not retrieve the verbatim "References Cited" table of US 11,548,934. My tooling returned narrative/specification text and Cited By tables of neighbouring documents, not the patent's own citation lists. I will therefore not present a fabricated citation table. Instead I separate references into (a) those verified as being cited in the '934 record by documentary evidence I retrieved, and (b) those that are in the record by necessary implication or are in the same narrow art neighbourhood and may appear in the count. Each is flagged.
- The granted claim text of US 11,548,934 is still not in hand (as flagged in the earlier Patent summary section). Anticipation under 35 U.S.C. § 102 is a claim-by-claim test requiring that a single reference disclose every limitation. Without the granted claims I can only map references to claim categories inferred from the specification. That limitation propagates into every row below.
No contradictions with the previously generated sections were found on bibliographic facts; one carry-over issue is re-flagged in § 6.
1. Prior-art framework applied
| Item | Value |
|---|---|
| Patent | US 11,548,934 B2, App. 15/781,028 (national phase of PCT/EP2016/079777, pub. WO 2017/093569 A1) |
| Priority / effective filing date | 2015-12-03 (PCT filed 2016-12-05) |
| Governing statute | AIA § 102 (effective filing date after 2013-03-16) |
| § 102(a)(1) window | Disclosures publicly available before 2015-12-03 — this captures the key patent and non-patent references, including PCT publications |
| § 102(a)(2) window | US patents / US application publications with an effective filing date before 2015-12-03 |
| Grace-period relevance | § 102(b)(1)(A) does not rescue the applicant's own 2013 PCT publication (published ~2013-02-28, i.e. more than one year before 2015-12-03) |
A structural point that drives everything below: the applicant's own specification concedes the state of the art — "Recently, anti-fibrotic activity has been reported for C-terminal endostatin polypeptides but not for N-terminal endostatin polypeptides, in TGF-beta- and bleomycin-induced fibrosis (WO 2011/050311; Yamaguchi et al. (2012), Sci. Transl. Med., 4, p. 136ra71)." That sentence is an admission that pre-2015-12-03 art already taught endostatin → fibrosis, and it frames the applicant's asserted point of novelty as N-terminal sequence + oligomerisation/dimerisation.
2. Patent citations — verified or strongly evidenced
2.1 WO 2013/026913 A1 — the most dangerous patent reference
| Field | Detail |
|---|---|
| Citation | WO 2013/026913 A1 (PCT; DKFZ / Abdollahi et al.) |
| Dates | Published ~2013-02-28 (est.); priority 2011-08-23 (US 61/526,535); family member US 2023/0341406 A1 |
| Description | Discloses protein oligomers comprising at least two NC-1 monomers of human collagen 18; Fc–NC-1 fusion proteins; and fusion proteins comprising an endostatin peptide (or endostatin-derived peptide) plus the RGD and/or PHSRN motif of Fibronectin. The instant specification states verbatim: "SEQ ID NOs: 1-17 are also depicted in WO 2013/026913, the disclosure content of which is incorporated herewith by reference." |
| § 102 status | § 102(a)(1) — PCT publication more than one year before the effective filing date. The common-ownership exception of § 102(b)(2)(C) is unavailable because that provision applies only to § 102(a)(2) art, and § 102(b)(1)(A) fails on timing. |
| Potential § 102 anticipation | Claim category A (oligomer composition) — if the granted claim covers an oligomer of ≥2 NC-1 monomers / ≥2 endostatin domains / ≥2 endostatin N-terminal peptides, this reference is a serious single-reference anticipation candidate, since it discloses the same oligomer architecture by the same applicant. Also category B/C (methods) to the extent the '934 method claims recite the oligomer without a limitation absent from WO '913; and category E (Fc fusion protein) and category F (kit). |
| Why it matters | This is the same inventive entity's earlier disclosure in the same field. If WO 2013/026913 discloses an NC-1 oligomer for treating fibrosis or a fibrosis-linked condition, the '934 claims are exposed to a § 102(a)(1) anticipation attack (or, in the alternative, § 103). The only safe harbour would be a claim limitation genuinely absent from WO '913 (e.g. the specific fibrosis indication, the Gln7→Cys dimerisation mutant, or the KiH-Fc architecture) — none of which I can check without the granted claims. |
2.2 US 7,524,811 B2 — N-terminal endostatin peptides
| Field | Detail |
|---|---|
| Citation | US 7,524,811 B2, "Anti-angiogenic peptides from the N-terminus of endostatin" |
| Dates | Filed 2006-02-28 (App. 11/364,855); granted 2009-04-28 (verified from the FPO record) |
| Assignee | Children's Medical Center Corporation |
| Description | Claims anti-angiogenic peptides derived from the N-terminal region of endostatin, including the zinc-binding motif (His1/His3/His11), pharmaceutical compositions, and antitumor uses. The instant specification expressly directs the reader to it: "N-terminal peptides of the collagen 18 endostatin domain are shown in Tjin et al., loc. cit., or in U.S. Pat. No. 7,524,811 or EP1668129 B1." |
| § 102 status | § 102(a)(1)/(a)(2) — published and granted well before 2015-12-03. |
| Potential § 102 anticipation | Category A, but only as to the sub-genus "at least two N-terminal peptides of the collagen 18 endostatin domain." The reference discloses the peptide, not necessarily a dimer/oligomer of it, so on its face it anticipates only if the granted claim is not limited by oligomerisation. Category E (fusion protein) if the claim is drawn to an N-terminal-peptide–Fc molecule. It is unlikely to anticipate category B/C method claims premised on oligomer-driven Fibronectin/VEGF/MMP binding, because the reference does not disclose that mechanism. |
2.3 US 8,206,718 B2 / EP 1 107 989 B1 — "immunofusin" Fc–endostatin
| Field | Detail |
|---|---|
| Citation | US 8,206,718 B2 and EP 1 107 989 B1, "Expression and export of angiostatin and endostatin as immunofusins" (Bergers / Javaherian et al.) |
| Dates | Earliest priority 1998–1999; EP granted with German translation filed 2010-05-12 (per the EPO legal-events record); US granted 2012 (est.) |
| Assignee | EPO record lists Merck Patent GmbH as owner (verified from the legal-events data I retrieved) |
| Description | Expresses endostatin (and angiostatin) as immunoglobulin-Fc "immunofusins," giving a dimeric endostatin molecule with prolonged half-life. This is the archetypal Fc–endostatin disclosure and the direct antecedent of the '934 specification's "FcE" construct (two Fc chains, disulfide-linked, each extended to one endostatin, so the two endostatin moieties become a dimer as a result of the Fc dimer). |
| § 102 status | § 102(a)(1)/(a)(2) — far predates 2015-12-03. |
| Evidence of citation in the '934 record | I retrieved the Google Patents Cited By table of US 8,206,718 and of EP 1 107 989 B1, and each lists US 11,548,934 B2 (2015-12-03 / 2023-01-10 / Deutsches Krebsforschungszentrum). This establishes a citation relationship between the '934 record and these immunofusin documents. |
| Potential § 102 anticipation | Category A (oligomer) — because the Fc forces dimerisation of two endostatin domains, this reference discloses "at least two endostatin domains of collagen 18" in an Fc-linked complex. If granted claim 1 is generic to "at least two endostatin domains of collagen 18," this is a strong § 102(a)(1) anticipation candidate. It also squarely bears on category E (Fc fusion protein). It is weaker against category B/C method claims (it is directed to anti-angiogenic/anti-tumour use, not fibrosis), though the '934 specification itself asserts the oligomer binds Fibronectin/VEGF/MMP-2/MMP-9 — a mechanism the immunofusin art does not articulate. |
2.4 EP 1 668 129 B1 — anti-angiogenic endostatin peptides
| Field | Detail |
|---|---|
| Citation | EP 1 668 129 B1 |
| Dates | Family with ~2004–2005 priority; granted pre-2015 (exact grant date not verified in this session) |
| Description | Anti-angiogenic peptides derived from endostatin. Cited expressly in the instant specification alongside US 7,524,811 and Tjin et al. as a source of N-terminal peptides of the collagen 18 endostatin domain. |
| § 102 status | § 102(a)(1) (EP publication). |
| Potential § 102 anticipation | Category A, sub-genus "at least two N-terminal peptides of the collagen 18 endostatin domain" — subject to the same caveat as US 7,524,811 (peptide disclosure ≠ oligomer disclosure). |
2.5 Older endostatin patent documents appearing in the same citation neighbourhood
The following were surfaced in the reference apparatus of the endostatin/immunofusin family documents I retrieved. I cannot confirm that each appears in the '934 "References Cited" table; treat them as neighbourhood art that an examiner would have had before them, and verify before relying on any of them for a § 102 position.
| Citation | Date | Description | Provisionally relevant claim category |
|---|---|---|---|
| WO 2011/050311 A1 | Published 2011 (est. 2011-05-05) | Anti-fibrotic activity of C-terminal endostatin polypeptides in TGF-β- and bleomycin-induced fibrosis; conceded by the applicant in the '934 background. | Category B — the closest subject-matter match on fibrosis, but it teaches C-terminal polypeptides, not the oligomeric N-terminal/NC-1 constructs claimed. Timing is the key point: it is squarely § 102(a)(1) art. |
| US 5,854,205 (O'Reilly et al., Children's Medical Center) | Granted 1998-12-29 | "Therapeutic antiangiogenic compositions and methods"; the foundational endostatin patent | Category A (endostatin per se), background |
| US 6,653,098 B1 (Violand et al.) | Granted 2003-11-25 | "Method of producing mouse and human endostatin" | Production-method art; weak § 102 relevance |
| US 6,017,949 (D'Amato et al.) | Granted 2000-01-25 | "Method of regulating the female reproductive system through angiogenesis inhibitors" | Category B (endometriosis is an enumerated '934 indication) |
| US 2006/0122374 A1 (Mertins et al.) | Published 2006-06-08 | "Albumin-fused anti-angiogenesis peptides" | Category E — fusion-mediated half-life extension/oligomerisation of endostatin peptides |
| US 2006/0258583 A1 (Folkman et al.) | Published 2006-11-16 | "Anti-angiogenic peptides for treating or preventing endometriosis" | Category B (endometriosis) |
| US 2004/0073007 A1 (Chillemi et al.) | Published 2004-04-15 | "Antiangiogenic peptides" | Category A |
| US 2002/0103129 A1 (Ge et al.) | Published 2002-08-01 | "Small peptides having anti-angiogenic and endothelial cell inhibition activity" | Category A |
| WO 2000/063249 A1; WO 2000/026368 A2; WO 1999/062944 A2; WO 1999/048924 A1; WO 1999/039702 A2; WO 1999/029855 A1; WO 1997/015666 A1; WO 2000/011033 A2; WO 2000/060945 A1; WO 2000/067771 A1; WO 2002/030982 A2; WO 2002/068457 A2; WO 2005/021756 A1; WO 2005/042566 A2 | 1997–2005 | Endostatin polypeptides, derivatives and anti-angiogenic compositions | Mostly category A background |
3. Non-patent citations (the § 102(a)(1) printed-publication art)
These are cited verbatim in the '934 specification and are therefore certainly part of the record as applicant-acknowledged art. Several are genuine § 102(a)(1) anticipation candidates against method claims because they disclose endostatin's use in fibrosis models.
| Reference | Date | Description | Potential § 102 relevance |
|---|---|---|---|
| Yamaguchi et al., Sci. Transl. Med. 4:136ra71 (2012) | 2012 | Anti-fibrotic activity of C-terminal endostatin polypeptide in TGF-β- and bleomycin-induced fibrosis | Category B. The single most on-point printed publication on endostatin→fibrosis. If the granted method claim is not limited to oligomeric N-terminal constructs, this reference plus the WO 2011/050311 companion are the primary § 102(a)(1) threat. Because the applicant's own data show the C-terminal peptide ineffective in the RILF model, the claims likely exclude C-terminal — which is precisely the limitation that would defeat anticipation. |
| Tjin et al., Cancer Res. 65:3656 (2005) | 2005 | Identifies the N-terminal 27-aa endostatin peptide as the anti-tumour domain; the specification relies on it for the N-terminal peptide definition (and requires retention of His1/His3/His11) | Category A / E. Anticipates N-terminal peptide sub-genus if oligomerisation is not a claim limitation. |
| Lee et al., Clin Cancer Res. 14:1487 (2008) | 2008 | Endostatin fused to an IgG Fc domain; half-life extended beyond one week | Category A / E. Supports anticipation of an Fc–endostatin dimer claim and undercuts any argument that Fc-driven endostatin dimerisation was novel. |
| Boehm et al., Biochem. Biophys. Res. Commun. 252:190 (1998) | 1998 | Zinc binding of endostatin is essential for anti-angiogenic activity | Background; relevant to the His1/His3/His11 limitation |
| Sasaki et al., EMBO J. 17:4249 (1998) | 1998 | Domain structure of NC-1 (association region / hinge / endostatin domain) | Background; the '934 claim terms are taken directly from this paper |
| Ding et al., PNAS 95:10443 (1998) | 1998 | Endostatin zinc site; endostatin dimerises at high concentration | Category A. Directly relevant to the "oligomer" limitation and to obviousness of dimeric endostatin |
| Oh et al., PNAS 91:4229 (1994); Genomics 19:494 (1994) | 1994 | Cloning of mouse and human collagen 18 | Background |
| O'Reilly et al., Cell 88:277 (1997); Folkman, Exp. Cell Res. 312:594 (2006); Bergers et al., Science 284:808 (1999) | 1997–2006 | Endostatin as an endogenous angiogenesis inhibitor | Background; supports motivation to modify endostatin |
| Capon et al., Nature 337:525 (1989); Lo et al., Protein Eng. 11:495 (1998); Gordon et al., J. Clin. Oncol. 19:843 (2001); Holash et al., PNAS 99:11393 (2002) | 1989–2002 | Fc-fusion technology; half-life extension of angiogenesis inhibitors | Category E; § 103 backbone rather than § 102 |
| Heliasvaara et al., Exp. Cell Res. 307:192 (2005) | 2005 | MMP cleavage of the NC-1 hinge region | Background |
| Ali & Imperiali, Bioorg. Med. Chem. 13:5013 (2005) | 2005 | Non-natural oligomerisation scaffolds | Category A, artificial oligomerisation-domain limitation |
| Wijelath et al., Circ. Res. 99:853 (2006) | 2006 | Fibronectin domain structure / integrin α5β1 binding | Background for the RGD/PHSRN limitation |
| Rubin et al., Int. J. Radiat. Oncol. Biol. Phys. 33:99 (1995); Movsas et al., Chest 111:1061 (1997); Raghu et al., Am. J. Respir. Crit. Care Med. 183:788 (2011); Gurujeyalakshmi et al. (1996, 1999); Hallahan et al., J. Natl. Cancer Inst. (2002) | 1995–2011 | Radiation- and bleomycin-induced lung-fibrosis models; IPF diagnosis | Background for category B/C/D; evidentiary for enablement rather than anticipation |
4. Ranking: the most relevant prior art for US 11,548,934
- WO 2013/026913 A1 — same applicant, same oligomer architecture, published >1 year before priority, expressly incorporated for SEQ ID NOs 1–17. § 102(a)(1). Highest risk.
- US 8,206,718 B2 / EP 1 107 989 B1 (immunofusins) — Fc-mediated endostatin dimer; a Cited By relationship to the '934 is documented in the records I retrieved. § 102(a)(1)/(a)(2).
- WO 2011/050311 A1 + Yamaguchi et al. 2012 — endostatin (C-terminal) for fibrosis; conceded by the applicant. § 102(a)(1) against any method claim not limited to oligomeric N-terminal/NC-1 constructs.
- US 7,524,811 B2 and EP 1 668 129 B1 — N-terminal endostatin peptides, expressly incorporated into the '934 definition set. § 102(a)(1)/(a)(2) against the peptide sub-genus.
- Lee et al. 2008 + Ding et al. 1998 — Fc–endostatin half-life and spontaneous endostatin dimerisation. § 102(a)(1) against the oligomer/dimer and Fc-fusion limitations.
5. Provisional § 102 anticipation matrix (claims unknown — hypothesis only)
| Inferred claim category | Best § 102 candidate | Anticipation assessment |
|---|---|---|
| A — oligomer of ≥2 NC-1 monomers | WO 2013/026913 A1 | Plausible anticipation; same architecture in the same applicant's own earlier publication |
| A — oligomer of ≥2 endostatin domains | US 8,206,718 / EP 1 107 989 (immunofusin) | Plausible; Fc forces a two-endostatin dimer. Also Ding 1998 (concentration-dependent endostatin dimer) |
| A — oligomer of ≥2 N-terminal endostatin peptides | US 7,524,811; EP 1 668 129 B1; Tjin 2005 | Anticipates only if the granted claim does not require oligomerisation |
| B — treating fibrosis / fibrosis-associated disease | WO 2011/050311 + Yamaguchi 2012 | Anticipates only if the claim is not limited to oligomeric N-terminal/NC-1 species; the specification's own efficacy data (C-terminal peptide ineffective in RILF) suggest such a limitation is present |
| C — VEGF-related / MMP-related disease | No single anticipatory reference identified | The oligomer-specific Fibronectin/VEGF/MMP-2/MMP-9 binding mechanism (FIGS. 9–12) appears to be the applicant's own contribution; § 103 is the more realistic attack |
| D — detection/diagnosis | No single anticipatory reference identified | Labelled endostatin/DOTA-imaging art may support § 103 |
| E — Fc fusion protein | US 8,206,718 / EP 1 107 989; Lee 2008 | Strong candidate if claim is not further limited by the Gln7→Cys mutant or the KiH architecture |
| F — polynucleotide / vector / host cell / kit | US 7,524,811; WO 2013/026913 | Routine-art categories; anticipate only if claim recites no distinguishing sequence or architecture |
6. Explicit uncertainties and contradictions to carry forward
- The "References Cited" table of US 11,548,934 was not retrieved. Everything in § 2.5 is neighbourhood art, not a verified citation list. Do not present § 2.5 as the patent's citation count without independent verification on the USPTO PatentCenter "References Cited" tab or the front page of the issued patent.
- Granted claim text still unavailable. This remains the single most consequential gap: § 102 anticipation cannot be adjudicated, only hypothesised, without the claims. This confirms (and does not contradict) the caveat in the earlier Patent summary section.
- Assignee conflict persists. Today's searches again show Deutsches Krebsforschungszentrum as the assignee on FPO/Google/Chinese-aggregator records, while the earlier section noted a 2026-04-30 reassignment to Heidelberg Biotech GmbH. The databases are not reconciled; no correction has been applied.
- Date anomaly persists. Current date supplied for this task is 2026-04-26; recorded reassignment events remain dated 2026-04-30. Reported literally, not auto-corrected.
- Same-number caution observed. Two distinct documents surfaced in searches and were not conflated with US 11,548,934: US 9,370,934 and US 11,535,038 (unrelated Epson/ITC context), and a PubMed ID 11548934 cited inside GB 2562502 A. None of these is US 11,548,934.
- Family members cited by their own distinct numbers (not to be merged with the '934): WO 2013/026913 A1, US 2023/0341406 A1, US 2021/0363225, US 2023/0382975 — all DKFZ/Heidelberg endostatin-NC-1 family filings with different priority chains.
If you can supply the issued patent's front page (References Cited) and the granted claims, I can convert the matrix in § 5 into a claim-by-claim § 102 chart with element-by-element mapping. Without those two documents, the honest position is that the strongest § 102 candidates are WO 2013/026913 A1, the immunofusin patents (US 8,206,718 / EP 1 107 989), and WO 2011/050311 + Yamaguchi et al. 2012, with everything else operating primarily under § 103.
Generated 9/12/2026, 12:49:21 AM
Obviousness
Combinations of prior art that suggest the claimed invention would have been obvious under 35 U.S.C. § 103.
I'll ground this analysis by pulling the prior-art landscape for this patent — both the references cited in the specification and any patent/technical literature on oligomeric endostatin and fibrosis.
Good — that surfaced the key prior-art family (WO 2013/026913 / EP 2561888) and the endostatin-peptide antifibrotic art. Let me pull two more threads: the '934 granted claim text, and the immunofusin / fibrotic-disease composition references.
Obviousness Analysis — US 11,548,934 B2 under 35 U.S.C. § 103
0. Scope, framework, and cross-reference to prior sections
This section builds on — and does not repeat — the bibliographic summary and the litigation check already produced. Two carry-overs matter here:
- Claim text. As flagged in the Patent Summary, I could not retrieve the verbatim granted claims of US 11,548,934. For this § 103 analysis I therefore use the specification (authoritative text supplied) plus the verbatim claim 1 of the same family's later continuation, US 12,577,291 B2, as a scope proxy (Patsnap Eureka — US12577291B2). That proxy claim 1 reads, in relevant part: "A method for treating or ameliorating a matrix metalloproteinase (MMP)-related disease … comprising administering … a protein oligomer comprising (i) at least two NC-1 monomers of collagen 18 or (ii) at least two endostatin domains of collagen 18 or (iii) at least two N-terminal peptides of the collagen 18 endostatin domain … wherein the NC-1 monomer of human collagen 18 comprises a heterologous oligomerization domain comprising an Fc domain from knobs‑into‑holes (KiH)‑engineered human IgG…" — i.e., the '934 claims are, on this proxy, broader (no KiH limitation).
- Effective filing date. Priority 2015‑12‑03; therefore AIA § 102/103 applies (post‑16 March 2013). All art below predates 2015‑12‑03, so no date reconciliation is needed. (The entry labelled "Prior art date 2015‑12‑03" on the Google Patents record is that page's label for the priority date, not an independent prior-art date.)
The "Prior Art section" set. The cited-reference list carried on the family's US 12,577,291 record is compact and is the anchor for this analysis (Patsnap, Patent Citations):
| Ref | Identity | Relevance |
|---|---|---|
| US 8,206,718 B2 / EP 1107989 B1 | Bergers et al., Expression and export of angiogenesis inhibitors (angiostatin/endostatin) as immunofusins | Fc–endostatin fusion (dimerizing, half-life-extending) |
| JP 2007084459 A | Composition for treating fibrotic disease | Endostatin/composition in fibrosis |
| JP 2014529605 A | Japanese family member of WO 2013/026913 / EP 2561888 — DKFZ, Means and methods for treating angiogenesis‑related diseases | Oligomeric NC‑1/endostatin, Fc fusions, fibronectin/VEGF binding |
| US 7,524,811 B2 | Javaherian, Anti‑angiogenic peptides from the N‑terminus of endostatin | N‑terminal endostatin peptide as active domain |
| US 8,206,718 B2 | (as above) | — |
Supplementary literature grounding the mechanism (all pre‑2015): Kuo 2001 JCB 152:1233; Sasaki 1998 EMBO J 17:4249; Ding 1998 PNAS 95:10443; Tjin 2005 Cancer Res 65:3656; Wijelath 2006 Circ Res 99:853; Rehn 2001 PNAS (endostatin/α5β1); Yamaguchi & Feghali‑Bostwick 2013; Wan 2013 Respir Res 14:56; Feghali‑Bostwick E4 (Sci Transl Med 2012). Several are cited in the '934 specification itself.
1. The single most important reference: WO 2013/026913 / EP 2561888 (DKFZ, pub. 2013‑02‑27/28)
This is the applicants' own earlier application, and the '934 specification expressly incorporates it: "SEQ ID NOs: 1‑17 are also depicted in WO 2013/026913, the disclosure content of which is incorporated herewith by reference." By the applicant's own admission, the sequence set relied on in '934 was already published ~2 years 10 months before the '934 priority date.
What it discloses (per the DKFZ technology-transfer sheet and the CN 104271151 B / family text):
- "NC1 rather than monomeric endostatin [is] the key physiologic molecule exerting antiangiogenic effects."
- "Synthetic dimerization of endostatin via Fc‑conjugation … better mimics the effects of the natural trimeric NC1."
- "Oligomerization of endostatin as observed in NC1 is important for its binding to a large number of extracellular matrix proteins including Fibronectin and cytokines such as VEGF."
- Fc–NC‑1 fusion constructs (mouse Fc–NC‑1, SEQ ID NO 3/5), endostatin dimerization by Gln7→Cys disulfide, and enterokinase-cleavable linkers.
- The anti‑angiogenesis indication list expressly includes scleroderma and hypertrophic scars/keloids — fibrotic conditions.
- Fibronectin RGD/PHSRN motif fusion proteins (SEQ ID NOs 7, 11, 12, 13, 17).
Sources: DKFZ P‑1000 technology sheet; DKFZ 254704 sheet; CN104271151B — NC‑1‑containing proteins; WO 2013/026913 family listing.
Prior-art status — no escape hatch. Because WO 2013/026913 is a printed publication, it is § 102(a)(1) art. The AIA's common-ownership exception (§ 102(b)(2)(C)) reaches only § 102(a)(2) art, and the § 102(b)(1) grace period is unavailable (a) for a different inventive entity — the DKFZ sheet names Abdollahi, Javaherian and Tong‑Young Lee, whereas '934 names Abdollahi, Javaherian, Debus, Zhou — and (b) in any event because publication was far more than one year before the priority date. It cannot be removed from the prior art.
2. Combination A — the oligomer/VEGF/MMP claims: WO 2013/026913 + Kuo 2001 + Sasaki 1998
Claim elements mapped: "protein oligomer comprising at least two NC‑1 monomers / endostatin domains / N‑terminal peptides"; native trimerization domain; Fc (heterologous) oligomerization domain; Gln7→Cys artificial domain; fibronectin/VEGF/MMP binding; VEGF‑ and MMP‑related disease treatment.
- WO 2013/026913 discloses each oligomer genus — NC‑1 trimers, Fc‑NC‑1 dimers, the Q7C endostatin dimer — and already assigns them the same utility (anti‑angiogenic, anti‑tumour), including the fibronectin/VEGF binding rationale.
- Kuo et al. 2001 JCB 152:1233 (invoked by the '934 specification itself to explain the C7 disulfide) teaches that NC1/endostatin oligomerization is functionally determinative and discloses the engineered C7 dimer.
- Sasaki 1998 EMBO J 17:4249 (also cited in '934) teaches the domain architecture — association region / hinge / endostatin — i.e., the native trimerization domain.
Motivation to combine: express. WO 2013/026913 tells the skilled artisan that the oligomer binds more partners and outperforms monomer endostatin; Kuo and Sasaki supply the two known oligomerization mechanisms. This is KSR's "simple substitution of one known element for another" and "known technique to improve similar devices in the same way."
Assessment: strong. The oligomer per se, and its use in VEGF‑related disease, appear obvious — arguably anticipated for the specifically disclosed species (Fc‑NC‑1, ES dimer, SEQ ID NOs 7/13). For MMP‑2/‑9 binding specifically, I have not located pre‑2015 art expressly disclosing oligomer-selective MMP‑2/9 binding, and I flag that element as the weakest link in this combination.
3. Combination B — the fibrosis claims: WO 2013/026913 + endostatin‑antifibrotic art (Yamaguchi 2013 / WO 2011/050311 / Wan 2013 / E4)
This is the most probative combination for the '934 fibrosis claims.
The fibrosis art is dense and predates 2015:
- Yamaguchi & Feghali‑Bostwick 2013, "Role of endostatin in fibroproliferative disorders — as a candidate for anti‑fibrosis therapy" — an explicit review concluding endostatin "may have the therapeutic potential for inhibiting fibrosis" (PubMed 24390105).
- Wan et al. 2013, Respir Res 14:56 — endostatin ameliorates bleomycin‑induced pulmonary fibrosis in rats, inhibiting VEGF/VEGFR‑2 and ERK1/2 (PMC3668162).
- WO 2011/050311 A1, Use of endostatin peptides for the treatment of fibrosis — endostatin peptides E1–E4 reduce FN/Col1α1 and α‑SMA, attenuate bleomycin dermal and pulmonary fibrosis, and work when given 3 days after the fibrotic trigger (WO2011050311A1).
- E4 peptide, Sci Transl Med 2012 — potent antifibrotic activity in TGF‑β and bleomycin models (Science).
Motivation to combine: the two references pull in the same direction on the same molecule family. Endostatin is known to treat fibrosis; the artisan simultaneously knows (i) that monomeric endostatin has poor pharmacokinetics and poor efficacy ("endostatin has as monomer poor efficacy"; half‑life ~2 h vs ~2 weeks for Fc‑endostatin — DKFZ sheet), and (ii) that oligomerization solves precisely that problem. Substituting the disclosed, superior oligomeric NC‑1/endostatin for monomeric endostatin to obtain greater potency and half‑life is a design incentive with a reasonable expectation of success, not an act of invention. The bleomycin and thoracic‑irradiation fibrosis models relied on in '934 were already the art's standard models.
Assessment: strong, subject to one patentee counter — the '934 specification itself reports that a C‑terminal peptide (E4/mP1) "was not effective to improve most investigated parameter of fibrosis development." That is the applicant's own unpublished data, not prior art, and the counter cuts both ways: it is a narrow argument about a specific fragment, not about the oligomeric genus that the prior art already flagged as superior.
4. Combination C — Fc‑fusion and half‑life: US 8,206,718 / EP 1107989 + WO 2013/026913
Claim elements: heterologous Fc oligomerization domain; Fc N‑ or C‑terminal placement; cleavable linker.
- US 8,206,718 B2 / EP 1107989 B1 (Bergers et al.) disclose expression and export of angiostatin and endostatin as immunofusins — IgG‑Fc fusions chosen for dimerization and half‑life.
- The '934 specification itself concedes the general technique: "angiogenesis inhibitors linked to an immunoglobulin Fc domain have shown to increase the half life" (citing Capon 1989; Gordon 2001; Holash 2002) and "Fusion of the Fc domain … has been found to enhance the production and secretion of the fusion proteins."
Motivation: KSR's "known technique" prong. Fc fusion for half‑life extension and dimerization was conventional and predictable by 2015. Assessment: strong.
The KiH‑engineered Fc element (SEQ ID NOs 25/26/28/30) is a narrower question: knobs‑into‑holes Fc heterodimerization was itself well known, but using it to force a defined NC‑1 valence is a more specific design step, and I have not verified that WO 2013/026913 (as opposed to the later 2021/2023‑priority filings) discloses KiH. Flag: this is the element where '934's narrower family members (e.g., US 12,577,291) most plausibly survive.
5. Combination D — the N‑terminal‑peptide claims: Tjin 2005 + US 7,524,811 + Fc‑fusion art
Claim elements: "at least two N‑terminal peptides of the collagen 18 endostatin domain"; residues 1‑132/1‑27/1‑25 of SEQ ID NO 19; the 27‑mer ("Superstatin," SEQ ID NO 13).
- Tjin et al. 2005, Cancer Res 65:3656 — the N‑terminal 27‑aa peptide is the anti‑tumour/anti‑angiogenic domain of endostatin (cited throughout the '934 spec).
- US 7,524,811 B2 and EP 1668129 B1 — claim N‑terminal endostatin peptides, including fragments retaining histidines 1/3/11 (the zinc site). Both are cited in the '934 specification.
- Ding 1998 PNAS 95:10443 (cited in '934) teaches the N‑terminal zinc‑binding site forms a dimer at higher concentration.
Motivation: once the N‑terminal peptide is known to be the active domain, and Fc‑fusion is known to dimerize peptides and extend half‑life, dimerizing that peptide via Fc (or via a Cys at the corresponding position) is the routine, predictable route. Assessment: moderate‑to‑strong, with the caveat that the anti‑fibrotic utility of the oligomeric peptide specifically is less squarely disclosed than for full‑length endostatin.
6. Combination E — MMP/VEGF indications and diagnostic claims
- MMP‑related disease: '934's own definition is broad — "benign and malignant diseases where MMP activation contributes to the pathophysiology," encompassing local tumour invasion/metastasis (glioblastoma, pancreatic, lung cancer) and post‑radiotherapy fibrosis. WO 2013/026913 already frames the oligomer's utility around tumour invasion/metastasis and ECM remodelling. Mapping that onto an "MMP‑related disease" label is a naming exercise over known biology, not a patentable difference.
- Diagnostic/detection claims: '934 contemplates the human Superstatin peptide conjugated to DOTA for ⁶⁸Ga PET. Peptide–DOTA–⁶⁸Ga imaging chemistry was fully conventional by 2015 (and is taught as routine chelation chemistry generally). Combining a known targeting peptide with a known chelator/label is obvious absent unexpected targeting data, which the specification does not appear to supply.
- Combination/dosage claims (angiostatin; anti‑PD‑1/PD‑L1; 0.1‑1 mg/kg/day; IV/IT/subcutaneous/IP): US 8,206,718 teaches angiostatin co‑administration; checkpoints were a known class; and dose/route selection is per se obvious as a result-effective variable requiring only routine optimisation (In re Aller; Pfizer v. Apotex).
7. Secondary considerations — how they are likely to fare
| Consideration | Likely weight | Reason |
|---|---|---|
| Unexpected results (oligomer binds fibronectin/VEGF; monomer does not) | Low | This is precisely the finding DKFZ had already published in WO 2013/026913 / its tech-transfer sheet before the priority date. A result disclosed in the prior art cannot be "unexpected." |
| Superior anti‑fibrotic potency of oligomer vs. C‑terminal peptide | Low–moderate | The comparison is against a fragment the applicant selected; the prior art already taught the oligomer as the superior form. |
| Long‑felt need (no effective fibrosis therapy) | Low | Pirfenidone/nintedanib were approved/known by 2015, and endostatin's own PK problem was expressly acknowledged and pre‑solved by Fc fusion. |
| Teaching away | Weak | No reference disparages oligomeric endostatin for fibrosis. |
| Nexus | Weak | Any unexpected data are not shown to be coextensive with the full genus (NC‑1 monomer OR endostatin domain OR N‑terminal peptide; native OR Fc OR artificial oligomerization). |
8. Bottom line
- Most likely to be found obvious: (1) claims to the oligomer per se and to VEGF‑related use — over WO 2013/026913/EP 2561888 alone, or in view of Kuo 2001 and Sasaki 1998; (2) fibrosis method claims — over WO 2013/026913 + {Yamaguchi 2013 / Wan 2013 / WO 2011/050311 / E4}; (3) Fc‑fusion and dosage/route/combination claims — over US 8,206,718 / EP 1107989 plus routine optimisation.
- Where '934 most plausibly retains patentable weight: claim elements tying the oligomer to KiH‑engineered IgG1 Fc (SEQ ID NOs 25/26/28/30), the specific Q7C substitution in combination with Fc‑release, and — if demonstrated — oligomer‑selective MMP‑2/‑9 binding, for which I did not locate express pre‑2015 disclosure. Notably, the family itself pursued those narrower features in US 12,577,291 B2 (KiH‑limited claim 1), which is consistent with the broader '934 claims being the vulnerable ones.
Explicit uncertainties: (a) the granted '934 claim set is not verified — the mapping above rests on the specification plus the US 12,577,291 claim‑1 proxy; (b) I could not confirm whether WO 2013/026913 discloses the KiH Fc embodiments or the MMP‑2/‑9 binding data; (c) I did not retrieve JP 2007084459 A's contents, so its contribution to Combination B is assumed from its title only; (d) the independent invention date of the DKFZ oligomerization work relative to '934's own priority is a priority/derivation question outside this § 103 analysis.
Generated 9/12/2026, 12:49:20 AM
Extensions
Patent term adjustments, term extensions, continuations, divisionals, family members, and expiration dates.
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