US 5827739

I'll search for this specific patent's records and any litigation/docket information.

Let me verify the claim set and check for litigation history.

Let me check for the specific litigation record and any recent appellate activity.

US 5,827,739 — Summary

Important caveat up front: I searched public web-accessible patent databases (Google Patents, Justia Patents, uspto.report, and CourtListener/Unified Patents litigation records surfaced through those pages). I did not directly query USPTO PatentCenter/PAIR or the Federal Circuit's own 2026 docket system, so the litigation portion below is based on secondary aggregators and should be verified at the source. I found no Federal Circuit 2026 (or any-year) docket activity for this patent number. I also did not return results for any other number; the data below pertains specifically to 5,827,739 (US5827739A) only.

Bibliographic data

Sources: https://patents.google.com/patent/US5827739/en ; https://patents.justia.com/patent/5827739

Continuity note (interpreted literally): The specification states this is a continuation of Ser. No. 08/302,241 (filed Sep. 8, 1994, pending), which is a continuation of 08/165,533 (filed Dec. 13, 1993, abandoned), which is a continuation of 07/852,390 (filed Mar. 16, 1992, abandoned), which is a continuation of 07/595,733 (filed Oct. 10, 1990, issued as U.S. Pat. No. 5,122,464), which is a continuation of 07/117,071, filed as PCT/GB87/00039 (Jan. 23, 1987), abandoned. One aggregator lists the 07/117,071 U.S. filing date as October 23, 1987, which conflicts slightly with the specification's "filed as PCT/GB87/00039 jan. 23, 1987" — I flag this rather than resolve it.

Abstract (verbatim)

"Recombinant DNA sequences which encode the complete amino acid sequence of a glutamine synthetase, vectors containing such sequences and methods for their use, in particular as dominant selectable markers, for use in co-amplification of non-selected genes and in transforming host cell lines to glutamine independence."

Independent claims — plain-language overview

The patent has four claims, of which two are independent (claims 1 and 2); claims 3 and 4 depend from claim 2.

Claim 1 (independent — method): A method of giving a cell line the ability to survive in medium that lacks glutamine. The method has two steps: (a) providing a vector that encodes the complete amino acid sequence of glutamine synthetase (GS); and (b) transforming a host cell that either completely lacks GS activity or has reduced GS activity with that vector. In plain terms: put a full-length GS gene into a GS-deficient cell so the cell can make its own glutamine.

Claim 2 (independent — composition of matter, DNA): An isolated DNA encoding the complete amino acid sequence of GS, limited to hamster GS, where the hamster GS comprises the amino acid sequence of the Chinese hamster GS shown in FIGS. 2a–2d. In plain terms: the isolated polynucleotide that codes for the full Chinese hamster GS protein as disclosed in the sequence figures. (Note the claim is species-limited to hamster and tied to the FIG. 2 sequence, rather than claiming any GS genus.)

Claim 3 (dependent on claim 2): A vector (e.g., plasmid/expression vector) that comprises the isolated hamster GS DNA of claim 2.

Claim 4 (dependent on claim 3): A host cell transformed with the vector of claim 3.

Practical significance described in the specification: The disclosed GS gene/vectors are used as (i) a dominant selectable marker conferring resistance to GS inhibitors such as methionine sulphoximine (Msx) and phosphinothricin, (ii) an amplifiable marker for co-amplifying a non-selected gene (tPA is exemplified; immunoglobulins, hGH and TIMP are also named), and (iii) a means of converting cells (notably hybridoma/myeloma) to glutamine-independent growth. The specification reports high copy numbers (~10,000–15,000 copies/cell) with the pSVLGS.1 construct in CHO-K1 cells after two rounds of Msx selection.

Litigation / docket status (verify at source)

• The Google Patents page for US5827739 carries a Darts-IP "first worldwide family litigation filed" link (family ID 10591815) and a Unified Patents litigation record for a U.S. case in the District of Maryland, case 8:07-cv-03177 (source: District Court; jurisdiction: Maryland District Court). I did not independently confirm the parties or outcome of that 2007 case; the aggregator's link is https://portal.unifiedpatents.com/litigation/Maryland%20District%20Court/case/8%3A07-cv-03177.
• I found no CAFC 2026 docket entry, appeal, or other appellate activity tied to 5,827,739. Given the patent's listed expiration of 2015-10-27, 2026 appellate litigation on this patent is unlikely, though I cannot categorically exclude later-filed actions.
• The Google Patents assignment timeline shows a 2006-08-01 security agreement recorded to "MPM BIOVENTURES III-QP, L.P., AS ADMINISTRATIVE AGENT" with assignor "PharmAthene, Inc." I could not confirm that this record specifically encumbers US5827739 (it appears in the family/timeline feed), so treat it as unverified.

Related family members (context, not the subject patent)

The GS expression system from this family is widely cited in later patents. Related Celltech/Glasgow GS patents referenced alongside US5827739 include US 5,122,464 (the parent that issued from 07/595,733), US 5,591,639, US 5,770,359, US 5,879,936, US 5,981,216, and US 5,658,759. Also relevant is GB 2,237,288 A (Bebbington & Yarranton, Celltech) on GS-based amplification.

Confidence / uncertainty statement

• Bibliographic data and the four-claim set are drawn from Google Patents, Justia, and uspto.report, which agree and match the authoritative full text supplied; confidence is high.
• The Maryland case 8:07-cv-03177 is reported by a secondary aggregator only; parties/outcome are unverified, and "no CAFC activity" reflects a negative search result, not a certified docket check.
• The exact U.S. filing date of the earliest application (07/117,071: Oct. 23, 1987 per one aggregator vs. the PCT reference in the specification) is unresolved.
• I am not providing legal advice; patent claims should be construed by counsel against the granted claim text and prosecution history.

I'll research litigation involving US patent 5827739 using the sources you've indicated.

The general searches returned unrelated matters. Let me dig into the specific litigation lead on the patent's Google Patents page (a Maryland District Court case) and search litigation databases directly.

I found a key case. Let me verify its details and outcome, and check for any other litigation in the patent family.

Litigation involving US Patent No. 5,827,739

Important methodological note: I searched for the exact number 5827739 / 5,827,739 and did not accept results for similar-looking numbers. Web searches for this patent number returned very little directly; the main substantive lead was the litigation entry already flagged on the patent's own Google Patents page (a Maryland District Court case), which I then corroborated. Below is what the retrieved sources actually support, with the limits of each source stated.

Case found

Lonza Group AG v. Northwest Biotherapeutics, Inc.

• Court / jurisdiction: U.S. District Court for the District of Maryland
• Case number: 8:07-cv-03177
• Filing date: November 27, 2007 (as listed in the docket/patent-litigation reporting)
• Plaintiff: Lonza Group AG (referred to in some press reporting as "Lonza Group Ltd.")
• Defendant: Northwest Biotherapeutics, Inc. ("NWBT")
• Cause of action: 35 U.S.C. § 271 patent infringement
• Patent asserted (relevant): U.S. 5,827,739 — "Recombinant DNA Sequences, Vectors Containing Them and Method for the Use Thereof" — asserted together with a group of related gene-expression patents: U.S. 5,122,464; 5,591,639; 5,658,759; 5,770,359; 5,879,936; 5,891,693; and 5,981,216.
• Accused product: NWBT's DCVax® products (initially including DCVax®-Prostate), on the theory that NWBT used Lonza's gene-expression (glutamine synthetase/vector) technology.
• Status/outcome: Lonza amended its complaint on December 13, 2007 to withdraw all infringement allegations relating to products other than DCVax®-Prostate, leaving only that one product accused. NWBT denied infringement and stated it would "fight the remaining Lonza claims vigorously."
  • Sources: patentdocs.net summary (reposted on siliconinvestor.com), the Justia docket listing for the Maryland case, and a Lonza/NWBT press release of December 20, 2007 (biospace.com).

Caveat on outcome: The sources I retrieved establish the filing, the identity of the patents (including the '739), the parties, and the December 2007 amendment narrowing the claims. They do not establish a final judgment, dismissal, or settlement of the Maryland case. I could not confirm the ultimate disposition from the retrieved material and will not guess at it.

Related, but NOT confirmed to involve the '739

• There was an earlier, first Lonza suit against NWBT filed July 27, 2007 in the U.S. District Court for the District of Delaware, alleging infringement of "certain gene expression patents" by NWBT's DCVax® products. That Delaware suit was dismissed (by agreement of the parties) and Lonza then filed the Maryland action. The press release does not specify which patent numbers were in the Delaware complaint, so I cannot confirm the '739 was asserted there. (Source: biospace.com press release, Dec. 20, 2007.)

Other matters checked and ruled out (to avoid conflating patent numbers)

• MedImmune, Inc. v. Genentech, Inc. (and the related Celltech/Genentech interference) involved Celltech's U.S. 4,816,397 "Boss" patent and Genentech's 6,331,415 ("Cabilly II") — not the '739.
• The Celltech v. MedImmune UK action (cited in the Festo amicus brief) concerned a humanized-antibody patent, not the glutamine-synthetase vector patents — not the '739.
• The Google Patents page for US 5,827,739 carries a generic "Family has litigation" flag with a link to a Darts‑ip family record (family ID 10591815). That flag denotes litigation somewhere in the patent family, and does not by itself identify the '739 as an asserted patent; the Maryland case above is the matter I could specifically tie to the '739.

Bottom line

Based on the sources retrieved, the only litigation I can specifically tie to US 5,827,739 is Lonza Group AG v. Northwest Biotherapeutics, Inc., No. 8:07-cv-03177 (D. Md., filed Nov. 27, 2007), in which the '739 was one of eight Lonza gene-expression patents asserted (ultimately narrowed to DCVax®-Prostate). I do not have a confirmed disposition for that case, and I found no other litigation specifically naming the '739.

If you need the disposition pinned down, the next steps would be pulling the Maryland docket directly (PACER for 8:07-cv-03177) and the Darts‑ip family record (family 10591815). I was not able to retrieve a decisive final-outcome document within this session, so I am flagging that gap rather than filling it in.

Would you like me to draft a PACER/Darts‑ip retrieval request to close out the outcome question?

I'll verify the structured block's default against web sources before writing.

Let me run a few more targeted checks before concluding.

One more verification pass on the litigation trail and reexamination history.

Proceedings overview

Total AIA trial proceedings on US 5,827,739: zero. The structured "PTAB proceedings on file" block supplied in this task — the canonical USPTO ODP list — returns no IPR, PGR, or CBM for this patent, and my independent web searches (patent number, patentee "Celltech"/"Lonza," GS-expression-system art, and IPR-filing-year queries) surfaced no PTAB petition, institution decision, Final Written Decision, or CAFC appeal involving it. There is therefore no breakdown by status to give — nothing was invalidated, nothing was sustained, nothing settled, and nothing was denied institution, because nothing was ever filed.

The bottom-line defensive posture is nonetheless maximally favorable to a defendant, but for a reason entirely unrelated to PTAB: the patent is expired. Google Patents records an "Anticipated expiration" of 2015-10-27 with legal status "Expired – Lifetime," consistent with a 1986-01-23 priority date and a 20-year term measured from the earliest US filing in the chain. Because the patent has now been expired for roughly eleven years, a demand letter citing it is stale on its face — see the strategic summary below on 35 U.S.C. § 286.

Proceedings list

No proceedings to enumerate. Per the task's constraint that I not invent proceeding numbers, I am deliberately not creating placeholder entries. For auditability, here is what I checked and what it returned:

Litigation trail (context, not PTAB). The Google Patents record carries a "Family has litigation" flag and two entries that are worth naming because they are the only adversarial history I could find on this patent:

1. A "First worldwide family litigation filed" record pointing to the Darts-IP family tracker: https://patents.darts-ip.com/?family=[10591815](/patent/10591815)
2. A US case filed in Maryland District Court, case 8:07-cv-03177, per the Unified Patents litigation portal: https://portal.unifiedpatents.com/litigation/Maryland%20District%20Court/case/8%3A07-cv-03177

I could not verify in this session whether the Maryland action actually asserted the '739 patent, whether it named Celltech/UCB, the University of Glasgow, or a licensee as plaintiff, or how it terminated — my verification searches were truncated. Treat the Maryland case as a lead to pull on a PACER/Unified Patents pull, not as an established fact about this patent.

Assignment note. The Google Patents reassignment record dated 2006-08-01 to MPM BIOVENTURES III-QP, L.P. as administrative agent is a security agreement (assignor: PharmAthene, Inc.), not a transfer of title to US 5,827,739. Recorded assignees remain the University of Glasgow and Celltech R&D Ltd. Do not read that entry as a change in ownership of this patent.

Strategic summary

Claim status: no claim was ever canceled, sustained, or tested at the PTAB — because no petition was ever filed. The patent issued with a small claim set — four claims as displayed on Justia (https://patents.justia.com/patent/[5827739](/patent/5827739)): claim 1 to a method of endowing a cell line with glutamine-independent survival by transforming a GS-activity-deficient host cell with a vector encoding complete glutamine synthetase; claim 2 to isolated DNA encoding complete hamster (Chinese hamster, FIGS. 2a–2d) GS; claim 3 to a vector comprising that DNA; and claim 4 to a host cell transformed with that vector. All four stand as issued, unamended by any post-grant trial. Note that if the patent was ever narrowed, the narrowest instrument would have been ex parte reexamination or a certificate of correction, not an AIA trial — I found no evidence of either, but I also could not exhaustively confirm that negative.

Estoppel landscape: there is none, and that cuts against the patent owner, not the defendant. Section 315(e)(2) estoppel only arises from a petitioner that reached a Final Written Decision. With no IPR ever filed on this patent, no party is estopped from raising any prior-art ground, and no invalidity ground has been "used up" at the PTAB against these claims. A defendant therefore has the full menu — §§ 102, 103, and 112 in district court or an IPR (subject to the expiration considerations below) — with no § 315(e) constraints and no § 325(d) discretionary-denial risk from prior PTAB treatment of the same art. Whether that menu is worth ordering from is a separate question, addressed next.

Pattern signals are weak, and the timing is the real story. Neither check revealed a serial petitioner, a defensive aggregator, or an aggressive PTAB-appeal posture. Two structural facts explain the silence. First, AIA trials only became available on 2012-09-16; this patent expired roughly three years later on 2015-10-27, leaving a narrow window in which a challenger would have had to act. Second, and more importantly, there was little reason to file — the commercial GS selection/amplification technology is a licensing program, not a litigation program. Search results indicate the related GS-system patents (US 5,770,359 and US 5,747,308, co-assigned with the University of Glasgow) were licensed by Lonza Biologics to "over 70 companies" (per the Enhanced Expression / NS0 platform literature and the BioPlan Synagis analysis), and that Lonza Group plc is the successor holder of the Celltech Biologics GS platform. A broadly licensed, revenue-producing patent family attracts licensees, not IPR petitioners. Note this is context about the family, sourced from secondary literature; I did not verify the current recorded owner of US 5,827,739 beyond the Google Patents assignee data.

One nuance to keep straight: an expired patent remains eligible for IPR — the PTAB will institute on a lapsed patent because claims can be cancelled retroactively and the estoppel/challenge questions survive. So "no IPR" is not because the patent expired; it is because, during the three-year overlap, nobody paid to file. The expiration matters for the far more practical reason below.

Recommended next steps

If you have received a demand letter citing US 5,827,739, the expiration date is your primary defense, not validity. The patent's anticipated expiration is 2015-10-27; today is 2026-09-27. Under 35 U.S.C. § 286, a patentee may recover damages only for infringement committed within six years before the filing of the complaint. The last day on which the patent could have been infringed is 2015-10-27, and that is more than six years and eleven months in the past. Any damages recovery on this patent is time-barred as a matter of arithmetic, independent of infringement, validity, or claim construction. If the demand letter also invokes continuing conduct, the response is simply that the patent term ended and post-2025 conduct cannot infringe it.

Do not spend IPR money here. With the damages window closed, an IPR on US 5,827,739 would be a solution in search of a problem — the PTAB cannot give you a better outcome than "the patent is expired and unenforceable for damages." Reserve IPR budget for live family members or later-generation GS/expression-system patents if those are what is actually being asserted.

Verify the assertion's true target before responding. Two open threads need a PACER pull: (1) the Maryland District Court case 8:07-cv-03177 (https://portal.unifiedpatents.com/litigation/Maryland%20District%20Court/case/8%3A07-cv-03177) — confirm whether the '739 was ever a pleaded patent and how it resolved; and (2) the Darts-IP family-litigation record at https://patents.darts-ip.com/?family=10591815. If a demand letter's theory actually depends on sibling patents (US 5,770,359, US 5,747,308, US 5,591,639, US 5,981,216) rather than the '739 specifically, confirm each sibling's expiration date individually — they share the 1986-era priority chain and should be expired as well, but I did not verify each one in this session and will not assert it.

Absence as signal. Where a patent has been actively asserted, IPRs follow. That this patent — a foundational GS selection marker with a very broad claim set and heavy commercial use — drew no AIA petition across the entire 2012–2015 window is best explained by licensing rather than litigation as the monetization strategy. That is the correct read of the record, and it means you should look for this patent in a license agreement, not a complaint.

Confidence and limitations. High confidence: no AIA trial proceedings on US 5,827,739 (structured ODP data plus multiple independent searches agree); the 2015-10-27 anticipated expiration; the 1986-01-23 priority date; the assignee and inventor data. Lower confidence, flagged inline: the specific subject matter and outcome of the Maryland case 8:07-cv-03177; whether any ex parte reexamination or reissue certificate exists; the current recorded owner; and the expiration dates of the sibling GS patents. My verification searches were cut off by a step limit before I could close those four items, so they are stated as leads rather than findings. Consult the PTAB E2E portal (https://ptab.uspto.gov/) and the PTAB decisions search (https://developer.uspto.gov/ptab-web/#/search/decisions) directly to confirm the zero-proceedings result before relying on it in a filing.

I'll research the assignment record for US 5827739 before assembling the report.

Data-access note: The USPTO Assignment Center is a JavaScript application that my research tooling cannot query programmatically, and no mirror (uspto.report, patents.google.com legal events, EPO/Espacenet register) exposed reel/frame numbers or correspondent-of-record names for this patent within my search budget. Everything below is labeled by source and confidence; no reel/frame numbers or correspondent names are stated because I could not verify any, and I will not invent them.

Inventors

Unusual patterns — none found. Both inventors stayed with their 1986 employers long past the priority date: Bebbington was still publishing GS/NS0 work out of Celltech in 1992, and Wilson remained at Glasgow. There is no evidence of simultaneous inventor departure preceding a fire-sale. What is structurally notable is a university + industry co-ownership at filing — a UK public university co-owning with a UK biotech — which is the reason this family has two institutional owners rather than one.

Original assignee

Two co-assignees on the face of the patent: University of Glasgow and Celltech Therapeutics Ltd.

• University of Glasgow — public UK university; operating, never dissolved. Not a product company; its stake is purely licensing-driven.
• Celltech Therapeutics Ltd (Slough, UK) — recombinant-DNA and biopharmaceutical operating company. Primary line of business: recombinant protein/biologic R&D; Celltech (as Celltech Biologics) ran the Slough contract-manufacturing business and the NSO cell line franchise.
• Did they ship a product embodying the claims? Yes, and it is the reason this patent matters. The claimed subject matter (a recombinant DNA sequence encoding the complete GS amino acid sequence, plus vectors containing it) is the kernel of the GS Gene Expression System™ — later branded GS System® / GS Xceed®. Lonza's own materials state the system is "owned and licensed by Lonza" and that "over 80 biotechnology and pharmaceutical companies and over 70 academic laboratories worldwide" use it (Lonza press release, Basel, 2007-03-07). A peer-reviewed review states the system "is based [on] patents issued to Celltech Biologics plc, now assigned to Lonza Group plc, subsidiary of Alusuisse-Lonza Group," and that "over 70 companies have licensed GS System technology" (Biotechnol. Prog. review, ref. 27). So the original assignee shipped/licensed a commercial embodiment — this is not a paper patent.
• Current status of Celltech: acquired, not dissolved. Celltech Group plc was acquired by UCB S.A. (UCB Bioproducts) in mid-2004; the Celltech biologics/GS business and the Slough manufacturing site had earlier passed to the Alusuisse-Lonza side and became Lonza Biologics plc. Google Patents lists the current assignee of record as "University of Glasgow; Celltech R&D Ltd" — i.e. the Celltech side of the title appears to still sit in a Celltech R&D Ltd (UCB) entity of record, while Lonza holds the GS System commercially and enforced these patents in court. That divergence (record assignee vs. commercial/enforcement owner) is the single most important unresolved question in this chain — see the caveat under NPE signals #2.

Assignment timeline

Record status legend: [GP] = Google Patents "Legal Events" for US5827739 (derived from USPTO reassignment data, no page images); [2°] = secondary source; [CT] = court docket. No entry below carries a verified reel/frame or correspondent, because none was retrievable.

• 1986-01-23 (priority) / recording date not retrieved — Reel not retrieved / not retrieved

  • Conveyance: implied invention assignment to co-employers (no separate recorded instrument retrieved)
  • Assignor: Richard Harris Wilson (University of Glasgow) and Christopher Robert Bebbington (Celltech)
  • Assignee: University of Glasgow and Celltech Therapeutics Ltd
  • Correspondent: not retrievable
  • Context: academic–industrial co-ownership at first filing (GB priority; PCT/GB87/00039 filed 1987-01-23).

• 1995-06-07 / recorded 1995-06-07 [GP] — Reel not retrieved / not retrieved

  • Conveyance: application filing / priority claim (not a title transfer)
  • Assignor: n/a — applicants
  • Assignee: University of Glasgow; Celltech Therapeutics Ltd
  • Correspondent: not retrievable
  • Context: filing of continuation 08/476,567 (the application that issued as '739) in a 10-year continuation chain running back through 07/117,071 (PCT/GB87/00039) → 07/595,733 → US 5,122,464. No title change.

• 1998-10-27 / recorded 1998-10-27 [GP] — Reel not retrieved / not retrieved

  • Conveyance: patent grant (not an assignment)
  • Assignor: n/a
  • Assignee: University of Glasgow; Celltech Therapeutics Ltd
  • Correspondent: not retrievable
  • Context: issuance. Title unchanged from filing.

• ~1996–2004 (exact date not retrieved) [2°] — Reel not retrieved / not retrieved

  • Conveyance: corporate transfer of the Celltech biologics/GS business (reported as assignment of the GS patents to Lonza Group plc, subsidiary of Alusuisse-Lonza Group)
  • Assignor: Celltech Biologics plc / Celltech Therapeutics Ltd (Celltech group)
  • Assignee: Lonza Group plc (Lonza Biologics plc operating entity; later Lonza Sales AG)
  • Correspondent: not retrievable
  • Context: internal/corporate divestment, not an NPE transfer — the Slough biologics business and the GS System changed hands as a going concern. Date and instrument unverified; this is the key gap in the chain.

• 2004 (mid-year) [2°] — no assignment recorded against this patent; corporate-level event

  • Conveyance: merger/acquisition (Celltech Group plc acquired by UCB S.A.)
  • Assignor: Celltech Group plc shareholders
  • Assignee: UCB S.A. / UCB Bioproducts
  • Correspondent: not retrievable
  • Context: public-company acquisition — the Celltech equity, and with it any retained Celltech interest in this family, moved to UCB.

• 2006-08-01 / recorded 2006-08-01 [GP] — Reel not retrieved / not retrieved

  • Conveyance: Security Agreement (as indexed by Google Patents)
  • Assignor: PHARMATHENE, INC.
  • Assignee: MPM BIOVENTURES III-QP, L.P., AS ADMINISTRATIVE AGENT
  • Correspondent: not retrievable
  • Context: Almost certainly an indexing artifact, not a link in this chain. PharmAthene is a biodefense company with no documented relationship to the Glasgow/Celltech GS family, and this identical "MPM BIOVENTURES III-QP, L.P. / SECURITY AGREEMENT / Assignor: PHARMATHENE, INC." tuple is surfaced by Google Patents on numerous unrelated patents. Even if a security interest existed, a security agreement is a lien, not a title transfer. Flagged, not credited. Verify at the Assignment Center before relying on it either way.

• 2007-03-07 [2°] — no assignment recorded

  • Conveyance: License (non-exclusive, worldwide) — Lonza → UCB
  • Assignor/owner of record: Lonza Group Ltd ("the GS Gene Expression System™, which is owned and licensed by Lonza")
  • Assignee/licensee: UCB
  • Correspondent: n/a (not a USPTO recording)
  • Context: strong corroboration that by March 2007 Lonza — not Celltech/UCB — held the GS rights, and that UCB (Celltech's acquirer) was now a licensee of its own former technology.

• 2007-11-27 [CT] — no assignment recorded

  • Conveyance: none; first infringement suit naming this patent
  • Plaintiff: Lonza Group AG
  • Defendant: Northwest Biotherapeutics, Inc.
  • Venue: D. Md., No. 8:07-cv-03177 (filed 2007-11-27), asserting US 5,122,464; 5,591,639; 5,658,759; 5,770,359; 5,827,739; 5,879,936; 5,891,693; 5,981,216 over Northwest's manufacture/use/sale of DCVax® products. Source: docket summary reproduced at siliconinvestor/patentdocs; also indexed on Google Patents as "Family has litigation" and in the Unified Patents litigation portal.
  • Correspondent: not retrievable
  • Context: operating-company assertion by the GS System's commercial owner — eight patents asserted together as a technology stack, not a lone patent asserted for toll revenue.

• 2015-10-27 [GP] — no assignment

  • Conveyance: none — anticipated expiration
  • Context: term ran to 2015-10-27, i.e. 17 years from the 1998-10-27 grant, under the pre-URAA 17-year-from-grant alternative. The patent is expired; no current infringement exposure.

If the Assignment Center in fact holds no post-issuance records tying US5827739 to Lonza, read this timeline accordingly: the only recorded title on the face of the patent is University of Glasgow + Celltech Therapeutics Ltd, and Lonza's 2007 standing would then rest on an exclusive licence rather than a recorded assignment of this particular patent number. Those two readings have materially different consequences and I could not resolve between them with the sources available.

Timeline diagram

timeline
    title Ownership of US 5827739
    1986 : Priority filing Glasgow and Celltech
    1987 : PCT application filed
    1992 : Parent patent 5122464 issues
    1995 : Continuation application filed
    1998 : Patent issued 27 Oct 1998
    2004 : Celltech acquired by UCB
    2007 : Lonza licenses GS System to UCB
         : Lonza sues Northwest Biotherapeutics
    2015 : Patent expires 27 Oct 2015

(The 2006 MPM BioVentures/PharmAthene security-agreement entry is deliberately omitted from the diagram pending verification — see the flagged entry above.)

NPE / troll-pattern signals

1. Shell-entity transfer — not present. Every named party is a university or an operating company: University of Glasgow, Celltech Therapeutics Ltd, Lonza Group plc, Lonza Sales AG, UCB. No "IP / Holdings / Ventures / Licensing" LLC appears as assignee, and no registered-agent-service address was located. The only entity with an NPE-style name in the record (MPM BIOVENTURES III-QP, L.P.) appears solely in the unverified 2006-08-01 security-agreement entry, is a venture-capital fund acting as collateral agent, and concerns an assignor (PharmAthene) with no documented link to this family — a lien, not a shell transfer, even on its face.

2. Known asserter in the chain — not present. No Acacia, Marathon, IV, IPNav, Wi-LAN, Conversant/Mosaid, Vringo, Pendrell, Innovatio, MPHJ, Lumen View, Round Rock, Document Generation Corp or Spangenberg entity appears anywhere in the chain or in the 2007 docket. The plaintiff of record is Lonza Group AG, a Swiss CDMO/life-sciences group. Caveat that cuts the other way: Lonza's business model for these patents is pure licensing (80+ licensees, GS System®), and Lonza does not itself ship the therapeutic products at issue — so by the functional "does it sell the patented invention" test, Lonza is a licensor of the invention, not a manufacturer of an article. I am calling this signal not-present because Lonza is a genuine operating company in the contract-manufacturing and cell-line-supply business and is on no public NPE list, but a reader applying a stricter functional definition could reasonably score this unclear.

3. Repeat correspondent across the chain — unclear / not assessable. No correspondent-of-record name or firm was retrievable for any entry. I have no basis to identify recurring counsel, and I explicitly decline to name one. This is the single largest evidentiary hole in this report and the thing to pull first from the Assignment Center's "correspondent" column.

4. Cascading transfers — not present. The chain is the opposite of cascading: priority 1986 → grant 1998 → commercial move to Lonza (reported ~1996–2004) → UCB acquisition 2004 → litigation 2007 → expiry 2015. Roughly two decades between the meaningful title events, with no cluster of LLC-to-LLC transfers inside 24 months.

5. Pre-litigation transfer — not present / no evidence. The only litigation is dated 2007-11-27 (D. Md. 8:07-cv-03177). I found no assignment executed within six months before that date; the Lonza ownership position arises from the Celltech biologics divestment years earlier and is corroborated by Lonza's own March 2007 press release describing the system as "owned and licensed by Lonza." No venue-engineering transfer is visible. Marked as a negative finding contingent on the reel/frame gap.

6. Bankruptcy fire-sale — not present. No Chapter 7/11 anywhere in the chain. Celltech's exit was an acquisition by UCB (2004), not an insolvency; the GS assets moved to Lonza by corporate divestment, not by a bankruptcy estate sale.

7. Privateering — not present. Lonza litigated in its own name as plaintiff; it did not hand the patents to a proxy NPE to assert on its behalf against competitors. The inverse pattern (asset transferred to a third party who then sues) is absent.

8. Defensive aggregator (anti-NPE) — not present. The chain does not terminate at RPX, AST, LOT, Unified or OIN. It terminates at expiry (2015-10-27) with the technology still held commercially by Lonza and licensed to UCB and 80+ others.

Verdict

Operating-company assertion.

Lonza Group AG — the commercial owner of the GS Gene Expression System, which it states it "owns and licenses" and which has 80+ corporate licensees, and which it licensed back to Celltech's acquirer UCB in March 2007 — filed D. Md. 8:07-cv-03177 on 2007-11-27 asserting US 5,827,739 as part of an eight-patent technology stack against Northwest Biotherapeutics' DCVax® products. That is a technology owner enforcing a stack it actually exploits, not an NPE toll operation: there is no shell-entity transfer, no listed NPE in the chain, no cascading LLC transfers, no pre-suit assignment within six months of the complaint, and the chain's only non-operating element is a university co-assignee. This verdict is moderate rather than high confidence on the record dimension because I could not retrieve a single reel/frame or correspondent entry — the sources for Lonza's title are Lonza's own press materials, a peer-reviewed review and the 2007 docket, while Google Patents' recorded current assignee still reads "University of Glasgow; Celltech R&D Ltd." Resolving whether Lonza holds this patent by assignment or by exclusive licence would not change the verdict class (either way the asserter is an operating licensor), but it should be confirmed.

Verification links:

• USPTO Assignment Center — search by patent number 5827739: https://assignmentcenter.uspto.gov/ (legacy mirror: https://assignment.uspto.gov/patent/index.html — search 5827739; retrieve the reel/frame and the correspondent column, which are the two fields missing here)
• Google Patents legal events for US5827739: https://patents.google.com/patent/US5827739/en
• 2007 litigation docket summary: https://www.siliconinvestor.com/readmsg.aspx?msgid=24127441 and https://portal.unifiedpatents.com/litigation/Maryland%20District%20Court/case/8%3A07-cv-03177

I'll research US patent 5827739 and its prior art citations.

Let me get more detailed citation data from the Justia and USPTO/Google Patents records.

Prior Art Analysis: US 5,827,739

1. Patent Under Review (confirmed from USPTO/Google Patents record)

Subject matter of the claims: A recombinant DNA sequence encoding the complete amino acid sequence of a glutamine synthetase (GS); vectors containing it (including GS + a second "desired protein" coding sequence, e.g. tPA); host cells transformed therewith; a method for co-amplifying a non-GS gene by selection in progressively increasing GS inhibitor (Msx/phosphinothricin); use as a dominant selectable marker; and use to confer glutamine independence (especially in hybridoma/myeloma cells).

Important preliminary caveat — anticipation vs. obviousness. Because the effective priority date is 23 January 1986, most of the references listed below are cited as §103 (obviousness) background art, not as §102 anticipatory art. True §102 anticipation requires a single reference disclosing every element of a claim — including a recombinant DNA sequence encoding the complete amino acid sequence of GS. None of the references I located discloses the complete GS coding sequence except the patent's own family member. The claim mapping below is therefore stated as "most relevant to / closest to potential §102" and should be verified against the verbatim granted claims (which I could not retrieve in full). I flag below where a reference is genuinely §102(a)/(b) art vs. post-priority-date art.

2. U.S. Patent References Cited

2.1 — US 4,399,216

• Full citation: Axel, R. et al., "Processes for inserting DNA into eucaryotic cells and for producing proteinaceous materials," US 4,399,216.
• Filed / Published (granted): Filed Feb. 25, 1980; granted Aug. 16, 1983. → Valid pre-1986 §102(a)/(b) art.
• Brief description: Discloses co-transformation of eukaryotic (mammalian) cells with (i) DNA coding for a desired protein (DNA I) and (ii) an amplifiable gene for a dominant selectable marker (DNA II), linked or unlinked, followed by selection in successively higher concentrations of an inhibitor to co-amplify the desired gene. Specifically names DHFR, CHO cells, and interferon.
• Potential §102 mapping: Most relevant to the co-amplification and dominant-selectable-marker method claims and the transformed-host-cell claims. However, it does not disclose GS as the marker and does not disclose a GS-encoding sequence, so it cannot anticipate any claim reciting GS. Its relevance is as §103 art against the method claims where the only novelty is the choice of GS as the amplifiable marker.

2.2 — US 4,656,134

• Full citation: Ringold, G.M. (Board of Trustees of Leland Stanford Jr. University), "Gene amplification in eukaryotic cells," US 4,656,134.
• Filed / Published (granted): Filed Jan. 11, 1982; granted Apr. 7, 1987. → Filed before 1986 priority date (pre-AIA §102(e) art at minimum; substantive art as of its 1982 filing).
• Brief description: Discloses a DNA "unit" in which an amplifiable gene (e.g. DHFR) is positioned upstream of a second structural gene of interest, with the promoter for the amplifiable gene deliberately weaker than the promoter for the desired gene, so that selection increases copy number and expression of the desired gene. Teaches that the amplifiable gene can be under the control of regulatable promoters/operators.
• Potential §102 mapping: Most relevant to claims directed to a vector comprising a GS sequence together with a second desired-protein sequence, and to claims reciting a regulatable promoter for the GS gene (the "switch on during selection, then down-regulate" limitation in the patent's specification). Not anticipatory for GS-sequence claims; strong §103 art against the vector architecture claims.

2.3 — US 4,797,359

• Full citation: Finkelstein, D.B. et al., "Heat shock regulated production of selected and fused proteins in yeast," US 4,797,359.
• Filed / Published (granted): Granted Jan. 10, 1989. (Filed 1984–85; pre-priority filing.)
• Brief description: Discloses heat-shock-inducible regulatory sequences from yeast (e.g. HSP90) fused to a selected gene, allowing regulated (temperature-switched) expression in a transformed host.
• Potential §102 mapping: Relevant only to the patent's limitation that the GS-encoding sequence "is under the control of a regulatable promoter, such as a heat shock or a metallothionein promoter." It contains no GS teaching and cannot anticipate; it is §103 art supporting the regulatable promoter species of the vector claims. (This reference merely supports that heat-shock promoters were known regulators.)

2.4 — US 5,122,464

• Full citation: Wilson, R.H. and Bebbington, C.R., US 5,122,464.
• Filed / Published (granted): Issued June 16, 1992 (from application 07/595,733, filed Oct. 10, 1990, itself in the chain from PCT/GB87/00039, Jan. 23, 1987).
• Brief description: The earlier-issued family member / parent of the patent under review — same specification (GS cDNA encoding the complete CHO GS amino-acid sequence; pSVLGS.1, pSV2.GS, pZIPGS; Msx amplification).
• Potential §102 mapping: As a same-family parent, this is the only listed reference that itself discloses a DNA sequence encoding the complete amino acid sequence of GS. Its §102 relevance is chiefly via the obviousness-type double-patenting / §102(b) self-collision analysis (a patent cannot be its own prior art for §102(a)/(b) unless it qualifies as a distinct patent under §102(b)/§102(e); this is the classic In re ODP situation). It is not independent third-party prior art. All claims reciting the GS sequence/vector overlap its disclosure; whether it "anticipates" turns on exact claim wording and the §102(e)/§102(b) status of the parent.

2.5 — WO 86/06409

• Full citation: PCT international publication WO 86/06409.
• Published date (as listed): April 1986 — i.e., after the 23 Jan. 1986 priority date. → Not §102(a)/(b) art; potentially §102(e) art only if it qualifies (a WO designating the US and published in English can qualify as §102(e) art from its international filing date, but not from a "April 1986" publication if that is post-priority).
• Brief description: Listed among the cited documents; the record I retrieved does not set out its subject matter in detail. (I could not independently verify its disclosure with high confidence, so I flag this rather than guess.)
• Potential §102 mapping: Indeterminate. Because it post-dates the 1986 priority date, it can only bear on claims if it qualifies as §102(e) art. I do not have high-confidence subject-matter details for this reference and will not fabricate a claim mapping.

(Note: I retrieved the citation list from the Justia and Google Patents records of US 5,827,739. The Justia "Referenced Cited – U.S. Patent Documents" block should be treated as the authoritative list of record citations; I could not confirm whether additional US references exist beyond those above.)

3. Non-Patent Literature of Record (the substantive §102(a)/(b) art)

These are the references most likely to have driven the examination and are the strongest candidates for §102(a)/(b) between 1978 and early 1986:

(I have cited these as they appear in the record; the string "Watsen" appears literally in the citation listing and I have not auto-corrected it.)

4. Bottom-Line Assessment

1. No listed third-party reference discloses a recombinant DNA sequence encoding the complete amino acid sequence of GS. The only reference in the set that does is the patent's own earlier family member, US 5,122,464 (self-collision / double-patenting, not third-party anticipation). The closest third-party GS reference, Sanders & Wilson (1984), discloses only a partial, unsequenced genomic fragment.
2. §102 anticipation therefore appears unavailable for the core "complete GS sequence" claims (Claim 1-type) on this record.
3. §103 obviousness is the operative theory for the method/vector/marker claims, with Axel (US 4,399,216) + Ringold (US 4,656,134) + Sanders & Wilson (1984) + Young & Ringold (1983) forming the strongest combination, and Finkelstein (US 4,797,359) supplying the "regulatable/heat-shock promoter" species.
4. Date verification needed: Kaufman (1986) and WO 86/06409 (April 1986) post-date the 23 Jan. 1986 priority date and can only be prior art under pre-AIA §102(e) (US patents/applications and qualifying WO publications), not §102(a)/(b) — verify their exact publication dates before relying on them.

Confidence and limitations: I have high confidence in the patent bibliographic data, continuity chain, assignees, and the record citation list (from the Google Patents and Justia records of US 5,827,739). I do not have the verbatim granted claim set in front of me, so the claim-number mapping is stated functionally rather than by literal claim number; it should be confirmed against the granted claims. I could not independently verify the subject matter of WO 86/06409 and have deliberately not invented a description for it.

I'll ground this analysis in the prior art actually associated with this patent. Let me first pull the claim set and the cited references, since the rendered page you supplied omits both the numbered claims and the front-page "References Cited" list.

I now have the actual claim set. Let me confirm it and pull the parent patent's cited art, since US 5,827,739 is a continuation in a long chain.

I have the claim set and the cited art. Let me verify a few key references that matter for the § 103 analysis.

Obviousness Analysis — U.S. Patent 5,827,739 under 35 U.S.C. § 103 (pre‑AIA)

0. Note on the source page and my evidentiary basis

The Google Patents rendering you supplied contains a "Prior art keywords" field (vector, dna, cells, msx, gene) and a "Prior art date" of 1986‑01‑23, but it does not contain an enumerated "Prior Art" reference list (Google Patents renders cited references only on certain pages; the delivered text does not include them). Rather than invent one, I reconstructed the art of record from two verifiable sources:

1. The front page of the parent patent, US 5,122,464 ("Method for dominant selection in eucaryotic cells," same inventors, same family, appl. 07/595,733), which lists the "References Cited" — retrieved at https://uspto.report/patent/grant/[5122464](/patent/5122464)
2. The references cited in the specification of US 5,827,739 itself (authoritative text you provided).

I flag below where I could not verify a date, page range, or the substance of a reference.

Governing law. The application was filed 7 June 1995 with a priority date of 23 January 1986 (GB 8601597; PCT/GB87/00039, published as WO87/04462). Because it was filed before 16 March 2013, pre‑AIA §§ 102/103 govern. KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398 (2007), and In re Kubin, 561 F.3d 1351 (Fed. Cir. 2009), both apply the pre‑AIA statute and are therefore directly relevant.

Claims at issue (verified via Justia, https://patents.justia.com/patent/5827739 — only four claims were granted):

1. The art of record

Statutory references (all pre‑dated the 1986 priority date):

Printed publications (all before 23 Jan. 1986 unless noted):

• Wilson, R.H., Heredity 49:181 (1982) — extensively amplified GS genes in Msx‑resistant mammalian cell variants.
• Young & Ringold, J. Biol. Chem. 258(18):11260–11266 (1983) — mouse 3T6 cells over‑producing GS via Msx/MSO selection; GS mRNA enriched (i.e., GS gene amplification).
• Sanders & Wilson, EMBO J. 3(1):65–71 (1984) — cloning of an 8.2 kb BglII fragment "containing DNA coding for GS" from the Msx‑resistant CHO line KG1MS. This is the single most important reference.
• Donn, Tischer, Smith & Goodman, J. Mol. Appl. Genet. 2:621–635 (1984) — herbicide‑resistant alfalfa selected by GS gene amplification; GS‑encoding sequences used to confer resistance.
• de Saint Vincent et al., Cell 27:267–277 (1981) — cloning and reintroduction of a functional CAD gene as a "dominant amplifiable genetic marker" (PALA selection), usable in cells with an intact endogenous CAD gene.
• Wigler et al., PNAS 77:3567–3570 (1980) — "transformation of mammalian cells with an amplifiable dominant‑acting gene" (quoted in the background of US 4,656,134).
• Subramani, Mulligan & Berg, Mol. Cell. Biol. 1:854–864 (1981) — pSV2 expression vectors (SV40 early promoter + polyA); the very vector the applicants modified.
• Pennica et al., Nature 301:214 (1983) — cloning/expression of human tPA cDNA.
• Gubler & Hoffmann, Gene 25:263–269 (1983); Michelson & Orkin, JBC 257:14773 (1982); Vieira & Messing, Gene 19:259–268 (1982); Huynh, Young & Davis (1985) — routine cDNA synthesis, tailing/linkering, pUC and λgt10 cloning.
• Johnson & Piskiewicz, BBA 827:439–446 (1985) — bovine brain GS peptide/terminal sequences.
• Kabak et al. (1978) 134:237–245 and Velkov, Soviet Genetics 18 (1982) — GS‑deficient/mutant cell systems (cited of record; I did not retrieve these texts).
• Hayward, Hussain, Wilson, Lyons, Woodcock, McIntosh & Harris, Nucleic Acids Res. 14:999–1008 (1986) — "cloning and nucleotide sequence of cDNA for an amplified glutamine synthetase gene from the Chinese hamster." Applicants' own work (Wilson is a named inventor) — see §5.
• Kaufman et al., PNAS 83:3136–3140 (1986) — cited of record, but published after the 23 Jan. 1986 priority date; not prior art to these claims (flagging this because it appears on the parent's face and is sometimes mistakenly relied on).

Applicant admissions in the specification (usable as prior art under § 103): the entire "Background" section — that DHFR/MTX was the standard co‑amplification system; that it required a DHFR⁻ host and "there is at present only one cell line known which lacks the gene encoding DHFR"; that MTX "is a potential carcinogen"; that "at least three or more" rounds of amplification were needed; that GS is inhibited by Msx; and — critically — that "Cell lines are known which lack the GS gene. Moreover, there are available schemes whereby such cell lines may be selected."

2. Claim 1 — glutamine‑independent survival by transformation with a GS vector

Combination A (primary): Sanders & Wilson 1984 + Wilson 1982 + Young & Ringold 1983 + Ringold US 4,656,134 + the applicant's own admission that GS‑deficient cell lines and selection schemes were known.

Combination B: de Saint Vincent 1981 (dominant amplifiable marker concept) + Ringold US 4,656,134 (class of amplifiable genes) + Sanders & Wilson 1984 (the GS gene cloned) + Subramani 1981 (expression vectors).

Combination C (anticipatory‑flavored): any pre‑1986 cloning of a complete bacterial GS gene (e.g., Anabaena glnA, described in Nature 306:337–342, 1983 — cited second‑hand in EP 0 333 033; I did not verify this citation directly), placed in a plasmid and used to complement a GS‑deficient host. Claim 1 is not limited to eukaryotic or mammalian GS, so a plasmid‑borne complete glnA transforming a glutamine auxotroph to prototrophy would appear to read on it literally.

Motivation / rationale:

• The claim's result (growth without exogenous glutamine) is the definitional function of GS, which the specification itself states is "responsible for the synthesis of glutamate and ammonia using the hydrolysis of ATP." A POSITA knew that supplying a functional GS gene to a GS⁻ cell restores glutamine prototrophy.
• Complementation of metabolic auxotrophies with cloned genes, and selection in metabolite‑free medium, was a standard, well‑established technique (Ringold US 4,656,134 expressly describes amplification "by maintaining a low or zero concentration of an essential metabolite").
• The fed‑medium (glutamine‑free/gln‑free) selection format was already the operational context of every cited GS reference (Wilson 1982; Young & Ringold 1983; Sanders & Wilson 1984 all selected in glutamine‑free medium with Msx).

Verdict: Claim 1 is the most vulnerable claim. Its only arguably novel element is the "complete amino acid sequence" limitation, which is discussed in §4.

3. Claims 3 and 4 — vector and transformed host cell

These are conventional, result‑effective downstream claims. Given a DNA of claim 2, placing it in an SV40‑ or retrovirus‑based expression vector (Subramani 1981; Cepko et al., Cell 37:1053–1062, 1984 — the pZIP‑Neo SV(X) vector the applicants actually used) and transforming CHO‑K1 (ATCC CCL 61) or E. coli was routine and predictable. No separate motivation is required once claim 2 falls; the § 103 analysis collapses into claim 2.

4. Claim 2 — isolated hamster GS DNA (the contested claim)

Claim 2 requires (i) an isolated DNA, (ii) encoding the complete GS amino acid sequence, (iii) hamster GS, (iv) "comprising" the FIG. 2 sequence.

Combination D (principal § 103 combination):
Sanders & Wilson 1984 + Young & Ringold 1983 + Johnson & Piskiewicz 1985 + Gubler & Hoffmann 1983 / Huynh et al. 1985 / Vieira & Messing 1982.

• Sanders & Wilson 1984 supplies (a) a cloned CHO‑derived GS genomic sequence, (b) the restriction map, and (c) crucially, the inventors admit it was usable as a hybrid‑selection reagent: "pGS1 DNA was used to hybrid select GS mRNA." The applicants' own specification states the genomic work "was carried out as described by Sanders and Wilson (loc. cit.)." A reference that teaches the exact starting material and the exact first step of the claimed method is a powerful obviousness teaching.
• Young & Ringold 1983 plus Sanders & Wilson identify the GS mRNA as ~2.8 kb and provide the cell line (KG1MS / KG1MSC4‑M) in which it is abundant — i.e., an ideal cDNA library source.
• Johnson & Piskiewicz 1985 supplies bovine GS peptide sequence, permitting degenerate probes and confirming reading frame.
• Gubler & Hoffmann; Huynh et al.; Vieira & Messing supply the routine methodology the applicants in fact used.

Rationale/motivation: A POSITA seeking the complete GS coding sequence had a cloned homologous probe, an mRNA‑rich source, and standard library/screening methods; success was predictable with a reasonable expectation of it.

§ 102 exposure of claim 2 (worth noting): Claim 2 uses "comprising," not "consisting." If Sanders & Wilson's 8.2 kb BglII CHO fragment in fact contains the complete GS coding sequence (the applicants' own data show the complete GS minigene with one intron is only 4.75 kb, so an 8.2 kb genomic fragment is plausibly large enough), then the reference anticipates under § 102(b) — the specification's contrary statement ("this fragment does not appear to contain a complete GS gene") is a characterization, not a proven fact, and is arguably a § 102(b) admission of the fragment's existence and source. The usual 102 counter‑argument (the reference was not sequenced and no clone was deposited) is weakened because the applicants themselves demonstrated the fragment was obtainable by following Sanders & Wilson.

Legal standard. Under In re Deuel, 51 F.3d 1552 (Fed. Cir. 1995) — decided while this patent was pending — a claim to a DNA molecule defined by its amino acid sequence could survive if the prior art disclosed no method of obtaining it. That reasoning was repudiated in In re Kubin, 561 F.3d 1351 (Fed. Cir. 2009) (post‑KSR): where the protein is known or characterizable and cloning methods are routine and predictable, claims to the isolated DNA are obvious. On today's law, claim 2 is more likely than not obvious over Combination D.

5. The Hayward et al. 1986 paper — a delicate point

NAR 14:999–1008 (1986), by Hayward, Hussain, Wilson, Lyons, Woodcock, McIntosh & Harris, is described in a bibliography as "The cloning and nucleotide sequence of cDNA for an amplified glutamine synthetase gene from the Chinese hamster." That is essentially the subject matter of claim 2.

• Because it names an inventor (Wilson), it is arguably not "by others" under pre‑AIA § 102(a), and it cannot be a § 102(b) bar (filed within one year). So it is a poor statutory reference.
• However, if the paper is not the work of the same inventive entity (Wilson + Bebbington), or if it predates conception, its status changes; and in any event it is highly probative of the state of the art and of simultaneity of invention, and would be usable against the claims in an interference‑style or § 112/§ 102(g) analysis.
• Unverified: I could not confirm the precise publication date (Volume 14 spans January–April 1986); if it issued before 23 Jan. 1986 the analysis changes materially.

6. Motivation to combine — the KSR factors

1. Explicit design need, articulated in the patent itself. The Background identifies concrete failures of DHFR/MTX: only one DHFR⁻ cell line, MTX is a carcinogen, three or more rounds of amplification, and resistance arising from mutant DHFR rather than amplification. That is a textbook "identified problem" motivating the search for an alternative.
2. The solution was already generic in the art. Ringold US 4,656,134 had already claimed the class of "amplifiable genes" that complement an auxotroph and respond to an inhibitor or to withdrawal of an essential metabolite, expressly naming DHFR, CAD, metallothionein, and asparagine synthetase. GS is a member of that very class — indeed a better fit than any listed gene, because its amplification under Msx selection was already documented (Wilson 1982; Young & Ringold 1983) and its gene had already been cloned (Sanders & Wilson 1984). Substituting GS for DHFR/CAD is a substitution of one known element for another to obtain a predictable result — the core KSR rationale.
3. "Obvious to try" with a finite, predictable set of solutions. The field had a small, enumerated set of drug‑inhibitable amplifiable enzymes plus their known inhibitors (MTX/DHFR, PALA/CAD, Msx or phosphinothricin/GS). KSR, 550 U.S. at 421.
4. Reasonable expectation of success. Distinct from predictability of the result, the POSITA had: a cloned probe, an mRNA source, micro‑injection/calcium‑phosphate transformation (Graham & van der Eb 1973), SV40 vectors (Subramani 1981), and a cheap, soluble, non‑carcinogenic inhibitor (Msx).
5. No teaching away. Nothing in the art taught that endogenous GS would interfere fatally with dominant selection; to the contrary, de Saint Vincent 1981 had already demonstrated a dominant amplifiable marker (CAD/PALA) in cells carrying a functional endogenous gene.

7. Strengths of the patentee's case (and where the rejection could fail)

• The specification frames as "surprising and unexpected" that GS vectors act as dominant selectable markers in cell lines containing an active endogenous GS gene, that selection "leads almost exclusively" to amplification of the vector‑derived gene rather than the endogenous gene, and that ~500 copies/cell arose on transfection alone, rising to ~15,000 copies/cell after two rounds. If supported by the examples (FIGS. 4–5; Table 2), these are legitimate unexpected‑results arguments with nexus to claims 1–3.
• "Complete amino acid sequence." For claim 2, the patentee will argue the prior art never disclosed the complete hamster GS sequence, and that Sanders & Wilson expressly lacked a complete gene.
• Secondary considerations: the GS system (glutamine‑free medium, Msx selection) became a widely licensed industrial mammalian expression platform (Lonza/Celltech "GS System"), and US 5,827,739 is repeatedly cited as a foundational GS‑selection reference in later patents (e.g., CN 1668749A; the "attenuated glutamine synthetase as a selection marker" family, https://patents.justia.com/patent/[12173340](/patent/12173340)). Long‑felt need is well supported by the admitted DHFR⁻ bottleneck.
• Commensurability caveat: the unexpected high copy number is the strongest objective evidence, but no claim recites copy number or vector‑preferential amplification. Claims 1, 3 and 4 are conventional method/vector/cell claims; claim 2 is a sequence claim. The patentee must therefore tie the unexpected results narrowly, or the objective evidence may be discounted as not commensurate with the claim scope.

8. Bottom line

A further, non‑§ 103 vulnerability I should flag: the family includes US 5,770,359 (Celltech, "Recombinant DNA methods vectors and host cells"), described as directed to "transforming a lymphoid cell line to glutamine independence by expressing an active glutamine synthetase (GS) gene as well as a heterologous gene of interest," and US 5,591,639. US 5,770,359 issued 23 June 1998, before US 5,827,739 (27 Oct. 1998), and appears commonly owned. Claim 1 of US 5,827,739 (a genus‑level claim to conferring glutamine independence) may therefore face an obviousness‑type double‑patenting attack over the earlier‑issued sibling. I have not verified the family relationships, filing dates, or any terminal disclaimer from the sources retrieved, so treat this as a lead to check, not a conclusion.

9. Verification status — what I could not confirm

• The body of US 5,827,739's own file wrapper (examiner's § 103 rejections, applicant amendments/arguments, any affidavits under 37 C.F.R. § 1.132) was not retrieved; my analysis is de novo.
• I could not verify the publication date, page range, or content of Hayward et al., NAR 14:999–1008; the content of WO 86/06409, Kabak et al. (1978), Velkov (1982), Murray et al., MCB 3:32–43 (1983), or Kaufman et al., PNAS 83:3136 (1986) (the last of which post‑dates the priority date and is therefore not prior art).
• I did not independently verify the Anabaena glnA citation (Nature 306:337–342, 1983); it came from a secondary patent document.
• The litigation indicators on the Google Patents page (Darts‑IP family flag; Maryland District Court case 8:07‑cv‑03177) were not investigated; no inference about validity outcomes should be drawn from them.