US 11402392

I'll search for authoritative information on US 11402392, including any 2026 litigation activity.

Let me run more targeted searches.

Let me try more targeted queries.

Summary: US 11,402,392 B2

Important scope note up front: I could not find any CAFC 2026 docket activity, or any litigation/PTAB record, tied to US 11,402,392. Searches for the number returned hits for different patents that merely share the "'392" short form (e.g., U.S. 10,193,392 wireless power transfer, Scramoge v. Apple/Volkswagen IPRs; U.S. 9,083,204; U.S. 5,869,392 "Kimura"). Per your instruction, I am not reporting those as results for 11,402,392. Likewise, the authoritative full text you supplied does not include the granted claims section — it is specification text that ends mid-sentence ("the present disclo…"). So my claim overview below is inferred from the specification's stated aspects and numbered embodiments, not read from the granted claim set, and is flagged accordingly.

Bibliographic data (high confidence — consistent across the Google Patents full text, Justia, and FreePatentsOnline)

Related family members appearing in the record: US 11,635,440 B2 (from 17/843,470), US 2023/0341421 A1 (from 18/305,586), and EP 3788062 A1 ("Methods of diagnosing and treating based on site-specific tau phosphorylation"). A confirmatory NIH license and reassignment to "WASHINGTON UNIVERSITY" (2022-06-09) appear in the assignment records; note that one assignor entry is literally recorded as "BATMAN, RANDALL" — I am reporting that string as it appears and not auto-correcting it, though it is almost certainly a typo for Bateman.

Abstract (as given in the authoritative record)

The patent relates to quantifying tau phosphorylation at specific amino acid residues (notably T181, T205, and T217) in an isolated tau sample from a subject, optionally with total tau, to predict time to onset of mild cognitive impairment (MCI) due to Alzheimer's disease (AD), stage subjects, guide treatment decisions, select subjects for clinical trials, and evaluate therapeutic efficacy, using deviations from a control population without brain amyloid plaques (defined by PET imaging and/or Aβ42/40 in CSF).

Plain-language overview of the independent claims

Caveat: the granted claims were not in the material provided. The following describes the independent claim(s) as they read in the specification's claim-style passages and numbered embodiments; treat exact claim wording as unverified.

The patent's independent claims are treatment claims (as the title signals — "Methods of treating…"). The specification's own articulations of the concept include:

1. Core treating method (the apparent Claim 1-type subject matter): A method for treating a subject in need thereof, comprising:

• (a) providing an isolated tau sample obtained from the subject and measuring tau phosphorylation at one or more residue selected from T181, T205 and T217, and optionally measuring total tau; and
• (b) administering a pharmaceutical composition to the subject when the measured phosphorylation level(s) "significantly deviate from the mean" in a control population without brain amyloid plaques (as measured by PET imaging and/or Aβ42/40 in CSF).
• "Significantly deviate from the mean" is expressly defined as at least 1σ, preferably ≥1.3σ, more preferably ≥1.5σ, and even more preferably ≥2σ above or below the mean.

1. Ratio-based treating method (variants): Same as above but computing a ratio — either between phosphorylation sites (e.g., p-T217/p-T205, p-T181/p-T205, p-T181/p-T217) or between a phospho-site and total tau (e.g., p-T217/total tau, p-T205/total tau, p-T181/total tau) — and administering when the ratio meets specified σ thresholds.

2. Two-sample / longitudinal treating method: Providing a first and second isolated tau sample (collected at different times), measuring phosphorylation at (i) T181 and T205, (ii) T217 and T205, or (iii) T181, T217 and T205, optionally total tau; calculating the change; and administering a pharmaceutical composition when phosphorylation at T181 and/or T217 decreases or stays the same while phosphorylation at T205 (and optionally total tau) increases.

3. Threshold/progression-oriented variants: Administering when p-T217 and/or p-T181 is about 1.5σ or above (in some embodiments 2σ or above) while p-T205 is about 1.5σ or below (in some embodiments 2σ or below) — correlating with roughly 10–25 years (or 10–20 years) from onset of MCI due to AD in the disclosed model; and variants where the sites are about 15 years or less / about 10 years or less from onset.

Supporting specification content the claims draw on: treatment/staging timing figures (p-T217 first deviates ~21 years, p-T181 ~19 years, total tau ~17 years, p-T205 ~13 years before onset); a disclosed example control-population percentage-of-tau ratio of pT181 = 21.7 ± 2.3, pT205 = 0.34 ± 0.13, pT217 = 1.2 ± 0.66 (Table 3, mutation non-carriers); and a defined CSF amyloid cut-off of Aβ42/40 < 0.12 by mass spectrometry (Patterson et al., Annals of Neurology, 2015).

What I could not verify

• Exact granted claim language and claim count for US 11,402,392 — the provided authoritative text omits the claims. My overview is reconstructive and should be confirmed against the USPTO Patent Center / Google Patents "Claims" tab before being relied on.
• No CAFC 2026 docket, district court case, or IPR/PGR involving US 11,402,392 was found in the searches performed (search date April 26, 2026). Absence of results is not proof of absence — I recommend a direct check of the CAFC docket (e.g., PACER/CAFC CM-ECF) and USPTO PTAB/Patent Center for this specific number.
• The earlier pre-grant publication surface (e.g., US 2020/0400689, US 2022/0317136) appeared in results for the same family title; those are separate documents and not the granted patent.

I'll search for litigation involving US patent 11402392.

Let me try more targeted searches on litigation databases.

Let me try more specific litigation-database searches.

Summary answer

No litigation involving U.S. Patent No. 11,402,392 ("the '392 patent") was found in the sources I was able to search. I could not identify any district court case (including D. Del., E.D. Tex., W.D. Tex., C.D. Cal., or N.D. Ill.), any ITC Section 337 investigation, any IPR/PGR petition, or any CAFC appeal in which the '392 patent is the patent-in-suit or a patent-in-controversy.

What I searched and what I found

I want to be explicit about a limitation, per your instruction not to fabricate: the absence of search hits is not affirmative proof that no suit exists, but I have no grounded evidence of any case, and I am not willing to invent party names, case numbers, or filing dates.

Important caveats on identifier precision (as instructed)

• I did not auto-correct identifiers. A very large fraction of false-positive results in these searches involved different patents sharing a partial number, e.g.:
  • U.S. Patent No. 11,447,023 ('023 patent, The NOCO Company v. Winplus North America, C.D. Cal. 8:23-cv-00269) — not the patent you asked about.
  • U.S. Patent No. 10,193,392 (Apple v. Scramoge Technology, IPR2022-00529) — not relevant.
  • U.S. Patent No. 10,215,392 (Golight Inc. v. Feniex Industries, 1:23-cv-01186) — not relevant.
  • U.S. Patent No. RE43,023 / 9,233,023 (Alcon/LenSx litigation) — not relevant.
  • JP 11402392 A (Japanese published application, EPO Global Patent Index) — not the same identifier.
• Accordingly, none of these are reported as litigation against US 11,402,392.

Patent context (from the document you supplied, for the enforcement analysis)

• Patent: US 11,402,392 B2, "Methods of treating based on site-specific tau phosphorylation."
• Assignee: Washington University in St. Louis (WUSTL). Inventors: Nicolas Barthelemy, Randall Bateman, Eric McDade.
• Application: US 17/368,403, filed 2021-07-06 (continuation-family member); granted/publication date: 2022-08-02.
• Priority: PCT/US2019/030725 (WO2019213612A1); the Google Patents record lists a 2018-05-03 prior-art date and a 2019-05-03 PCT priority claim. Anticipated expiration: 2039-05-03.
• Related US family members identified in the record: US 11,635,440 B2 (from US 17/843,470) and US 20230341421 A1 (from US 18/305,586) — relevant if you are monitoring the family for enforcement, since a plaintiff might assert a sibling patent rather than the '392 patent itself.
• Government interest: a confirmatory license to the National Institutes of Health was recorded 2023-12-06 (assigned from Washington University). This is a licensing record, not litigation.
• Subject matter: mass-spectrometry (IP-MS/PRM) measurement of site-specific tau phosphorylation (T111, S113, T181, S199, S202, S208, T153, T175, T205, S214, T217, T231) with diagnostic, staging, treatment, and clinical-trial-enrollment claims.

Recommended next steps to verify

Because litigation coverage is incomplete in general web indexes, and because WUSTL's tau portfolio has been commercially relevant (WUSTL's tau/Aβ assets have been associated with its spinout C2N Diagnostics, though I found no litigation tying C2N to this patent), I'd confirm through:

1. PACER / CourtListener RECAP — full-text search for "11,402,392" and "11402392," and for "Barthelemy" / "Bateman" / "McDade" as inventors.
2. Unified Patents Portal (portal.unifiedpatents.com/litigation) — patent-number lookup, which indexes district court and PTAB records.
3. USPTO Patent Center / Assignment and PTAB — check for IPR/PGR petitions naming the '392 patent, and for any assignments or exclusive licenses (e.g., to a diagnostics company) that would signal enforcement intent.
4. Docket Navigator / Lex Machina — patent-level litigation reports (paywalled; most reliable for litigation history).
5. ITC EDIS — search Section 337 investigations for the patent number.

If you'd like, I can run additional targeted searches (e.g., a specific docket/party name, or the sibling patent 11,635,440) if you can share a candidate plaintiff, defendant, or district.

Proceedings overview

Total AIA trial proceedings on file for US 11,402,392: zero. The structured "PTAB proceedings on file" block — sourced from the USPTO Open Data Portal — returns no IPR, PGR, CBM, or derivation proceeding for this patent, and targeted web searching (petitioner names, the patent number in both 11,402,392 and "11402392" forms, assignee "Washington University," and the family member US 11,635,440) surfaced no AIA trial in which this patent was the challenged patent, the patent owner, or otherwise involved. Searching the number in the PTAB/CAFC corpus returns only unrelated patents that share the "'392" short form (e.g., 10,193,392, 5,869,392, 11,381,285) — I am not reporting those as results for this patent.

Breakdown by status: active 0 / claims invalidated 0 / claims sustained 0 / settled 0 / institution denied 0 / appeals 0.

Bottom line for a defendant: there is no PTAB roadmap and no PTAB estoppel. Nothing about this patent has been canceled, and nothing has been blessed as patentable either. The patent is best described as untested rather than hardened — WUSTL has never had to defend it at the Board. That is a two-edged signal: no precedent exists to help you, but also no institution-denial history or FWD that would let the patent owner claim the claims have survived scrutiny. (I also confirm the caveat from the prior section: the authoritative text supplied for this patent is specification text that ends mid-sentence and does not include the granted claim set, so I cannot enumerate claim numbers here. Do not rely on my reconstructive claim overview; pull the issued claims from USPTO Patent Center first.)

Per-proceeding detail

No proceedings to report

• Type: n/a
• Filed: n/a
• Status: The canonical structured field reads, verbatim: "The USPTO ODP API returns no AIA trial proceedings for this patent as of the most recent ingest."
• Judge panel: n/a
• Petition grounds: n/a
• Institution decision: n/a
• Final Written Decision: none issued — so there is no claim-level disposition to quote, and I will not characterize any claim as canceled, confirmed, or construed.
• Settlement / termination: n/a
• Appeal: no FWD and no rehearing/Director Review decision exists to appeal; no CAFC docket tied to this patent was identified.
• Defensive value: Neutral-to-favorable for a defendant today. You cannot free-ride on someone else's win, but you also inherit zero § 315(e) estoppel and a patent whose claims have never been tested under the lower (preponderance) PTAB standard.

Verification caveat (stated plainly): the absence of results is not proof of absence. The ODP ingest can lag newly filed petitions by weeks, and petitions are conventionally not public until a Notice of Filing Date Accorded issues. Before relying on "no PTAB activity" in a client memo, check the PTAB E2E docket directly for this patent number at https://ptab.uspto.gov and search CourtListener at https://www.courtlistener.com/?q=%2211%2C402%2C392%22. I could not complete a fully exhaustive docket-by-docket sweep within the search budget available.

Strategic summary

Claim-by-claim status — CANCELED / SUSTAINED / UNTESTED. Every claim of US 11,402,392 is UNTESTED. There are no canceled claims (no FWD), no claims sustained (no FWD or institution-denial decision on the merits reaching patentability), and therefore no "surviving claims" list to give you. Contrast this with the family's litigation-adjacent reality: the patents in this portfolio are licensed by WUSTL to C2N Diagnostics (per the published author disclosures, which state that tests using these phosphorylation-site methods are licensed to C2N and that Bateman and the University hold equity in C2N). That means the realistic assertion scenario is a competitor diagnostics/lab-developed-test company facing a WUSTL licensee or WUSTL itself — and the assertion target is filing claims not present in your source text, which I cannot confirm. Confirm the claim set before building any invalidity theory.

Estoppel landscape. Because no IPR/PGR was ever instituted, § 315(e)(2) estoppel is empty — no petitioner, and no privy of any petitioner, is barred from any ground. For a defendant now being asserted against: every § 102 and § 103 ground based on patents and printed publications remains available, both at the Board and in district court. Two clocks matter, and neither appears to have started:

• § 315(b) — the one-year bar runs from service of a complaint alleging infringement of this patent. I found no complaint asserting it, so the bar is not triggered and an IPR can be filed at any time.
• § 315(a)(1) — filing a DJ action of invalidity first bars a later IPR by that party. If you are contemplating both, file the IPR first or coordinate counsel.

Note that the patent estate here is government-funded (the record carries an NIH confirmatory license and a "government has certain rights" statement), and the patent owner is a private university — so there is no Eleventh Amendment sovereign-immunity obstacle to institution, and no state-actor immunity argument available to WUSTL.

Pattern signals. No petitioner has filed even once, so there is no General Plastic / follow-on-petition problem for a first mover; the Board's § 314(a)/§ 325(d) discretion will be exercised on a clean slate. There is no defensive aggregator (no Unified Patents-type petitioner) anywhere in the chain. The patent owner has no PTAB appeal history on this patent, so no read on how aggressively WUSTL litigates at the Board. Institution policy under the current Director's discretionary-denial briefing regime (see e.g. Dabico Airport Sols. Inc. v. AXA Power ApS, IPR2025-00408, Paper 21 (PTAB June 18, 2025), designated Jan. 9, 2026, weighing patent age/settled expectations; and Revno Techs., Inc. v. Cerebrum Sensor Techs., Inc., IPR2025-00632, Paper 20 (Director Nov. 3, 2025), precedential) means merits strength is doing more work again — a strong § 103 petition against a 2018-priority biomarker claim is the right posture, not a purely procedural one.

One portfolio-level warning. This patent is a continuation (17/368,403, filed 2021-07-06, priority 2018-05-03 via PCT/US2019/030725 / WO 2019/213612 A1) and the family is active: US 11,635,440 B2 (from 17/843,470), US 2023/0341421 A1 (from 18/305,586), and EP 3788062 A1 all appear in the record. Invalidating US 11,402,392 alone may not clear your freedom to operate — a sibling with materially similar claims may be waiting behind it. No PTAB activity surfaced on 11,635,440 either, so the same clean-slate analysis applies there.

Recommended next steps

1. Do not yet treat "no PTAB activity" as final. Re-verify against PTAB E2E (https://ptab.uspto.gov) and the ODP AIA-trial endpoint for US 11,402,392, and check whether any newly accorded petition has issued a Notice of Filing Date. If a petition has recently been filed by a third party, the § 315(b) joinder route (§ 315(c)) could let you ride an instituted trial — that option disappears if the first petition is denied.
2. Obtain the granted claims. The source text provided omits the claim set entirely; nothing in this report should be used to characterize claim scope or claim numbers. Pull the issued claims and the file history (prosecution history estoppel and any applicant statements about σ-thresholds or the T205/T217 directionality limitation will be prime § 112 and claim-construction ammunition — the specification's own embodiments recite thresholds like "above 1.5σ," "above 2σ," and "below 1.5σ," which invites indefiniteness and written-description attacks).
3. Pre-2018-05-03 art is the battleground. The claims have a 2018-05-03 priority date. CSF p-tau181 assays were commercially established well before then, and the specification itself frames the advance as site-specific stoichiometry rather than tau measurement generally — so build the § 103 case around what a POSA already knew about phosphorylated-tau measurement as of May 2018. (Flag: I did not verify specific references; treat this as a search strategy, not a validity opinion.) Note the inventors' own Barthélemy et al. J. Exp. Med. 2020 paper and the 2020 Janelidze/Palmqvist/Karikari/Thijssen plasma p-tau literature are after the priority date and therefore not § 102/103 art against this patent.
4. If you are a defendant, there is no FWD to link to and no canceled claim to quote — the honest answer is that the patent's claims are all live and all unadjudicated. Budget for a first-filed IPR (with a Fintiv/Sotera stipulation if you are also in district court litigation) rather than looking for a shortcut.
5. Monitor the siblings. Set docket and prosecution alerts on US 11,635,440, US 2023/0341421, and EP 3788062 — a PTAB or EPO outcome on any of them is the best available early read on how this family fares under adversarial scrutiny.

I'll research the assignment record for US 11,402,392 before drafting.

The generic searches returned irrelevant hits. Let me query more specifically.

Let me try to pull the specific assignment PDFs and the USPTO record directly.

Assignment & Ownership Reconstruction — US 11,402,392 B2

Scope caveat, stated up front (important): I was able to retrieve the events in the ownership chain from the authoritative Google Patents legal-events record you supplied and from corroborating full-text sources, but I could not retrieve the reel/frame numbers, execution dates, or correspondent data from USPTO Assignment Center within this session (the assignment PDFs for application 17/368,403 did not surface in indexed search, and USPTO Assignment Center itself is not directly queryable by this tool). Per your constraints, I am not fabricating reel/frame numbers or correspondent names; every field I could not verify is marked [not retrieved] with the exact verification step in the "How to verify" note. Nothing below should be treated as a substitute for a direct Assignment Center pull.

Inventors

Pattern notes:

• No fire-sale / mass-departure pattern. All three inventors were WashU personnel, and WashU remained the applicant and assignee throughout. A university inventor moving to the university's own commercialization spin-out (C2N) is the opposite of the portfolio-fire-sale tell; it is a classic academic tech-transfer signature.
• Inventorship differs across the family. The conflict-of-interest disclosure attached to a related WashU publication (DZNE record 163710, PDF p.5) names "Drs. Barthelemy, Bateman, McDade and Sato and other inventors" as beneficiaries of the licensed WashU IP. Sato is not an inventor on US 11,402,392 — so inventorship is not uniform across the family (see also US 11,085,935, US 11,635,440, US 2023/0341421, US 12,493,043). Worth flagging in any inventorship/standing diligence.
• Recorded name anomaly (carried over from the earlier section): the assignment record lists an assignor literally as "BATMAN, RANDALL". That string is reported as recorded; it is almost certainly a typo for Bateman, but I have not auto-corrected it. If real, it is a chain-of-title defect to flag (an assignment executed by a "Batman" who is not a named inventor).

Original assignee

Washington University in St. Louis (WUSTL) — a private research university, not a product company.

• Product embodying the claims? WashU itself ships no product. The technology has been licensed for commercialization, evidently to C2N Diagnostics, a WashU spin-out in St. Louis. C2N commercializes the PrecivityAD2 blood test, the flagship analyte of which is plasma p-tau217 — i.e., squarely within the T217 subject matter of this patent. Evidence: the DZNE-hosted WashU conflict-of-interest disclosure (record 163710, DZNE-2022-00449, p.5) states WashU IP including "Methods of diagnosing AD with phosphorylation changes" "can be or is licensed," that licensing income may flow to Barthelemy, Bateman, McDade and Sato, that the IP is "being licensed ... to C2N," and that "Dr. Holtzman and the University have a financial investment in C2N." Treat this as a disclosure in a scientific paper, not a USPTO record — no license was found recorded in the chain.
• Primary line of business: academic research and technology transfer (WashU Office of Technology Management).
• Current status: operating, not acquired, not dissolved, not in bankruptcy.

Assignment timeline

The Google Patents legal-events record (from the authoritative text) shows the following recorded events. Reel/frame, execution dates, and correspondent fields could not be retrieved and are marked accordingly. I list them in the order and with the language the record uses.

• 2021-07-06 (application filed) / recorded 2021-07-06 — Reel [not retrieved]

  • Conveyance: Application filed by / initial ownership
  • Assignor: n/a (applicant filing)
  • Assignee: Washington University in St. Louis (WUSTL)
  • Correspondent: [not retrieved]
  • Context: US continuation 17/368,403 filed by the university applicant, claiming priority to PCT/US2019/030725 (priority 2018-05-03). Not a transfer.

• 2022-06-09 (executed date [not retrieved]) / recorded 2022-06-09 — Reel [not retrieved]

  • Conveyance: Assignment (record labeled "reassignment"; substance = inventor → university)
  • Assignor: BATMAN, RANDALL and BARTHELEMY, Nicolas
  • Assignee: WASHINGTON UNIVERSITY
  • Correspondent: [not retrieved] — if a firm name recurs here across the sibling patents (11,085,935 / 11,635,440 / 12,493,043), flag it; I could not confirm recurrence in this session.
  • Context: Internal/intake confirmation — formalization of the inventors' pre-existing assignment obligation to their university employer; no change of beneficial owner.

• 2022-06-09 (executed date [not retrieved]) / recorded 2022-06-09 — Reel [not retrieved]

  • Conveyance: Assignment (record labeled "reassignment")
  • Assignor: MCDADE, Eric
  • Assignee: WASHINGTON UNIVERSITY
  • Correspondent: [not retrieved]
  • Context: Same as above — separate instrument covering the third inventor.

• 2022-06-09 (executed date [not retrieved]) / recorded 2022-06-09 — Reel [not retrieved]

  • Conveyance: Assignment (record labeled "reassignment")
  • Assignor: BATMAN, RANDALL and BARTHELEMY, Nicolas (this entry appears a second time in the Google Patents legal-events list)
  • Assignee: WASHINGTON UNIVERSITY
  • Correspondent: [not retrieved]
  • Context: Second/duplicate recording — likely the same instrument re-recorded against a sibling application in the family, a correction, or a duplicate indexing entry. This duplication is a data-quality flag, not evidence of a new transfer. Confirm at Assignment Center whether two distinct reel/frames exist or whether it is an indexing artifact.

• 2022-08-02 — patent issued to Washington University. Not an assignment.

• 2023-12-06 (executed date [not retrieved]) / recorded 2023-12-06 — Reel [not retrieved]

  • Conveyance: Confirmatory License (record labeled "reassignment")
  • Assignor: WASHINGTON UNIVERSITY
  • Assignee: NATIONAL INSTITUTES OF HEALTH (NIH), U.S. DEPT. OF HEALTH AND HUMAN SERVICES (DHHS), U.S. GOVERNMENT
  • Correspondent: [not retrieved]
  • Context: Bayh-Dole confirmatory license — NOT an ownership transfer. The U.S. Government (via NIH funding) takes a nonexclusive, nontransferable, irrevocable, paid-up license and march-in rights (35 U.S.C. § 202(c)(4)). This record is typically filed when the contractor executes an assignment/exclusive license or files/records the patent. Its practical significance here: it is a marker that WashU executed a covered instrument (commonly an exclusive license) in late 2023 — consistent with, but not proof of, the C2N commercialization license.

Summary of ownership: the patent has never left the original assignee (WashU). There is no recorded transfer to any LLC, aggregator, or asserter, and no recorded post-issuance change of beneficial ownership.

Timeline diagram

timeline
    title Ownership of US 11402392
    2018 : Priority application filed
    2019 : PCT application filed by Washington University
    2021 : US 17 368 403 filed as continuation
    2022 : Inventors assign rights to Washington University
         : US 11402392 issues to Washington University
    2023 : NIH confirmatory license recorded

NPE / troll-pattern signals

Verdict

Insufficient data — with the affirmative finding that there is no NPE pattern here.

I am forced into "Insufficient data" strictly because the verdict taxonomy's NPE buckets all require a transfer-to-asserter event that does not exist, "Defensive / non-asserting" requires termination at a defensive aggregator (not met — the NIH confirmatory license is a government-interest record, not a defensive aggregator), and "Operating-company assertion" requires the owner to be shipping a product and suing competitors (not met — WashU ships nothing and asserts nothing). The substantive conclusion is stronger than the label: all recorded events — the 2022-06-09 inventor→WASHINGTON UNIVERSITY assignments and the 2023-12-06 WASHINGTON UNIVERSITY→NIH confirmatory license — keep or confirm ownership in the original academic assignee, with no transfer to any LLC, aggregator, or known asserter. What I could not verify is the reel/frame-level detail (reel/frame, execution date, correspondent), and that gap is the sole reason for the label.

How to verify (2 minutes, closes the gap):

1. Go to https://assignmentcenter.uspto.gov/ → search by patent number 11402392 (and cross-check application 17/368,403).
2. For each of the 3 records dated 2022-06-09 and the 1 record dated 2023-12-06, capture Reel/Frame, Execution Date, and Correspondent.
3. See whether the third 2022-06-09 record is a genuinely distinct reel/frame or a duplicate indexing entry.
4. Pull the recorded confirmatory license document text — it sometimes identifies the exclusive licensee (expected: C2N Diagnostics) and would convert the §7 finding from "unclear" to confirmed.
5. Optionally repeat for siblings 11,085,935 / 11,635,440 / 12,493,043 — if any of those shows a transfer away from WashU, that would materially change the family-level picture.

I'll research the prior-art citations for US 11,402,392, focusing on the patent's own citation record (front-page references, "Patent Citations" and "Non-Patent Citations" on Google Patents / USPTO).

Let me try more specific queries to surface the actual citation lists on the patent's face.

Let me try to reach the patent's own front-page citation record via FreePatentsOnline and Justia.

Prior-Art Analysis — US 11,402,392 B2

"Methods of treating based on site-specific tau phosphorylation"
Priority: 2018-05-03 (PCT/US2019/030725 → WO 2019/213612 A1) | App. 17/368,403, filed 2021-07-06 | Granted 2022-08-02 | Assignee: Washington University in St. Louis | Inventors: Barthelemy, Bateman, McDade

0. Method, and three caveats you should read first

What I actually retrieved. I could not query USPTO Patent Center / PAIR directly, and the authoritative full text supplied earlier omits the front-page citation lists (it ends mid-sentence at "the present disclo…"). The citation record below is taken from mirrors that reproduce the USPTO (56) "References Cited" data — Justia Patents (patents.justia.com/patent/11402392, "Referenced Cited" section) and FreePatentsOnline — which agree on the U.S. and foreign document lists. Verify against the granted patent's printed front page before relying on it.

Caveat 1 — claim numbering is only partly verified. Earlier sections flagged that the granted claims were unavailable. I can now add one hard data point: the Justia claim text for 11402392 recites "28. The method of claim 15, wherein the isolated tau sample is a composition comprising tau, wherein tau has been purified from [blood or CSF]…" This confirms claims 15 and 28 exist and that 28 depends on 15. Beyond that, claim numbering in this analysis is inferred from the specification's claim-style passages. I flag every § 102 mapping accordingly.

Caveat 2 — "cited reference" ≠ "prior art." Under AIA § 102, a reference must (i) predate the 2018-05-03 effective filing date and (ii) be "by another." A very large fraction of this list is the applicant's own work (Bateman/Holtzman/WUSTL) and at least one entry is a same-family member. Those are cited for enablement/background, not because they anticipate.

Caveat 3 — false positives excluded. Consistent with the earlier sections, I excluded hits for other patents sharing partial numbers. One was especially seductive: a PTAB filing against a Quanterix "'092 patent" (Quanterix/Simoa single-molecule assays; parent app. 14/111,326) — not US 11,402,392. Excluded.

1. U.S. Patent Documents cited on the face of US 11,402,392

(Dates as listed by Justia. Titles are given where I am confident; otherwise marked "title not retrieved" — I will not invent them.)

2. Foreign patent documents cited

Note: the patent's own priority document, WO 2019/213612 A1 (2019-11-07), does not appear in its own citation list — correctly, since it is the priority application.

3. Non-patent literature cited

The NPL list is long (≈60 journal articles). Because the authoritative full text supplied omitted it, I recovered the comparable list from the sibling publication US 2022/0317136 A1 (same disclosure, same family) and cross-checked titles against the text. Treat the exact per-reference mapping to the '392 patent as unverified.

The NPL citations cluster into five groups:

(a) Site-specific tau phosphorylation / phospho-profiling (the only genuinely § 102-relevant cluster)

• Kimura, T., Sharma, G., Ishiguro, K. & Hisanaga, S.-i. (2018). "Phospho-Tau Bar Code: Analysis of Phosphoisotypes of Tau and Its Application to Tauopathy." Front. Neurosci. 12:44. → Published before 2018-05-03 → § 102(a)(1) printed publication. Directly addresses isomer-resolved tau phospho-profiling. This is the single most dangerous NPL citation for any claim drawn to "measuring site-specific tau phosphorylation."
• Neddens, J. et al. (2018). "Phosphorylation of different tau sites during progression of Alzheimer's disease." Acta Neuropathol. Commun. 6:52. → § 102(a)(1) if published before 2018-05-03 (a 2018 volume). Speaks directly to disease-stage-dependent phosphorylation at different sites — i.e., the staging concept. Anticipates nothing in the control-population/treatment limitations, but is strong § 103 art against any staging claim.
• Russell, C. L. et al. (2016). "Comprehensive Quantitative Profiling of Tau and Phosphorylated Tau Peptides in Cerebrospinal Fluid by Mass Spectrometry." J. Alzheimers Dis. 55:303-313. → Pre-critical-date. MS quantification of CSF p-tau peptides, including unmodified/phospho pairs. The closest anticipation candidate for any claim limited to "quantifying p-tau vs. total tau in CSF by MS."
• Mair, W. et al. (2016). "FLEXITau: Quantifying Post-translational Modifications of Tau Protein In Vitro and in Human Disease." Anal. Chem. 88:3704-3714. → Pre-critical-date MS stoichiometry of tau PTMs. Same limited anticipation exposure as Russell.
• Hanger, D. P. et al. (1998). "New phosphorylation sites identified in hyperphosphorylated tau… using nanoelectrospray mass spectrometry." J. Neurochem. 71:2465-2476. → Very early MS phospho-site mapping. § 102(a)(1) art but far narrower. No anticipation of the asserted combination.
• Matsuo, E. S. et al. (1994). Neuron 13:989-1002; Köpke et al. (1993) J. Biol. Chem. 268:24374; Liu et al. (1993) J. Neurosci. Res. 34:371; Bramblett et al. (1993) Neuron 10:1080; Grundke-Iqbal et al. (1986) JBC 261:6084. → Classical groundwork establishing that AD tau is hyperphosphorylated at specific residues. Background only.
• Hu, W. T. et al. (2013). "Reduced CSF p-Tau181 to Tau ratio is a biomarker for FTLD-TDP." Neurology 81:1945-1952. → Explicitly discloses a p-Tau181 : Tau ratio in CSF as a biomarker. This is the most structurally similar prior disclosure to the claimed ratio embodiments and deserves a full-text § 102/§ 103 review. It is directed at FTLD-TDP differential diagnosis, not amyloid-negative Alzheimer's staging, so it does not anticipate CL-1/CL-15.
• Ittner, A. et al. (2016). "Site-specific phosphorylation of tau inhibits amyloid-β toxicity in Alzheimer's mice." Science 354:904-908. → Site-specific phospho-function. Background/§ 103.
• Iqbal et al. (2005); Medina & Avila (2015); Wang & Mandelkow (2016); Malia et al. (2016) (AT8 epitope); Karch et al. (2012); Kanmert et al. (2015); Saman et al. (2012); Thomas et al. (2012). → Background on tau pathology, epitope mapping, secretion/truncation, methylation/ubiquitination.

(b) Kinetic / SILK platform and AD progression modelling (applicant's own domain)

• Sato, C., Barthélemy, N. R. et al. (2018). "Tau Kinetics in Neurons and the Human Central Nervous System." Neuron 97:1284-1298 (pub. 2018-03-21 → pre-critical-date). Inventor-authored. Relevant to measuring tau metabolism; does not disclose the claimed stratification/treatment rule.
• Xiong et al. (2016); Toledo et al. (2013); Mawuenyega-style metabolism work; McDade et al. (2018); Maia et al. (2013); Potter et al. (2013).

(c) DIAD/DIAN clinical and imaging cohort references

• Morris et al. (2012, DIAN network); Storandt et al. (2014); Ryman et al. (2014); Ridha et al. (2006); Quiroz et al. (2013, 2018); Lim et al. (2016); Gordon/Jack (A/T/N, NIA-AA framework 2018); Schöll et al. (2016); Villemagne et al. (2015); Su et al. (2015); Price & Morris (1991, 1999); Qian et al. (2017). → These underpin the clinical framing (preclinical AD, symptom-onset timing) and are § 103 material, not anticipatory.

(d) Analytical/statistical methods

• Peterson, A. C. et al. (2012). "Parallel Reaction Monitoring for High Resolution and High Mass Accuracy Quantitative, Targeted Proteomics." Mol. Cell. Proteomics 11:1475-1488. → Discloses the PRM technique used in the patent's Examples. Anticipates no claim on its own, but combined with (a)-group art it is the natural § 103 backbone for any claim reciting PRM.
• Luo et al. (2015) (bivariate correlation in family-clustered studies); Morris, J. C. (1993) (CDR); Folstein et al. (1975) (MMSE).

(e) Amyloid/Aβ biomarker references

• Klunk (2004) PiB-PET and Fagan (2006) CSF Aβ42 — cited in the specification for the amyloid-positivity definitions; also Vandermeeren et al. (1993) (tau sandwich ELISA). → Define the control-population construct the claims rely on; the prior art establishes amyloid status can be determined, but does not teach the claimed use of it as the normalizing denominator for phospho-site thresholds.

4. Bottom line: what the citation record actually shows

1. No cited reference anticipates the independent treatment claims (CL-1/CL-15) as I have reconstructed them. Anticipation requires one reference disclosing all elements — (i) an isolated tau sample, (ii) measurement at T181/T205/T217 ± total tau, (iii) the deviation-from-control-population criterion, (iv) the control population defined by absence of brain amyloid plaques as measured by PET and/or Aβ42/40 in CSF, and (v) administration of a pharmaceutical composition. The cited patent art is almost entirely (a) WUSTL isotope-kinetics filings or (b) generic anti-tau antibody/biomarker filings; neither delivers (iii)+(iv).

2. The citation list is dominated by the applicant's own prior work. Roughly half of the U.S. entries (U1, U3, U4, U5, U9–U16, U20, U22, U23) and three of the eleven WO entries (F2, F5, F7, F11) are Bateman/Holtzman/WUSTL. Under § 102(b)(2)(C) (common ownership) and, for U5/U22, identical inventive entity, these are materially weakened as § 102 art. Any invalidity theory built on them must be an obviousness theory with careful attention to the § 102(b)(2)(C) exception.

3. The real § 102 exposure sits in the NPL, not the patent citations. In descending order of threat:

• Kimura et al. 2018 (Phospho-Tau Bar Code) — pre-critical-date, isomer-resolved tau phospho-profiling.
• Russell et al. 2016 and Mair et al. 2016 (FLEXITau) — pre-critical-date MS quantification of phospho/unphospho tau peptide pairs.
• Neddens et al. 2018 — stage-dependent phospho-site changes.
• Hu et al. 2013 — CSF p-Tau181 : Tau ratio as a biomarker (the closest structural analogue to the claimed ratio embodiments).
  Each of these is a serious § 102/§ 103 reference for a narrowed claim (single-site measurement, or MS p-tau/u-tau quantification), and none reaches the full independent-claim combination. I have not verified the exact publication dates of the 2018-dated NPL items against the 2018-05-03 critical date in every case — this should be checked, since a publication date after 2018-05-03 removes § 102(a)(1) effect.

1. Flagged contradictions/updates to the earlier sections.

• Earlier sections stated the claim set was unavailable and that the overview was "reconstructive." This is now partly resolved: claims 15 and 28 are confirmed to exist, with claim 28 depending on claim 15 and adding the "purified from blood or CSF" limitation. The reconstructive overview is otherwise unchanged.
• Earlier sections found no litigation. My searches surfaced a PTAB proceeding against a Quanterix "'092 patent" and an Apple/Scramoge IPR against US 10,193,392 — both are different patents and are not reported here as activity involving US 11,402,392. Note that the anomaly is consistent with the earlier sections' caution about "'392"/"'023" short-form collisions.

1. Not verified / do not rely on without checking:

• The dates and effective filing dates of US 2018/0372720 A1 (Wildburger) needed for the § 102(a)(2) analysis.
• Titles for U8, U10, F3, F4, F6, F8, F9, F10 (listed as "title not retrieved").
• The exact NPL list of the '392 patent itself (I used the sibling US 2022/0317136 A1 list as a proxy).
• Whether any of the cited applications were copending/commonly owned at the relevant time, which controls the § 102(b)(2)(C) analysis.

If you can supply the granted claim set (or the file-wrapper IDS/892 forms), I can convert the "claim mapping" column from conditional to definitive and run a proper element-by-element § 102 chart against the top five NPL references.

I'll ground this analysis in actual prior-art references. Note up front: the authoritative text you supplied contains no explicit "Prior Art" section (the specification text ends mid-sentence), so I'll use the references the patent itself cites, plus the closest art I can find in searches, and flag where the record is incomplete.

Important: the search surfaced the actual granted claim sets of the sibling patent US 2022/0317136 (issued as US 11,635,440). Let me verify the granted claims of US 11,402,392 itself and pin down the key prior-art dates.

The record now shows the granted claim sets are "selecting a therapeutic agent" claims. Let me pin down the key prior-art dates and the actual granted claims of the '392 patent.

Obviousness Analysis — US 11,402,392 B2 (35 U.S.C. § 103)

0. Two record problems I must flag before analyzing

(a) The "Prior Art section" was not supplied. The task instructs me to "[u]se the results from the Prior Art section of this page." The authoritative full text you provided contains no "Prior Art" section — it is specification text that terminates mid-sentence ("the present disclo…"), and no prior-art search-result set was included in this prompt. I therefore built the analysis from (i) the references the patent itself cites in its specification/IDF (these are the closest thing to an on-record prior-art list for this document) and (ii) art I located by search. Where I rely on (ii), I say so.

(b) Contradiction with the earlier-generated sections. The earlier "Patent summary" section asserted that the '392's independent claims are (a) measure T181/T205/T217 → (b) administer when the level(s) significantly deviate from the mean, and that claim 1 was the "diagnosing" construct. The search record now shows the granted claims are "selecting a therapeutic agent" claims with express σ thresholds, in three independent-claim tiers. I flag this as a correction: the earlier claim characterization was reconstructive and is superseded by what follows.

1. The claims to be analyzed (as best established; verify against USPTO Patent Center)

Source: Justia's reproduction of the US 11,402,392 grant (patents.justia.com/patent/11402392) and the sibling US 2022/0317136/US 11,635,440.

The independent claims are methods for selecting a therapeutic agent comprising, substantively:

1. (a) providing an isolated tau sample from a subject and measuring tau phosphorylation at T205 together with T181 and/or T217 (in certain independent claims, plus at least one further site selected from T111, T153, S208, T231); and
2. (b) administering a therapeutic agent, wherein:
   • (i) T181 and/or T217 deviates from the mean of a control population without brain amyloid plaques (PET and/or Aβ42/40 in CSF) and T205 does not deviate → the agent prevents amyloid deposition from increasing or reduces existing plaque load; or
   • (ii) T181 and/or T217 deviates AND T205 deviates → the agent prevents amyloid deposition, reduces plaque load, prevents tau aggregation, or targets NFTs.

Dependents: the 1.5σ above / below thresholds (claims 4–9, 18–23); PET imaging as the diagnostic test (claims 3, 17); a very long Markush list of therapeutic agents (claim 10/24); kinase inhibitor / phosphatase activator (11–12); blood vs. CSF sample (13–14).

Caveat: the search layer returned overlapping claim text for the '392 and its sibling '11,635,440, so I cannot guarantee which independent-claim tier is literally "claim 1" of the '392. The substance above is stable across the family, but the exact claim numbering must be confirmed.

2. Legal framework

The '392 has an earliest effective filing date (EFD) of 2018-05-03 (PCT/US2019/030725; WO 2019/213612), so the AIA § 102/§ 103 regime governs. Obviousness requires (1) a teaching/suggestion/motivation to combine, (2) a reasonable expectation of success, and (3) all claim elements in the combination — KSR Int'l v. Teleflex, 550 U.S. 398 (2007); In re Kahn. A reference can be § 102(a)(2) art if it was effectively filed before the EFD even though it published later.

3. The prior-art picture (with § 102 status)

The grace-period/provisional-support issue — this drives the whole analysis

The specific insight the claims monetize — that p-T181 and p-T217 move first and in the opposite direction to p-T205 later, and that p-T205 rises after total tau — is not in R1. It appears in R8 (Nov 2017) and R9 (July 2018), both authored by the named inventors. R8 falls inside the grace period (excepted); R9 falls after the EFD (not art at all). If, however, the 2018-05-03 provisional does not support the staging/σ subject matter (a real risk — the provisional is not in the record I have), then the EFD for those claims slides to 2019-05-03, R9 becomes § 102(a)(1) prior art, and the position changes materially. Determine the provisional number and its disclosure before relying on any non-obviousness argument.

Also note: the family's own WO 2019/213612 (published 2019-11-07) is not prior art against the '392 (common family/after EFD). But a JP examiner (JP 2024513401A) used that very publication ("Washington Univ/612") as the closest art and reasoned that extending it to further tauopathy strata "would have been obvious … as determined through routine testing," showing how a national office treats the generic concept.

4. Grounds of rejection under § 103

Ground I — R1 (Barthélemy 2015) + R3 (Kolb '492) [+ R6]

Attacks claims 1–3, 4–14, and the T205+T217/total-tau tiers.

Motivation to combine (explicit in the art, not hindsight):

• R1 itself supplies the motivation: it closes by stating the MS method brings "new perspectives for AD diagnosis, therapy targeting and monitoring." An express "therapy targeting" cue in the primary reference is the paradigm KSR "design incentive."
• R3 supplies the therapeutic step and the patient-selection logic — it is a selection method ("determining whether a subject is suitable for anti-p217+tau antibody therapy") coupled to an administering step. Substituting the analytically superior MS read-out of R1 for R3's immunoassay read-out is a mere substitution of one known measurement technique for another to obtain the same information (KSR; In re Merck).
• Both references are in the same field (CSF tau biomarkers for AD) and address the same problem (identifying the right patients early enough to intervene), satisfying KSR's "interrelated teachings" rationale.
• Reasonable expectation of success is high: R1 already reports the discriminating performance; the only remaining step — treating a diagnosed AD-spectrum subject — is the ordinary practice of medicine (In re Kao).

Predicted scope of the rejection: the broad § (ii) tier (T181/T217 deviate and T205 deviates → administer any listed agent) is the most exposed. It reduces to "measure CSF p-tau at two/three known sites in a subject with elevated CSF p-tau and give an AD drug," which R1 + routine practice appears to render obvious.

Ground II — R1 + R2 + R3, further in view of the specification's own admissions

Attacks the additional-site tiers (T111, T153, S208, T231) and claims 10–12 (agent Markush / kinase inhibitor / phosphatase activator).

• The '392 admits that tau "can occur at over 80 different residues" and lists the therapeutic classes as known ("cholinesterase inhibitor… NMDA receptor antagonist… anti-Aβ antibody, an anti-tau antibody…"). Admissions in the specification are available as prior art (In re Nomiya).
• R1's MS platform inherently monitors multiple phospho-sites simultaneously; adding T153/T231 (which the patent's own FIG. 10 shows in CSF) or T111/S208 to the panel is routine panel expansion with a predictable benefit ("a finite number of identified, predictable solutions," KSR).
• Selecting a kinase inhibitor (e.g., GSK-3β, CDK5, MARK — all named in the family's own disclosure as the relevant tau kinases) or a PP2A phosphatase activator as the "therapeutic agent" is obvious to try against a tau-hyperphosphorylation target.

Ground III — the σ thresholds (claims 4–9, 18–23) are obvious as a matter of law

"[A]bout 1.5σ or above … and 1.5σ below" a control-population mean is the definitional statistical cut-off, and the specification itself recites a continuous range (1σ, 1.3σ, 1.5σ, 2σ, 2.5σ) — a classic "result-effective variable" optimized by routine experimentation (In re Aller; In re Boesch). Where a claim recites a numerical limitation and the specification presents it as a mere range, the burden shifts to applicant to show criticality. The claim's own parenthetical ("σ is the standard deviation defined by the normal distribution … in a control population without brain amyloid plaques") is a claim-drafting convention, not an inventive contribution.

Ground IV — the "control population without brain amyloid plaques as measured by PET imaging and/or Aβ42/40 in CSF" limitation

Taught by R6 (Klunk 2004 PiB-PET SUVR; Fagan 2006 CSF Aβ42; Patterson 2015 Aβ42/40 <0.12 by MS) — all cited inside the '392's own specification. Using the normal amyloid-negative cohort as the statistical reference population is the obvious baseline for any biomarker study.

Ground V — "selecting a therapeutic agent" as a claim category

Once R1 establishes the site-specific read-out and R3 establishes that p-tau status can select therapy, choosing the therapeutic agent from the known formulary based on the measured profile is the standard "treat-to-target" clinical paradigm; there is no new chemistry, no new mechanism, and no unexpected potency. KSR ("if a technique has been used to improve one device … a person of ordinary skill in the art would recognize that it would be obvious to use that technique with other devices"). Note in parallel that these claims are method-of-treatment claims with a diagnostic-selection step, so they will also attract § 101 Mayo scrutiny — a separate validity risk worth tracking, though outside this § 103 brief.

5. Counterarguments the applicant would (and should) press — and where they likely prevail

1. The asymptotic/ordered pattern is the invention, and it is the inventors' own post-priority work. R1 (2015) discloses that different sites change to different degrees in symptomatic AD (a static snapshot) — it does not disclose that pT205 rises at a different, later disease stage than pT181/pT217, nor that pT181/pT217 later decline. That asymmetry is what makes the § (i) tier ("T205 not deviating while T181/T217 deviate → give a plaque-reducing agent") a genuinely new staging logic. That disclosure originates in R8 (Nov 2017, within grace period) and R9 (July 2018, post-EFD) — neither is art. This is the strongest non-obviousness position, and it rests on the EFD holding at 2018-05-03.
2. Opposite-direction changes are unexpected. R1's own datum that S199 is hypophosphorylated while T217 is hyperphosphorylated, and the later observation that pT181/pT217 fall while pT205 rises, cut against the a priori expectation of uniform, monotonic hyperphosphorylation. A PHOSITA starting from the "hyperphosphorylated tau aggregates in NFTs" model would not have predicted site-discordant, stage-discordant dynamics (In re Soni — unexpected results).
3. The § (ii) tier is the weak flank — expect the applicant to defend on § (i) and the thresholds. If I were the examiner, I would press Strawman / KSR on the "(both deviate) → treat" tier while conceding the "(T205 does not deviate) → treat" tier needs R8/R9 or a very aggressive reading of R1.
4. Double-patenting overlap. The '392 and its siblings (US 11,635,440, from 17/843,470; US 2023/0341421 A1, from 18/305,586) share a specification and overlapping claim scope. Even if the § 103 rejection fails, obviousness-type double patenting is a standing exposure for the family.

6. Bottom line

• Strongest § 103 combination: Barthélemy 2015 (R1) + Kolb '492 (R3), optionally + Klunk 2004/Fagan 2006/Patterson 2015 (R6). R1 supplies every measurement limitation of claim 1's step (a) (T181/T205/T217 by MS in CSF) and the explicit "therapy targeting" motivation; R3 supplies the administering step and the patient-selection logic; R6 supplies the amyloid-negative control-population definition. Expect this combination to render the § (ii) tier and the additional-site tiers prima facie obvious.
• The decisive vulnerability is temporal, not technical. The claim set's distinctive content — the T205-vs-T181/T217 stage asymmetry and σ cut-offs — traces to the inventors' own Nov 2017 and July 2018 disclosures. If the 2018-05-03 provisional supports that content, § 102(b)(1)(A) removes R8 and R9 is not art, and the § (i) tier and threshold claims plausibly survive § 103. If it does not support that content, R9 becomes § 102(a)(1) art against an EFD of 2019-05-03, and the entire claim set becomes substantially weaker.
• Highest-value verification steps: (1) pull the granted claim set from USPTO Patent Center (the record I have is reconstructive); (2) obtain the 2018-05-03 provisional and map its disclosure against the staging/σ subject matter; (3) pull the full Kolb '492 priority chain (its 2018-03-05 provisional) to confirm § 102(a)(2) status; (4) check the file history for any § 103 rejection actually made and how it was overcome (the answer may already be on the record).

What I could not verify (stated rather than fabricated): the exact granted claim numbering/wording of the '392; the provisional application number and its content; the full Kolb '492 priority chain beyond the 2018-03-05 effective filing date shown by Google Patents/RPX; and whether any prior art beyond the specification's own citation list was cited during prosecution. No "Prior Art section" was present in the source document supplied.