United States Patent 10,004,792 (SEQ ID NO: 64 SLFPDSLIV) T-Cell Activation and Cancer Immunotherapy: Claim Scope, Likely Overlaps, and US Patent Landscape
US Patent 10,004,792 claims a cell-based cancer immunotherapy method centered on activated T cells that selectively recognize cancer cells presenting the peptide SLFPDSLIV (SEQ ID NO: 64) via human class I or II MEW molecules on antigen-presenting cells. The claims are written broadly across cancer indications, sourcing of T cells, activation and expansion conditions, and multiple antigen-loading routes (peptide-pulsed MEW, recombinant-virus expressing the peptide, dendritic cell/macrophage APCs), and they add composition-level adjuvant coverage.
What does US10,004,792 claim, in plain scope terms?
Core claim theme: a method for “eliciting an immune response” in a cancer patient by administering a population of activated T cells that recognize SLFPDSLIV presented by human class I or II MEW expressed on APCs. The activated T cells are generated by in vitro contacting with peptide-loaded human class I or II MEW molecules (or equivalent peptide loading on APC-expressed MEW on a cell), for a sufficient period to activate T cells.
Claim 1 sets the platform. Claims 2-18 add narrower optional limitations: autologous vs donor, T-cell source (TILs or PBMCs), in vitro activation and expansion, peptide-in-complex with class I MEW, recombinant virus expressing the peptide for APC infection, dendritic cells/macrophages, expansion in the presence of anti-CD28 and IL-12, CD8-positive cells, administration as a composition, and an adjuvant list that is unusually wide for a single patent (from TLR agonists and CpG to chemotherapeutics and biologics). Claim 15 ties the response to killing antigen-presenting cancer cells; claim 16 requires a cytotoxic T-cell response.
Indication coverage is broad and specific. Claim 1 enumerates a long list of cancers, with dependent claims calling out prostate cancer and non-small cell and small cell lung cancer.
Claim elements mapped to enforceable “design choices”
| Claim element |
What it covers |
Practical impact on accused products/processes |
| Activated T cells selectively recognizing SLFPDSLIV |
Functional recognition to a specific peptide |
Direct infringement is easier to argue if the same peptide epitope is used and results in T-cell recognition of cancer cells presenting that epitope |
| Presentation by “human class I or II MEW molecules” |
Requires peptide presentation via a specific HLA-like class I/II framework (“MEW”) |
Factual dispute likely focuses on what “MEW” corresponds to in the patentee’s system and whether the accused presentation route uses the same class I/II molecule family |
| T cells produced by contacting with peptide-loaded MEW molecules on APC surface |
In vitro activation mechanism |
If a competitor uses alternative priming (e.g., direct APC vaccination in vivo without the claimed in vitro contacting step), infringement depends on whether the method is still “producing” activated T cells by the claimed contacting |
| Recombinant virus expressing peptide (Claim 7/8) |
Alternative antigen delivery route |
Competitors using RNA/DNA vectors or peptide pulsing might avoid specific recombinant-virus steps unless they still fall within other independent claim elements |
| Expansion conditions with anti-CD28 and IL-12 |
Specific cytokine and costimulation |
Competitors using different cytokine cocktails (IL-2, IL-7/IL-15) may seek to avoid this dependent claim if the independent claim is not otherwise met |
| Composition with adjuvant (Claims 12-14) |
Broad adjuvant menu |
High overlap risk for combinations using many of the listed agents or “derivatives” (mixture of immunomodulators, chemo agents, biologics) |
| Autologous vs donor, TIL/PBMC sourcing |
Narrower operational variants |
Less likely to avoid infringement because independent claim 1 does not require a specific source |
| CD8-positive cells |
Phenotype restriction |
If competitor uses CD4-only or mixed products, it can affect dependent-claim exposure |
| Selected cancers enumerated in Claim 1 |
Indication limitation |
A competitor using the method in indications not listed can potentially avoid at least claim 1’s literal indication limitation (depending on infringement theory and claim construction) |
What does the “MEW” limitation likely do to claim breadth?
The claim uses “human class I or II MEW molecules.” The patent text you provided is claim language only; without the specification definitions and prosecution record, the term’s construction is the primary technical and legal pivot: whether “MEW” maps to a particular set of HLA alleles, a non-classical MHC family, or a specific construct name used in the patent family.
Why it matters commercially and for design-arounds
- If “MEW” is construed narrowly to particular HLA/alleles or engineered “MEW” molecules, competitors can reduce risk by using different presenting elements or peptide variants.
- If “MEW” is interpreted broadly to cover the human class I/II MHC system generally, the restriction becomes closer to “HLA class I or II peptide presentation,” increasing infringement risk across standard antigen presentation platforms.
How is the peptide SLFPDSLIV positioned relative to known epitope and neoantigen landscapes?
The claims anchor on one fixed peptide sequence: SLFPDSLIV (SEQ ID NO: 64). That makes the invention “epitope-specific” rather than “cancer-agnostic.”
Practical implication
- A competitor using any of: (i) different peptide sequences, (ii) altered anchor residues, (iii) different length peptides that bind but do not contain this exact nonamer/sequence exactly as claimed, or (iv) cross-reactive but sequence-different epitopes, can potentially evade peptide-sequence literal infringement.
- A competitor producing T cells against the same peptide but through different loading steps still risks direct infringement if the method includes the claimed “producing activated T cells by contacting with peptide-loaded human class I or II MEW on APC surface.”
What patents cover related approaches: peptide-loaded APC priming, virus-expressing peptide, and T-cell activation?
Below is the landscape logic that typically clusters around patents that overlap with US10,004,792. Without the full US patent number’s bibliographic and family data, listing specific other patent numbers would require pulling a patent database, which is not provided in the prompt. This section therefore focuses on claim-adjacent categories that, in practice, drive freedom-to-operate analysis for cell therapy manufacturing and antigen-loading workflows.
Likely overlapping patent clusters (by mechanism)
-
Peptide-pulsed APC / MHC presentation for T-cell activation
- Patents covering priming CD8 or CD4 T cells using peptide-loaded APCs.
- Typical variations: class I vs class II presentation; specific MHC molecules; dosing; activation protocols.
-
Recombinant virus expressing tumor peptides for antigen presentation
- Patents on using viral vectors to express tumor-associated peptides in APCs (dendritic cells or macrophages) to prime T cells.
- Common alternatives in competitive portfolios: adenovirus, poxvirus, lentivirus, or oncolytic viruses.
-
Expansion of activated T cells with anti-CD28 and IL-12
- IL-12-based Th1/cytotoxic skewing and anti-CD28 costimulation is a common motif.
- Patents may cover cytokine combinations, timing, and selection markers.
-
Adjuvant combinations for immunotherapy
- The adjuvant list in Claim 14 is broad and overlaps with many generic immuno-oncology combination patent themes:
- TLR agonists (CpG, poly(I:C))
- immune stimulators (GM-CSF, interferon-alpha)
- small molecules and combinations used as immunomodulators in trials (imiquimod/resiquimod, sunitinib, cyclophosphamide)
- checkpoint-unrelated but immunomodulatory agents (bevacizumab sometimes used in combination protocols)
- particulate adjuvants (PLG) and virosomes
- If the patent family has strong specification support, this claim language can create broad exposure for combination regimens.
-
Autologous TIL or PBMC derived activated T cells
- Manufacturing patents frequently claim general sourcing and activation of patient-derived T cells, which often creates cumulative infringement theories around any “activated T cells” administration protocol.
When does US10,004,792 lose exclusivity in the US?
No filing, priority, patent term adjustment (PTA), terminal disclaimer, continuation status, or maintenance history is provided. Without those facts, calculating the exact expiration date and exclusivity calendar cannot be done accurately.
What can be said from the claims alone
- This patent is a utility patent on a method of eliciting an immune response using specific antigen and activation scheme.
- There is no indication in the prompt that it has an FDA exclusivity regime akin to biologics exclusivity, since the claims are not tied to a specific branded biologic product in the information provided.
How strong is the patent estate for these claims?
From the claim draft provided, US10,004,792 is claim-structured for broad coverage within a narrow antigen anchor.
Strength indicators
- Single fixed epitope anchor (SLFPDSLIV) can be a strong evidentiary handle: infringement pivots on whether the defendant’s T cells recognize that exact peptide and whether cancer cells present it.
- Multiple operational embodiments are built into dependent claims (autologous vs donor, PBMC/TIL sources, APC types, virus infection, anti-CD28 + IL-12 expansion, adjuvants, CD8 phenotype). This increases the chance that at least one dependent claim matches a competitor’s actual protocol.
Weakness indicators
- “MEW” claim construction risk: if “MEW” is interpreted narrowly, the independent claim scope could contract sharply.
- Cancer indication list: Claim 1 requires the cancer be one of the enumerated set. If a competitor restricts use to non-listed cancers, it can avoid literal infringement for claim 1 (depending on how infringement is pleaded and whether the method is performed “in a patient who has cancer” falling in the list).
- Exact peptide sequence requirement: competitors can reduce exposure by switching to variant peptides, different lengths, or different target antigens.
What generic entry risks exist for a cell-based method patent?
There is no “generic entry” in the traditional small-molecule sense. The risk manifests as:
- Platform adoption risk: if a competitor can operationally implement the same steps, their product is “design-adjacent” even if it is biologically distinct.
- Process and combination risk: adjuvant combinations (Claim 14) and activation protocols (Claims 9, 7-8, 6) increase the number of infringement theories if competitors use standard immuno-oncology buildouts.
What patent litigation scenarios does a US10,004,792-type claim enable?
US10,004,792’s structure is consistent with two litigation models:
-
Protocol-based method infringement
- Plaintiffs focus on manufacturing and treatment steps: peptide-loaded MEW activation, expansion conditions, APC type, and administration in a patient with one of the listed cancers.
-
Combination regimen infringement
- Plaintiffs expand into adjuvant use based on Claim 12-14 when the accused therapy uses any of the listed adjuvants “selected from the group consisting of…” with “derivatives” terms broadening coverage.
For defense, common routes are:
- Avoid peptide-sequence identity.
- Change presentation machinery so “MEW” is not met.
- Use different cytokine/costimulation conditions to exit dependent claim coverage (especially anti-CD28 + IL-12).
- Restrict indication.
How does US10,004,792 compare with typical CAR-T and TCR-engineered epitope patents?
US10,004,792 is not a typical engineered receptor claim. It is closer to:
- adoptive transfer of activated T cells generated ex vivo using a peptide-MHC (MEW) presentation/priming approach.
Compared with CAR-T:
- CAR-T patents often claim chimeric receptors and vector constructs.
- US10,004,792 claims the priming and administration method tied to a specific peptide epitope and activation by peptide-loaded MEW on APCs.
Compared with TCR-T:
- TCR patents often focus on TCR sequences and engineered specificity.
- US10,004,792 focuses on functional recognition generated by contacting with peptide-loaded MEW on APC surface.
Commercially, this means US10,004,792 may collide with competitors who use “peptide-MHC stimulation to generate tumor-reactive T cells,” rather than those who engineer receptors.
What formulations are protected by US10,004,792?
The claims are not about a chemical formulation of a drug substance. The “composition” language (Claim 12) plus “adjuvant” language (Claims 13-14) indicates:
- a patient-administered cell composition (activated T cells) optionally combined with one or more adjuvants selected from a list of agents, including particulate formulations (PLG) and virosomes.
That creates exposure for combination regimens where the activated T cells are administered with any of the enumerated adjuvants.
Key takeaways
- US10,004,792 is epitope-specific around SLFPDSLIV (SEQ ID NO: 64) and claims activated T-cell generation by contacting T cells with peptide-loaded human class I or II “MEW” molecules on APC surfaces.
- Claim breadth is driven by multiple dependent claim variants covering T-cell sources, CD8 phenotype, APC types, virus-based peptide delivery, anti-CD28 + IL-12 expansion, and a wide adjuvant menu.
- The enforceability of the estate depends heavily on construction of “MEW” and the ability to prove that the accused product’s T cells recognize this exact peptide sequence and present it via the claimed class I/II MEW pathway.
- Indication limitations are explicit: the method is tied to a defined list of cancers in Claim 1, with prostate and lung subsets in dependent claims.
FAQs
1. Does US10,004,792 require autologous T cells?
No. Claim 1 covers activated T cells generally; claims 2-4 narrow to autologous cells and donor-derived variants.
2. Can a therapy avoid infringement by using a different peptide than SLFPDSLIV?
Yes, the claim is anchored to the exact amino acid sequence SLFPDSLIV (SEQ ID NO: 64).
3. What role does recombinant virus expressing the peptide play in infringement risk?
Claims 7-8 add recombinant-virus infected APCs as a dependent pathway. If a competitor does not use recombinant virus to express the peptide in APCs, those dependent claims may be avoided, but independent claim 1 may still be met if activation uses peptide-loaded MEW as claimed.
4. Do adjuvant choices create additional infringement pathways?
Yes. Claim 14 lists many specific adjuvants and “derivatives,” expanding risk if the accused cell therapy is administered with any listed agents (or derivatives) within the claimed composition context.
5. Is this patent a CAR-T or TCR-T patent?
The claims are not receptor engineering claims. They cover methods using activated T cells generated by peptide-loaded MEW/APC contacting and subsequent administration to elicit anti-cancer immune responses.
References (APA)
- United States Patent 10,004,792. (Claims excerpt provided in prompt).
