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Patent landscape, scope, and claims summary: |
United States Patent 10,093,934 (Method for Cancer Treatment Using “Type B” L-Nucleic Acids Binding SDF-1): Claim Scope, Validity Risk, and US Patent Landscape
What claims are in US Patent 10,093,934 and what do they cover for cancer treatment?
Core claimed invention: a cancer treatment method using a “type B L-nucleic acid” that binds SDF-1, where the nucleic acid includes (i) a specific 5’ flanking sequence, (ii) SEQ ID NO:52, and (iii) a specific 3’ flanking sequence, and where the 5’ and 3’ flanking sequences hybridize to each other.
Claim-by-claim scope (practical interpretation)
Claim 1 (independent, broadest):
- Patient has cancer.
- Administer a pharmaceutically effective amount of a type B L-nucleic acid (or homolog) that binds SDF-1.
- “Type B” is structurally tied to:
- 5’ flanking sequence + SEQ ID NO:52 + 3’ flanking sequence
- and the 5’ and 3’ flanking sequences can hybridize to each other.
- This is a sequence-defined nucleic acid binding SDF-1 claim framed as a method of treatment.
Claim 2 (combination breadth):
- Adds at least one modality among:
- irradiating
- conducting surgery
- exposing to cellular therapy
- or administering a further pharmaceutically active agent.
Claims 3–8 (tumor and adjunct framing):
- Claim 3: cancer includes hematological and/or solid tumors.
- Claim 5: hematological includes leukemia or myeloma.
- Claim 6: solid tumors include a long list (glioblastoma, colorectal, breast, lymphoma, prostate, pancreatic, renal, ovarian, lung).
- Claim 4: L-nucleic acid can be adjunct with a “primary treatment.”
- Claim 7: adjunct therapy sensitizes the subject to primary treatment.
- Claim 8: primary treatment can include agents/modalities from Claim 2.
Claims 9–15 (specific drug class/agent lists as “further pharmaceutically active agent”):
- Claim 9: further agent categories include antibodies, alkylating agents, anti-metabolites, plant alkaloids, plant terpenoids, and topoisomerase inhibitors.
- Claim 10: examples include leucovorin, methotrexate, tamoxifen, sorafenib, lenalidomide, bortezomib, dexamethasone, fluorouracil (spelled “flurouracil” in text), prednisone.
- Claim 11: antibodies include rituximab, ofatumumab, cetuximab, ibritumomab-tiuxetan, tositumomab, trastuzumab, bevacizumab, alemtuzumab.
- Claim 12: alkylating agents include cisplatin, carboplatin, oxaliplatin, mechlorethamine, cyclophosphamide, chlorambucil, doxorubicin, liposomal doxorubicin, bendamustine, temozolomide, melphalan.
- Claim 13: anti-metabolites include purine analogs/antimetabolites (purineazathioprine, mercaptopurine, fludarabine, pentostatin, cladribine).
- Claim 14–15: plant terpenoids (taxanes) and topoisomerase inhibitors (camptothecin, irinotecan, mitoxantrone).
Claims 16–18 (modification and residence time):
- Claim 16: the L-nucleic acid comprises a modification.
- Claim 17: modification includes HES moiety, PEG moiety, biodegradable modifications, or combinations.
- Claim 18: modification enhances residence time in host.
Key claim construction pressure points
- “Type B L-nucleic acid” is likely to be the pivot for infringement. If “type B” maps to a particular structural motif beyond merely being an L-oligonucleotide binding SDF-1, then literal infringement requires that motif. If “type B” is broad and defined only functionally plus flanking/SEQ ID architecture, the claim can be harder to design around.
- Hybridizable flanking sequences are another pivot. If flanks must hybridize intramolecularly to form a defined structure, then different fold/thermodynamics could reduce literal or could force reliance on doctrine-of-equivalents.
- “Binds SDF-1” is functionally stated but embedded in sequence structure. That creates dual arguments:
- for infringement: binding can be read onto the sequence-defined nucleic acid
- for invalidity: binding function may be argued as inherent or predictable given known aptamer/oligo scaffolds.
What patents likely compete with or overlap US 10,093,934 in the US market?
US Patent 10,093,934 claim language is characteristic of an SDF-1 targeting nucleic-acid platform using L-nucleic acids (often positioned as “D/L aptamer-like” or nuclease-resistant oligonucleotide therapeutics). The patent landscape for such programs typically contains overlapping families covering:
- SDF-1 binding sequence sets and structural “types”
- L-nucleic acid chemical modifications (PEG, HES, biodegradable moieties)
- therapeutic uses in cancer and in combination with radiation/surgery/chemotherapy/cellular therapy
- method-of-use and adjunct-sensitization theories
However, without the patent number’s full bibliographic data (assignee, priority, publication family) and without the intrinsic record (specification embodiments, definitions of “type B,” and the claim dependency graph beyond the excerpt), a complete, accurate US-family-to-family mapping cannot be produced.
Result: no comprehensive competitor list with verified US patent numbers, expiration dates, and ownership can be stated from the provided input.
When does US 10,093,934 lose exclusivity: what is the patent expiration and exclusivity timeline?
No reliable expiration timeline can be computed from the claim text alone. A patent’s US expiration requires at minimum:
- filing date / priority claim dates
- whether any terminal disclaimer exists
- whether PTA (patent term adjustment) applies
- whether the asset has any separate regulatory exclusivity (for small molecules/biologics) which usually does not extend composition-of-matter method claims in the same way as an NDA exclusivity period.
Because the necessary bibliographic data for US 10,093,934 is not included, the timeline cannot be calculated here.
How strong are the claims of US 10,093,934 against generic or “designed-around” SDF-1 L-nucleic acids?
Strength drivers for the patentee
- The independent claim is sequence-architecture constrained (5’ flank + SEQ ID NO:52 + 3’ flank + flanks hybridize). This often gives better enforceability than purely functional binding claims.
- The claim ties not only to the binding target (SDF-1) but also to specific oligo geometry.
Strength drivers can fail if:
- “Type B” is defined broadly in the specification such that many structurally distinct L-oligos fall within “type B.”
- the SEQ ID NO:52 is not truly limiting (for example, if “homolog thereof” is interpreted broadly in prosecution history).
- the flanking hybridization condition is met by many structurally different designs via predictable Watson-Crick complementarity.
Typical design-around strategies (in this claim class)
- Change the flanking sequences so they do not hybridize to each other intramolecularly (breaking the “can hybridize” limitation).
- Use an L-nucleic acid that binds SDF-1 but lacks the specific SEQ ID NO:52 and specific flanking architecture.
- Use a different backbone (outside L-nucleic acid definition) or incorporate modifications that alter fold such that the claimed structure is not met.
- Treat SDF-1 by inhibiting downstream signaling through other agents rather than administering the claimed L-nucleic acid.
Adjudication risk: because claim 1 is tightly framed around SEQ ID NO:52 and flanking hybridization, many design-arounds target those elements. The patentee would then litigate:
- whether “homolog thereof” encompasses the design-around sequence
- whether the designed flanks still “can hybridize” (means-capable-of binding standard)
- whether binding to SDF-1 is satisfied and how that is measured.
What validity challenges could invalidate or narrow US 10,093,934?
With only the claim set, the most plausible validity issues for this type of platform patent are:
1) Prior art obviousness for nucleic-acid aptamer-like SDF-1 binding
If the art already taught:
- SDF-1-binding nucleic acids (aptamers or oligonucleotide ligands),
- L-nucleic acid nuclease-resistance,
- and common conjugate modifications (PEG, HES),
then the incremental value could be argued as an obvious combination.
The sequence architecture requirement can be attacked if it is not meaningfully distinguishing.
2) Written description and enablement for “type B” and “homolog thereof”
“Homolog” plus a “type” classification often invites arguments that:
- the specification does not enable broad homologs across a wide sequence space
- the “type B” definition is not sufficiently precise.
3) Indefiniteness risk around “type B”
If “type B L-nucleic acid” is not clearly defined in the claims and the specification does not provide an objective boundary, indefiniteness can be argued. The flanking hybridization criterion helps, but the “type B” label could still be attacked if it depends on subjective/functional criteria.
4) “Can hybridize to each other” breadth
“Can hybridize” can be construed broadly if it only requires thermodynamic feasibility rather than a defined structure in solution. That can increase infringement breadth, but it also increases invalidity exposure if prior art structures are also capable of hybridization.
What formulation, modification, and delivery claims exist and how do they affect infringement?
Claims 16–18 add specificity around modifications and residence time:
- HES moiety
- PEG moiety
- biodegradable modifications
- combinations
- residence time enhancement
Implication: If an accused product uses a non-claimed modification (different hydrophilicity/residence time strategy) and does not meet claim 16’s modification limitation (for dependent claims), infringement is narrowed to claims 1–15. The modification claims can still matter under doctrine-of-equivalents, but dependent claim limitations usually constrain scope.
What cancer indications are claimed and how does the adjunct framing change enforceability?
Indications:
- Hematological cancers: leukemia, myeloma.
- Solid tumors: glioblastoma, colorectal, breast, lymphoma, prostate, pancreatic, renal, ovarian, lung.
Adjunct framing:
- L-nucleic acid is used as adjunct therapy or part of adjunct therapy with a primary treatment.
- The adjunct sensitizes to primary treatment.
This adjunct language often creates two litigation pathways:
- Direct infringement by prescribing a regimen that includes the claimed L-nucleic acid plus a primary modality and where the regimen functions as “adjunct/sensitization.”
- Evidentiary disputes about whether clinicians intended sensitization and whether the regimen meets the functional sensitization requirement (Claim 7). Even where sensitization is not an objective measurement, the patentee can use literature and mechanism evidence to satisfy “sensitizes.”
How do the “further pharmaceutically active agents” lists impact freedom to operate?
Claims 9–15 are constrained by category and by example lists.
FTO implication:
- If an accused therapy uses the claimed L-nucleic acid plus one of the listed agents or one that fits listed categories, the secondary step limitation is likely met.
- If an accused regimen uses a different modality outside categories (for example, an immunotherapy not listed, a different class, or supportive care only), it may avoid dependent claim limitations but still potentially infringe Claim 1 or Claim 2 if those are practiced.
What FDA pathway and regulatory status issues matter for this patent class?
This patent is a method-of-treatment patent for an oligonucleotide-like agent. Patent enforcement typically turns on:
- whether an investigational product or approved product includes the claimed L-nucleic acid sequence architecture
- whether the clinical regimen practiced falls within the claimed adjunct modalities and doses
No FDA regulatory status can be assessed from the claim excerpt alone.
Key business risk assessment: what could make US 10,093,934 commercially decisive?
- If the product’s active is a type B L-nucleic acid with SEQ ID NO:52 and hybridizing flanks, then the claim is likely to read directly on the core construct.
- If the company’s regimen includes adjunct chemotherapy/radiation/surgery/cellular therapy, then dependent claims may stack.
- If the product uses HES/PEG/biodegradable modifications for residence time, then dependent claim 16–18 add additional infringement hooks.
Key Takeaways
- US 10,093,934 is a regimen and sequence-architecture patent: the independent claim requires a type B L-nucleic acid binding SDF-1 with the 5’ flanking + SEQ ID NO:52 + 3’ flanking design where flanks can hybridize.
- Dependent claims expand into adjunct oncology combinations with radiation, surgery, cellular therapy, and a broad list of standard oncology agents (including antibodies, alkylators, antimetabolites, taxanes, and topoisomerase inhibitors).
- Modification claims (HES/PEG/biodegradable) target pharmacokinetics and can tighten infringement analysis if a competitor uses different conjugates.
- Validity risk concentrates on “type B” scope, homolog breadth, and prior-art obviousness in SDF-1 binding L-nucleic acids plus common residence-time modifications.
FAQs
- How do “homolog thereof” and sequence-architecture terms affect infringement for L-nucleic acids binding SDF-1?
- What evidence is usually used to prove “sensitizes the subject to primary treatment” under an adjunct therapy claim?
- Can a different SDF-1-binding L-oligonucleotide avoid infringement if it does not include SEQ ID NO:52?
- Do PEG/HES modifications create independent infringement risk even if the cancer regimen matches Claim 1?
- How do method-of-treatment claims get enforced when the accused product is the same but the clinician regimen differs from the patented adjunct combinations?
References
- United States Patent 10,093,934 (claims provided in prompt).
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