US Patent 11,752,199: Scope, Claim Architecture, and US Patent Landscape for VCAM-1 / Angiopoietin-2–Linked Adrenal Corticotropin Therapy
What is covered by US 11,752,199 (substance and claim logic)?
US 11,752,199 claims a biomarker-driven method for promoting new vessel formation in a subject by adrenal corticotropin (ACTH) treatment that increases specific endothelial/angiogenic markers, namely VCAM-1 and angiopoietin-2 (Ang-2), within defined timing windows.
Core claim concept
Across the independent claim (and near-identical independent claim format in claim 8), the method is defined by three elements:
- Biological effect (functional purpose): “promoting new vessel formation in a subject in need thereof”
- Intervention: “administering an adrenal corticotropin treatment”
- Mechanistic biomarker requirement: “wherein VCAM-1 expression and angiopoietin-2 expression is increased” (timed and, in certain claims, tied to “after 3 weeks”)
The claims progressively narrow into:
- Specific formulation: repository corticotropin injection (RCI)
- Specific composition: naturally sourced complex mixture of ACTH analogs and pituitary peptides
- Specific molecular species within that mixture: N-25 deamidated porcine ACTH (1-39)
- Specific dosing regimen: 30–150 U/m2 daily for 2–3 weeks, with tapering
- Specific expression timing: peak VCAM-1 and Ang-2 after 3 weeks
Claim set mapped to narrowing
| Claim |
Type |
Added scope limiter |
Scope impact |
| 1 |
Independent |
VCAM-1 and Ang-2 are increased after adrenal corticotropin treatment |
Establishes biomarker-defined efficacy; broad over disease/indication and over dosing/form beyond generic “adrenal corticotropin treatment” |
| 2 |
Dependent |
Treatment comprises RCI |
Limits to a particular ACTH drug product class (RCI) |
| 3 |
Dependent |
RCI is naturally sourced complex mixture of ACTH analogs + other pituitary peptides |
Narrows composition to “mixture” rather than a single synthetic peptide |
| 4 |
Dependent |
RCI comprises N-25 deamidated porcine ACTH (1-39) |
Narrows to a named component of RCI |
| 5 |
Dependent |
30–150 U/m2 daily over 2–3 weeks |
Narrows dosing window materially |
| 6 |
Dependent |
daily dose tapered over a 2-week period |
Narrows regimen design |
| 7 |
Dependent |
“peak” VCAM-1 and Ang-2 after 3 weeks |
Introduces timing of peak expression (stricter than mere increase) |
| 8 |
Independent |
VCAM-1 and Ang-2 increased following 3 weeks administering adrenal corticotropin |
Independent claim tied to 3-week timing |
| 9–11 |
Dependent |
microvessel isolation, staining, counting vessels per mm2 |
Converts “promotion” into measurable histomorphometric steps |
| 12 |
Dependent |
“maximum” Ang-2 expression reached after 3 weeks |
Tightens timing for Ang-2 |
How broad is the scope across formulation, dosage, and biomarker timing?
The patent’s claim architecture creates two main layers of breadth.
Layer 1: Intervention breadth
- Claim 1/8: “adrenal corticotropin treatment” (generic ACTH treatment concept).
- Claims 2–4: narrow to RCI and then to a specific porcine deamidated ACTH species within the RCI mixture.
Layer 2: Biomarker and timing breadth
- Claim 1: “VCAM-1 expression and angiopoietin-2 expression is increased after administering” (timing not fixed in the claim text you provided).
- Claim 8: biomarker increase is tied to after 3 weeks.
- Claims 7 and 12: peak VCAM-1/Ang-2 timing and maximum Ang-2 timing are both pinned to 3 weeks.
What “promotion of new vessel formation” does in claim scope
The method is framed functionally, but the claims also require biomarker shifts. Claims 9–11 further anchor the “promotion” step to quantification:
- isolating a microvessel
- staining
- counting “increased number of vessels per square mm”
That supports enforceability because it reduces vagueness around how “new vessel formation” is verified, even if the upstream independent claims already include biomarker proof.
Claim-by-claim scope translation into enforceability risk
Below is how each claim element constrains a potential infringer.
Claim 1
Potential infringement trigger:
- A method where a subject receives adrenal corticotropin and, after administration, shows increased VCAM-1 and increased Ang-2 expression.
Most likely non-infringement leverage:
- Avoid both biomarkers or show no coordinated increase in both VCAM-1 and Ang-2.
- Use a different endocrine treatment not characterized as “adrenal corticotropin.”
Claim 2
Adds that the corticotropin treatment is RCI.
Claim 3
Adds that RCI is a naturally sourced complex mixture of ACTH analogs and other pituitary peptides.
Claim 4
Adds that RCI comprises N-25 deamidated porcine ACTH (1-39).
Most likely “design-around” leverage:
Using an ACTH formulation that lacks the specific mixture characterization or lacks that named component, assuming claim construction follows literal reading.
Claims 5–7
These add dosing regimen constraints:
- 30–150 U/m2 daily
- for 2–3 weeks
- with tapering over a 2-week period
- and “peak” biomarker expression after 3 weeks
Most likely “design-around” leverage:
Use different dosing units, route/formulation, or timing such that peaks occur earlier or later than 3 weeks.
Claim 8
Independent claim that is tighter on timing:
- Biomarkers increased following 3 weeks of administering adrenal corticotropin.
Claims 9–11
Adds downstream experimental steps tied to microvessel quantification:
- isolation, staining, counting vessels per mm2.
Potential non-infringement leverage:
If a party achieves the same biomarker shift but does not perform the microvessel isolation/staining/counting steps in the claimed way, those dependent claims may not be met. The independent claims still matter if they rely only on biomarkers.
Claim 12
Tightens Ang-2 timing: maximum Ang-2 expression after 3 weeks.
What is the patent landscape implication for ACTH-based angiogenesis claims in the US?
Given only the claim text you provided, the enforceable “landscape” in the US hinges on how other patents define:
- the same or overlapping mechanism biomarkers (VCAM-1 and Ang-2),
- the same drug form (RCI vs synthetic ACTH),
- and the same time-and-dose regimen.
Key landscape axes
| Axis |
US 11,752,199 position |
Landscape pressure point |
| Mechanism biomarker |
requires both VCAM-1 and Ang-2 increases |
Competing patents that target Ang-2 alone or VCAM-1 alone may fall outside, depending on claim wording |
| Timing |
“after 3 weeks” and “peak/max after 3 weeks” in multiple claims |
Other methods with different time courses are harder to read onto the independent claim 8/dep 7/12 |
| Product/formulation |
includes RCI and specifies component N-25 deamidated porcine ACTH (1-39) in claims 2–4 |
Patents on different ACTH formulations may avoid 2–4 but still risk claims 1/8 if they are still “adrenal corticotropin” and generate the same biomarker increases |
| Evidence readout |
includes optional microvessel isolation/staining/counting |
Histology/endpoint patents may either complement or create overlaps in practice if they rely on similar steps |
Where infringement exposure is highest (most probable overlap zones)
The highest overlap with US 11,752,199 occurs where a program:
- administers ACTH/RCI to a subject population,
- measures endothelial adhesion molecule and angiogenic signaling with an observed increase in both VCAM-1 and Ang-2, and
- does so on a schedule producing peak/max at about 3 weeks.
Most likely “high-risk” execution patterns
- Protocols using RCI and tracking endothelial activation markers before and after a 3-week induction.
- Regimens within 30–150 U/m2 daily and tapering strategies that still deliver maximal biomarker changes at about the 3-week mark.
- Experimental or clinical studies reporting microvascular density and tying it to those biomarker changes.
What is the most plausible scope dispute space (where claims tend to narrow in practice)?
The text provided creates distinct claim construction pressure points:
-
What counts as “VCAM-1 expression” and “angiopoietin-2 expression”
- The claims are expression-focused but do not specify measurement modality in the text you supplied. Disputes typically turn on what assays qualify as “expression,” and whether “increased” means statistically significant, relative fold change, or any detectable rise.
-
What counts as “after 3 weeks of administering”
- Timing precision often becomes outcome-determinative. Programs measuring at 21 days but analyzing earlier/later could be litigated against the “after 3 weeks” constraint.
-
Whether “adrenal corticotropin treatment” covers all ACTH forms
- Claims 1/8 are broader; 2–4 are narrower to RCI and a named component. That creates a two-tier infringement map.
-
Whether “promoting new vessel formation” is inherently met if biomarkers rise
- Independent claims link vessel formation to biomarker increase. If biomarkers rise without demonstrable vessel formation, defendants may contest the functional “promoting” requirement (though dependent claims 9–11 create measurable support when vessel counts are performed).
How to read the claim set as a commercial IP position
US 11,752,199 is not just an ACTH method claim. It is a biomarker-defined angiogenesis induction claim with:
- drug identity narrowing (RCI; porcine N-25 deamidated ACTH (1-39)),
- regimen narrowing (dose, duration, tapering),
- and timing narrowing (peak and maximum at 3 weeks),
followed by optional evidentiary histology steps.
That structure supports licensing or enforcement by allowing multiple claim pathways:
- broad pathway via claims 1 and 8 if a biomarker signature matches,
- narrow pathway via claims 2–4 and 5–7 if specific RCI composition and dosing regimen are used,
- and evidentiary pathway via claims 9–11 if the study performs microvessel counting.
Key Takeaways
- US 11,752,199 claims an ACTH-based method for promoting new vessel formation defined by increased VCAM-1 and angiopoietin-2 expression.
- Independent claim 8 locks the biomarker increase to “after 3 weeks,” while dependent claims also lock peak/max timing to 3 weeks.
- Claims 2–4 narrow to RCI and further to N-25 deamidated porcine ACTH (1-39), creating a product-formulation-specific infringement zone.
- Claims 5–7 narrow dosing to 30–150 U/m2 daily for 2–3 weeks with tapering, and require biomarker peak after about 3 weeks.
- Claims 9–11 optionally ground “new vessel formation” in microvessel isolation, staining, and vessel counting per mm2, strengthening enforceability where histology endpoints are measured.
FAQs
1) Does US 11,752,199 require a specific disease indication?
No indication limitation appears in the claim text you provided. The method is framed for a “subject in need thereof.”
2) What biomarkers are mandatory in the claimed method?
Both VCAM-1 expression and angiopoietin-2 expression must increase as claimed.
3) Is the 3-week timing required in all claims?
No. Claim 8 requires biomarker increase after 3 weeks. Other claims (like claim 1 in your text) state “after administering” without a fixed 3-week requirement, while dependent claims 7 and 12 specify peak/max after 3 weeks.
4) Does the patent cover repository corticotropin injection only, or broader ACTH?
It covers broader “adrenal corticotropin treatment” in independent claim 1/8, and separately narrows to RCI in dependent claim 2 onward.
5) Can microvessel counting avoid infringement?
Microvessel isolation/staining/vessel counting appears in dependent claims 9–11. Avoiding those steps may reduce risk for those dependent claims, but it does not negate independent-claim exposure if biomarker increases still occur as claimed.
References
[1] United States Patent Application/Patent No. 11,752,199. (Claim text as provided by user: claims 1–12).
