P55gamma as Therapeutic Target for Aortic Dissection
Summary
The USPTO published patent application US20260091091A1 claiming p55γ as a therapeutic target for aortic dissection (AD). The inventors from China demonstrated that p55γ overexpression inhibits AD formation and elastic fiber degradation in β-aminopropionitrile fumarate (BAPN)-induced mouse models. The patent covers using p55γ as a screening target for drugs to prevent and/or treat AD.
What changed
The USPTO published patent application US20260091091A1, filed December 20, 2024, claiming p55γ protein as a therapeutic target for aortic dissection. The inventors identified that p55γ maintains phenotypic switching of vascular smooth muscle cells (VSMCs) and that manipulating p55γ expression affects AD formation and elastic fiber degradation in mouse models. The application covers methods of using p55γ to screen compounds for preventing or treating aortic dissection.
Pharmaceutical and biotech companies developing cardiovascular therapeutics should note this patent application as it establishes intellectual property claims around p55γ targeting for AD treatment. Research institutions conducting related work may want to evaluate freedom-to-operate before pursuing similar targets. No compliance actions or deadlines apply to third parties—this is an informational publication of patent claims.
Archived snapshot
Apr 2, 2026GovPing captured this document from the original source. If the source has since changed or been removed, this is the text as it existed at that time.
Use Of P55gamma As Therapeutic Target For Aortic Dissection (ad)
Application US20260091091A1 Kind: A1 Apr 02, 2026
Inventors
Chunmei CAO, Yang LI, Weiwei AN, Rilei DAI, Xun WANG
Abstract
Use of p55γ as a therapeutic target for aortic dissection (AD) is provided, belonging to the technical field of biomedicine. Over-expression of the p55γ inhibits formation of the AD and degradation of elastic fibers in mice induced by β-aminopropionitrile fumarate (BAPN); whereas knockdown of the p55γ in vascular smooth muscle cells (VSMCs) promotes the formation of the AD and the degradation of the elastic fibers induced by the BAPN. Mechanistically, the p55γ plays a role by maintaining phenotypic switching of the VSMCs, and knocking down the p55γ promotes phenotypic switching of the VSMCs from a contractile phenotype to a synthetic phenotype. The p55γ is used as a target in screening a drug for prevention and/or treatment of AD, such that a selected drug can effectively prevent and/or treat the AD, thus providing a new target for treating the AD.
CPC Classifications
A61K 38/45 A61K 48/005 A61P 9/00 C12Y 207/01153 G01N 33/6893 G01N 2333/91215
Filing Date
2024-12-20
Application No.
18989064
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