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|BeyondSpring Strengthens Intellectual Property Portfolio with Newly Granted U.S. Patent for Plinabulin|
The patent covers administering Plinabulin for treatment methods by which the brain tumor is metastatic, anaplastic astrocytoma, glioblastoma multiforme, oligodendroglioma, ependymomas or a combination thereof, with patent protection until 2036. Dr.
Plinabulin already has 69 patents granted in 34 countries, covering composition of matter and usage, among which 13 patents granted in the U.S. The composition of matter patent for Plinabulin is valid through 2025, with potential to extend five years to 2030.
“BeyondSpring has a robust patent portfolio surrounding Plinabulin, and the issuance of this latest patent extends our proprietary rights and further reinforces our global intellectual property position for our lead product,” said Dr. Huang. “Brain tumors represent a severe unmet medical need, especially metastatic brain cancer, for which the median overall survival for patients is 4.2 months. If Plinabulin can slow down metastasis to the brain, then this is an enormous contribution to the medical community.”
Plinabulin is currently in Phase 3 clinical development for the prevention of chemotherapy-induced neutropenia and as an anticancer therapy in non-small cell lung cancer.
Plinabulin, a small molecule derived from a marine fermentation product (phenylahistin), is BeyondSpring’s lead asset and is currently in late-stage clinical development for the prevention of chemotherapy-induced neutropenia (CIN) and as an anticancer therapy in non-small cell lung cancer (NSCLC). In addition to direct cytotoxic effects leading to tumor cell death, studies of Plinabulin's mechanism of action indicate that following tubulin binding, Plinabulin activates GEF-H1, a guanine nucleotide exchange factor. GEF-H1 affects downstream molecular pathways leading to increased dendritic cell maturation and antigen induced T-cell activation. With regard to CIN, nonclinical testing indicates that Plinabulin releases a chemotherapy induced block in the differentiation of bone marrow cells into neutrophils, allowing for a reduction in the incidence and duration of neutropenia.
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