Wednesday, November 1, 2023

PLGA-PEG-Azide and other polymers from PolySciTech used to create colon-targeting delivery system for treatment of ulcerative colitis

 

Ulcerative colitis is an autoimmune disease in which the body attacks parts of the colon or natural flora. Typical treatment with systemic immunosuppressants leads to significant side-effects. Researchers at University of North Carolina at Chapel Hill and University of Texas Southwestern Medical Center used PLGA (AP045), mPEG-PLGA (AK029), PLGA-CY5 (AV034) and PLGA-PEG-N3 (AI085) from PolySciTech division of Akina, Inc. (www.polyscitech.com) to create a delivery system targeting the colon and reduce autoinflammation. This research holds promise to provide improved treatment against this chronic disease. Read more: Au, Kin Man, Justin Wilson, Jenny Ting, and Andrew Wang. "An Injectable Subcutaneous Colon-Specific Immune Niche For The Treatment Of Ulcerative Colitis." bioRxiv (2023): 2023-10. https://www.biorxiv.org/content/10.1101/2023.10.03.560652.abstract

“As a chronic autoinflammatory condition, ulcerative colitis is often managed via systemic immunosuppressants. Here we show, in three mouse models of established ulcerative colitis, that a subcutaneously injected colon-specific immunosuppressive niche consisting of colon epithelial cells, decellularized colon extracellular matrix, and nanofibers functionalized with programmed death-ligand 1, CD86, a peptide mimic of transforming growth-factor-beta 1, and the immunosuppressive small molecule leflunomide, induced intestinal immunotolerance and reduced inflammation in the animals’ lower gastrointestinal tract. The bioengineered colon-specific niche triggered autoreactive-T-cell anergy and polarized pro-inflammatory macrophages via multiple immunosuppressive pathways, and prevented the infiltration of immune cells into the colon’s lamina propria, promoting the recovery of epithelial damage. The bioengineered niche also prevented colitis-associated colorectal cancer, and eliminated immune-related colitis triggered by kinase inhibitors and immune-checkpoint blockade.”

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