Q-Force (quercetin)

The most prevalent anti-cancer therapies used were lenvatinib (75% pts exposed) and nivolumab (73% pts) and the most prevalent regimen was gemcitabine/lenvatinib/oxaliplatin (33% of pts). Among repurposed agents, 50% were exposed to quercetin, 44% to celecoxib, and 14% to metformin... Patients with FLC undergo extensive molecular profiling with multiple novel therapeutic regimens being employed in real world practice. Aggregation of raw imaging scans is ongoing for central radiological review to measure depth and duration of response offered by the recorded therapeutic strategies. This dataset is a rich resource available to academic and government researchers to fuel research and define optimal treatment modalities.

P2, N=30, Recruiting, Temple University | Not yet recruiting --> Recruiting

PIM2 kinase regulates NK cell anti-myeloma activity by modulating TIGIT expression and energy metabolism.

In addition, SOD, GPX, GSR, HO-1, and Nrf2 showed decreased expression at 50 – 250 µM quercetin and OTA at IC50 value. These results suggest that quercetin may alleviate potential OTA-induced liver damage and oxidative stress through reducing cytotoxicity and enhancing the cellular antioxidant defense systems.

Kaempferol and Quercetin Dihydrate inhibit proliferation and induce apoptosis of myeloid neoplasms cells. PIM2 is an important target for the development and prognosis of acute myeloid leukemia and MDS. Kaempferol and Quercetin Dihydrate inhibit PIM2 kinase in myeloid neoplasms cells and subsequently participate in NF-κB expression, proliferation and regulation of myeloid neoplasms.

PIM2 kinase regulates NK cell anti-myeloma activity by modulating TIGIT expression and energy metabolism.Figure A.PIM2 was over expressed on NK cells from MM patients, the PIM2 kinase inhibitor improved NK cells function and decreased the expression of TIGIT. B.PIM2 kinase increased TIGIT expression on NK cell surface by up- regulated ETS-1. C.

Senolytics, such as the cocktail quercetin plus dasatinib (D+Q), show impressive effects in experimental models of pulmonary fibrosis... SOC drugs failed to trigger apoptosis in IPF senescent fibroblasts, nintedanib enhanced Bcl-2 levels and pirfenidone triggered the activation of the necroptosis pathway. SOC drugs elevated fibrotic and senescence markers in IPF lung fibroblasts. Together, these data demonstrated the inefficacy of SOC in targeting senescent cells in IPF.Funding: Cedars-Sinai Medical Center