Molecular docking confirmed that LT4 stably occupied the ATP‑binding pocket of PI3Kγ with a binding energy comparable to wortmannin and a conformation similar to antroquinonol. In conclusion, to the best of our knowledge, the present study is the first to comprehensively demonstrate the multi‑target anti‑CRC effects of LT4, highlighting its potential as a therapeutic agent, especially in KRAS‑mutant CRC.
The results revealed that 4-AAQB and erinacine A effectively suppressed breast cancer-induced osteoclastogenesis and migration, and reduced TGF-β and MMP-9 production via Erk or JNK signaling transductions, specifically in breast cancer cells or in breast cancer cells-induced osteoclasts. Based on these findings, either 4-AAQB or erinacine A showed promise in preventing breast cancer metastases in bone.
In this phase I/II trial, antroquinonol plus Gem/Nab-P showed good efficacy in survival and less adverse events than a first-line strategy of Gem/Nab-P for mPC patients. Clinical trial information: NCT03310632. >Abbreviations: mPC, metastatic pancreatic cancer; Gem/Nab-P, gemcitabine and nab-paclitaxel.#, data from U.S. FDA-approved Supplemental New Drug Application (NDA 21660/S-037) dated March 21, 2013 for paclitaxel protein-bound particles for injectable suspension (albumin-bound), 100 mg/vial.
over 2 years ago
Clinical • P1/2 data • Combination therapy • Metastases
P1/2, N=52, Active, not recruiting, Golden Biotechnology Corporation | Recruiting --> Active, not recruiting | Trial completion date: Jun 2022 --> Dec 2023 | Trial primary completion date: Jun 2022 --> Dec 2022
over 3 years ago
Enrollment closed • Trial completion date • Trial primary completion date • Combination therapy
Accordingly, to extent of our knowledge and previous studies, we demonstrated that 4-AAQB is an anti Pan-Cancer drug, and may inhibit pancreatic cancer EMT and metastasis and serve as a new therapeutic approach for patients with late-stage pancreatic cancer.
Serum or vascular endothelial growth factor (VEGF)-induced VEGF receptor 2 (VEGFR2), phosphoinositide 3-kinase (PI3K)/Ak strain transforming (Akt), and extracellular signal-regulated kinase ½ (ERK ½) phosphorylation were attenuated by 4AAQB in both PC3 and HUVEC. In conclusion, 4AAQB is a potential candidate for prostate cancer therapy.
Vascular endothelial growth factor A (VEGFA) expression, cell migration, and invasion were also inhibited by the 4-AAQB incubation. Overall, this combination treatment strategy might represent a novel approach for GEM-resistant pancreatic cancer.
4 years ago
Journal
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ABCB1 (ATP Binding Cassette Subfamily B Member 1) • ABCC1 (ATP Binding Cassette Subfamily C Member 1) • HMGB1 (High Mobility Group Box 1)
P1/2, N=52, Recruiting, Golden Biotechnology Corporation | Trial completion date: Jun 2021 --> Jun 2022 | Trial primary completion date: Jun 2021 --> Jun 2022
over 4 years ago
Clinical • Trial completion date • Trial primary completion date • Combination therapy
In summary, our findings provide strong evidence regarding the therapeutic effect of 4-AAQB on KRAS-mutant CRC cells. Furthermore, 4-AAQB effectively inhibits Ras singling in CRC cells, through which KRAS-mutant CRC can be resensitized to cetuximab.