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Artemisia gmelinii (Artemisia iwayomogi) has been used in traditional medicine to cure various infectious diseases such as cholecystitis, hepatitis, and jaundice. In this study, the Artemisiae Iwayomogii Herba ethanol extract was investigated for the ability to inhibit growth of hepatocellular carcinoma and its underlying mechanism involved. The antiproliferative effect of Artemisiae Iwayomogii Herba ethanol extract was evaluated using cell viability and proliferation assays. The effect of Artemisiae Iwayomogii Herba ethanol extract on apoptosis was measured using western blotting, terminal deoxynucleotidyl transferase-mediated dUTP-biotin end labeling staining, JC-1 staining, cytochrome c release, immunohistochemistry, and immunofluorescence in ex vivo mouse xenografts. Artemisiae Iwayomogii Herba ethanol extract inhibited hepatocellular carcinoma cell growth and proliferation in a dose-dependent manner. The apoptotic effect of Artemisiae Iwayomogii Herba ethanol extract was observed via increased levels of cleaved caspase-3 and cleaved PARP, as well as elevated numbers of terminal deoxynucleotidyl transferase-mediated dUTP-biotin end labeling-positive apoptotic cells. Artemisiae Iwayomogii Herba ethanol extract also decreased XIAP and Mcl-1 expression via loss of mitochondrial membrane potential. Additionally, Artemisiae Iwayomogii Herba ethanol extract inhibited hepatocellular carcinoma cell invasion and migration. In the ex vivo model, Artemisiae Iwayomogii Herba ethanol extract significantly inhibited tumor cell proliferation and increased the number of apoptotic cells with more activated cleaved caspase-3. A mechanistic study revealed that Artemisiae Iwayomogii Herba ethanol extract effectively suppressed the PI3K/AKT/mTOR signaling pathway in hepatocellular carcinoma cells. Our findings demonstrate that Artemisiae Iwayomogii Herba ethanol extract can efficiently induce apoptosis and inhibit the growth, migration, and invasion of human hepatocellular carcinoma cells, and simultaneously block PI3K/AKT/mTOR pathway. We therefore suggest Artemisiae Iwayomogii Herba ethanol extract as a novel natural agent for prevention and therapy of hepatocellular carcinoma. [ABSTRACT FROM AUTHOR]

A group of familiar faces to Incyte watchers has broken off to start their own biotech, [ABSTRACT FROM AUTHOR]

Adlai secured $97.5 million through an IPO and private placement to fund a phase 3 trial of an ex-Novartis asset in head and neck cancer. [ABSTRACT FROM AUTHOR]

This quarter's earnings season has been full of pipeline culls and partnership terminations, with at least 3 more biotechs reporting changes today. [ABSTRACT FROM AUTHOR]

Incyte is whittling down its R&D pipeline, scrapping six discovery programs to focus on eight remaining programs. [ABSTRACT FROM AUTHOR]

After meeting with the FDA, Kyowa Kirin and MEI Pharma have stopped development of their B-cell malignancy prospect zandelisib outside of Japan. [ABSTRACT FROM AUTHOR]

The data confirm the efficacy seen in an earlier trial, but the companies need an ongoing phase 3 to deliver to get the prospect to the U.S. market. [ABSTRACT FROM AUTHOR]

Eupatilin, a major flavonoid of plants in the genus Artemisia, has been shown to exhibit anti-inflammatory, anti-oxidative, and anti-tumor effects. However, the potential anti-atherogenic effects of eupatilin and any underlyingmechanisms have not been investigated. In the present study, we sought to determine the effects of eupatilin on phenotypes induced by the growth factor PDGF-BB in human aortic smooth muscle cells. Here we show that aortic sprouting as well as PDGF-BB-induced proliferation and migration of human aortic smooth muscle cells were significantly inhibited by eupatilin.We found that eupatilin inhibited PI3K activity, causing a direct effect on phosphorylation of the downstream kinases Akt and p70S6K. In parallel, eupatilin also inhibited the phosphorylation of MKK3/6-p38 MAPK and the MKK4-JNK pathway. Moreover we found that eupatilin exhibited stronger inhibition effects on PDGF-BB-induced proliferation and migration of human aortic smooth muscle cells than PI3K, p38 MAPK, and JNK pathway inhibitors. Taken together, our results indicate that eupatilin is a potent anti-atherogenic agent that inhibits PDGF-BB-induced proliferation and migration in HASMCs as well as aortic sprouting, which is likely mediated through the attenuation of PI3K, MKK3/6, and MKK4 activation. [ABSTRACT FROM AUTHOR]

By examining an Amgen med, a new Nature study offers better understanding of the mechanism behind PI3K-delta inhibitors' immune-mediated side effects. [ABSTRACT FROM AUTHOR]

Ever since last year's annual American Association of Cancer Research (AACR) meeting, Volastra's phone has been "ringing off the hook," according to CEO Charles Hugh-Jones, M.D. [ABSTRACT FROM AUTHOR]

The follicular lymphoma market is thinning out fast. Days after Gilead pulled an accelerated approval for Zydelig in the indication, Incyte has withdrawn a submission for approval of its rival PI3K inhibitor in response to talks with the FDA about confirmatory studies. [ABSTRACT FROM AUTHOR]

Existing clot busters have one major drawback: They can block the proper functioning of platelets, thereby increasing the risk of uncontrolled bleeding. A research team led by Monash University has found a way to target platelet activation in a manner that appears to address the pathological clumping of blood. [ABSTRACT FROM AUTHOR]