HS-173 - CAS 1276110-06-5
Catalog number: 1276110-06-5
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
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Description:
HS-173 is a potent PI3Kα inhibitor with potential anticancer activity. HS-173 inhibited the PI3K signaling pathway, and showed anti-proliferative effects on cancer cells. Also, HS-173 induced cell cycle arrest at the G(2)/M phase and apoptosis. In addition, HS-173 decreased the expression HIF-1α and VEGF which play an important role in angiogenesis. This effect was confirmed by the suppression of tube formation and migration assay in vitro. Furthermore, HS-173 diminished blood vessel formation in the Matrigel plug assay in mice. Therefore, HS-173 is considered as a novel drug candidate to treat cancer patients.
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Purity:
0.98
Appearance:
white to off-white solid powder
Synonyms:
HS-173; HS 173; HS173.
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Current Developer:
Inha University, Korea
1.Synergistic anticancer activity of HS-173, a novel PI3K inhibitor in combination with Sorafenib against pancreatic cancer cells.
Yun SM1, Jung KH, Lee H, Son MK, Seo JH, Yan HH, Park BH, Hong S, Hong SS. Cancer Lett. 2013 May 1;331(2):250-61. doi: 10.1016/j.canlet.2013.01.007. Epub 2013 Jan 20.
The RAF/MEK/ERK and PI3K/AKT pathways are highly implicated in the development of pancreatic cancer. The principal objective of this study was to assess the synergic effect between Sorafenib (a RAF inhibitor) and HS-173 (a novel PI3K inhibitor) to gain insight into novel therapeutic strategies for treating pancreatic cancer. We first investigated the cytotoxic effect of co-treatment with Sorafenib and HS-173 using the Calcusyn program. Combined treatment of the two drugs synergistically inhibited the viability of Panc-1 cells (combination index<1). Concomitantly, the co-treatment induced G2/M arrest and increased apoptosis with the loss of mitochondrial membrane potential. Apoptosis resulting from the co-treatment was accompanied by increased levels of cleaved caspase-3 and PARP as well as greater numbers of TUNEL-positive apoptotic cells compared to treatment with either drug alone. Furthermore, combined treatment with these drugs decreased the expression of HIF-1α and VEGF which play an important role in angiogenesis.
2.HS-173, a novel phosphatidylinositol 3-kinase (PI3K) inhibitor, has anti-tumor activity through promoting apoptosis and inhibiting angiogenesis.
Lee H1, Jung KH, Jeong Y, Hong S, Hong SS. Cancer Lett. 2013 Jan 1;328(1):152-9. doi: 10.1016/j.canlet.2012.08.020. Epub 2012 Aug 26.
We synthesized a novel imidazopyridine analogue, a PI3Kα inhibitor HS-173 and investigated anti-cancer capacity in human cancer cells. HS-173 inhibited the PI3K signaling pathway, and showed anti-proliferative effects on cancer cells. Also, HS-173 induced cell cycle arrest at the G(2)/M phase and apoptosis. In addition, HS-173 decreased the expression HIF-1α and VEGF which play an important role in angiogenesis. This effect was confirmed by the suppression of tube formation and migration assay in vitro. Furthermore, HS-173 diminished blood vessel formation in the Matrigel plug assay in mice. Therefore, HS-173 is considered as a novel drug candidate to treat cancer patients.
3.A novel imidazopyridine PI3K inhibitor with anticancer activity in non-small cell lung cancer cells.
Lee H1, Kim SJ, Jung KH, Son MK, Yan HH, Hong S, Hong SS. Oncol Rep. 2013 Aug;30(2):863-9. doi: 10.3892/or.2013.2499. Epub 2013 May 27.
Lung cancer is the leading cause of cancer-related mortality in the world, and non-small cell lung cancer (NSCLC) accounts for approximately 85% of all cases. Since more than 60% of NSCLC cases express the epidermal growth factor receptor (EGFR), EGFR tyrosine kinase inhibitors are used to treat NSCLC. However, due to the acquired resistance associated with EGFR-targeted therapy, other strategies for the treatment of NSCLC are urgently needed. Therefore, we investigated the anticancer effects of a novel phosphatidylinositol 3-kinase α (PI3Kα) inhibitor, HS-173, in human NSCLC cell lines. HS-173 demonstrated anti-proliferative effects in NSCLC cells and effectively inhibited the PI3K signaling pathway in a dose‑dependent manner. In addition, it induced cell cycle arrest at G2/M phase as well as apoptosis. Taken together, our results demonstrate that HS-173 exhibits anticancer activities, including the induction of apoptosis, by blocking the PI3K/Akt/mTOR pathway in human NSCLC cell lines.
4.A novel PI3K inhibitor alleviates fibrotic responses in fibroblasts derived from Peyronie's plaques.
Jung KH1, Ryu YL, Lee HS, Lee H, Son MK, Yan HH, Hong SW, Ryu JK, Hong S, Suh JK, Hong SS. Int J Oncol. 2013 Jun;42(6):2001-8. doi: 10.3892/ijo.2013.1905. Epub 2013 Apr 16.
Peyronie's disease (PD) is fibrosis localized in the tunica albuginea that is characterized by penile deformity and curvature. The pathogenesis of this disease remains unclear even though transforming growth factor-β (TGF-β)/smad signalling has been reported to be associated with PD. Recent studies have shown that phosphoinositide 3-kinase (PI3K)/Akt signalling regulates fibrotic responses including collagen synthesis and cell proliferation. Thus, we synthesized HS-173, a novel PI3K inhibitor, and determined whether this compound has anti-fibrotic effects on PD-derived primary fibroblasts. In this study, we found that HS-173 inhibited the growth of fibroblasts in a dose-dependent manner and induced apoptosis. In addition, HS-173 reduced the expression of α-smooth muscle actin (α-SMA), vimentin, PAI-1, fibronectin, collagen type I, collagen IV and TGF-β-activated smad2/3 in PD-derived primary fibroblasts. HS-173 blocked the PI3K/Akt signalling pathway by decreasing the activation of Akt, mTOR and P70S6K.
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CAS 1276110-06-5 HS-173

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