HS-173

Research use only, not for human use.

HS-173 is an effective PI3Kα inhibitor (IC50: 0.8 nM).

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.

HS-173 (0.1-10 μM) reduces the cell viability in a dose- and time-dependent manner. HS-173 shows a significant drug response by the inhibition of colony formation in pancreatic cancer cells dose-dependently. HS-173 inhibits TGF-β-induced cell migration and invasion in pancreatic cancer cells. HS-173 suppresses TGF-β-induced epithelial mesenchymal transition (EMT). HS-173 treatment reduces cell viability in two hepatic stellate cell lines in a dose and time dependent manner. HS-173 induces cell cycle arrest in the G2/M phase. HS-173 treatment increases the expression of cleaved caspase-3 and decreased that of Bcl-2 in the HSC-T6 cells. HS-173 inhibits the expression of profibrotic mediators and ECM degradation modulators in HSCs. The combination of Sorafenib and HS-173 synergistically inhibits cell proliferation in pancreatic cancer cell lines. The combination of Sorafenib and HS-173 inhibits key enzymes in both RAF/MAPK and PI3K/AKT signaling pathways.

HS-173 (10 mg/kg, i.p.) significantly increases expression of TUNEL, cleaves caspase-3 along with decreased expression of PCNA in tumor tissues. HS-173 treatment decreases p-AKT and p-Smad2 in tumor tissues. HS-173 (10 and 30 mg/kg) significantly decreases the metastatic burdens on the lung and liver. HS-173 (10 and 20?mg/kg) inhibits ECM accumulation and PI3K/Akt signaling in mice with CCl4-induced liver fibrosis animal model. HS-173 clearly suppresses the expression of p-Akt and p-P70S6K along with decreasing expression of collagen I and vimentin in the mice with CCl4-induced liver fibrosis.

HS173 | HS 173 | HS-173

Cytoskeleton/Cell Adhesion Molecules

Microtubule/Tubulin

PI3Kα

Cancer

——

1276110-06-5

422.46

C21H18N4O4S

>98% (HPLC)

DMSO : ≥ 26 mg/mL. 61.54 mM

S(=O)(=O)(Nc1cc(cnc1)c1ccc2n(c1)c(cn2)C(=O)OCC)c1ccccc1

ethyl 6-(5-(phenylsulfonamido)pyridin-3-yl)imidazo[1,2-a]pyridine-3-carboxylate

(-20℃)

With Ice Pack

≥ 2 years