Vps34-PIK-III_product_DataBase

Bioactivity

Vps34-PIK-III is an orally active and selective VPS34 inhibitor (IC50=18 nM). Vps34-PIK-III effectively inhibits autophagy and can be used as a molecular tool. vps34-PIK-III is also a PI3K inhibitor that inhibits the expression of genes in liver cancer stem cells (CSCs)[1][2][3].

Invitro

Vps34-PIK-III (1, 5, 10 µM; 24 h) inhibits autophagy and LC3 lipidation in DLD1 cells[1].Vps34-PIK-III (1, 5, 10 µM; 24 h) leads to an increase in the lipidated and nonlipidated forms of LC3 in DLD1 cells[1].Vps34-PIK-III (5 µM; 24 h) significantly decreases the expression of stemness genes in HCC cells[2].Vps34-PIK-III (5 µM; 24 h) suppresses liver CSCs via AMPK activation in Huh7 and MHCC97H cells[2]. Cell Viability Assay[1] Cell Line:

In Vivo

Vps34-PIK-III (10 mg/kg; p.o.; single) rapidly absorbed and shows moderate mean systemic clearance (30 mL/min/kg, approximately 33% of hepatic blood flow), with good oral bioavailability (F% = 47)[1]. Animal Model:

Name

Vps34-PIK-III

CAS

1383716-40-2

Formula

C17H17N7

Molar Mass

319.36

Appearance

Solid

Transport

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

Reference

[1]. Honda A, et al. Potent, Selective, and Orally Bioavailable Inhibitors of VPS34 Provide Chemical Tools to Modulate Autophagy in Vivo. ACS Med Chem Lett. 2015 Nov 13;7(1):72-6. [2]. Liu F, et al. PIK3C3 regulates the expansion of liver CSCs and PIK3C3 inhibition counteracts liver cancer stem cell activity induced by PI3K inhibitor. Cell Death Dis. 2020 Jun 8;11(6):427. [3]. Dowdle WE, et al. Selective VPS34 inhibitor blocks autophagy and uncovers a role for NCOA4 in ferritin degradation and iron homeostasis in vivo. Nat Cell Biol. 2014 Nov;16(11):1069-79.

PeptideDB

Vps34-PIK-III

CAS: 1383716-40-2 F: C17H17N7 W: 319.36