VPS34 inhibitor 1 (Compound 19)

Catalog No.S8456 Synonyms: PIK-III analogue

For research use only.

VPS34 inhibitor 1 (Compound 19, PIK-III analogue) is a potent and selective inhibitor of VPS34 with an IC50 of 15 nM.

VPS34 inhibitor 1 (Compound 19) Chemical Structure

CAS No. 1383716-46-8

Selleck's VPS34 inhibitor 1 (Compound 19) has been cited by 5 Publications

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Biological Activity

Description VPS34 inhibitor 1 (Compound 19, PIK-III analogue) is a potent and selective inhibitor of VPS34 with an IC50 of 15 nM.
VPS34 [1]
(Cell-free assay)
15 nM
In vitro

Compound 19 is extraordinarily selective over other lipid and protein kinases. The ability of compound 19 to prevent the degradation of autophagy substrates p62, NCOA4, NBR1, NDP52, and FTH1 is similar to PIK-III. In addition, treatment of cells with compound 19 leads to an increase in the lipidated and nonlipidated forms of LC3 similar to previous reports using PIK-III[1].

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
U2OS NGrCZW9HfW6ldHnvckBie3OjeR?= MoHkNkBpenN? NX\F[GhoUW6qaXLpeIlwdiCxZjDWVHM{PCCrbjDoeY1idiCXMl;TJINmdGy|IHnuZ5Vj[XSnZDDmc5IhOiCqcoOgZpkhT0[SLV\ZWmUhemWyb4L0[ZIh\2WwZTDhd5NigSxiSVO1NF0xNjB{Nd88US=> NHnDeGg9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{NkixPVY3QSd-Mk[4NVk3Pjl:L3G+
DLD1 NFnrfIZHfW6ldHnvckBie3OjeR?= NXf1bHRSOSC2bzCxNEB2VQ>? M4rudFI1KGi{cx?= MXnJcohq[mm2aX;uJI9nKF[SU{O0JIlvKGi3bXHuJGRNTDFiY3XscJMh[XO|ZYPz[YQh[XNicILleoVvfGmxbjDv[kBPS0:DNDDwdo91\WmwIHTl[5Ji\GG2aX;uJIF1KDFidH:gNVAhfU1iaX7jeYJifGWmIH\vdkAzPCCqcoOgZpkhX2W|dHXyckBjdG:2IHHuZYx6e2m| NXTFdFZuRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMk[4NVk3PjlpPkK2PFE6PjZ7PD;hQi=>
DLD1 MVPGeY5kfGmxbjDhd5NigQ>? MX2xJJRwKDFyIIXN MljNNlQhcHK| MXzJcohq[mm2aX;uJI9nKF[SU{O0JIlvKGi3bXHuJGRNTDFiY3XscJMh[XO|ZYPz[YQh[XNicILleoVvfGmxbjDv[kBxPjJiZHXndoFl[XSrb36gZZQhOSC2bzCxNEB2VSCrbnP1ZoF1\WRiZn;yJFI1KGi{czDifUBY\XO2ZYLuJIJtd3RiYX7hcJl{cXN? NFr6ZXU9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{NkixPVY3QSd-Mk[4NVk3Pjl:L3G+
DLD1 NGDkWnVHfW6ldHnvckBie3OjeR?= M4XsflEhfG9iMUCgeW0> MYCyOEBpenN? NXPERVZiUW6qaXLpeIlwdiCxZjDWVHM{PCCrbjDoeY1idiCGTFSxJINmdGy|IHHzd4V{e2WmIHHzJJBz\X[nboTpc44hd2ZiTlLSNUBxem:2ZXnuJIRm\3KjZHH0bY9vKGG2IEGgeI8hOTBidV2gbY5kfWKjdHXkJIZweiB{NDDodpMh[nliV3XzeIVzdiCkbH;0JIFv[Wy7c3nz NV;oW3A1RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMk[4NVk3PjlpPkK2PFE6PjZ7PD;hQi=>
DLD1 M33we2Z2dmO2aX;uJIF{e2G7 NGLpXVQyKHSxIEGwJJVO MoHMNlQhcHK| NXnEe2xrUW6qaXLpeIlwdiCxZjDWVHM{PCCrbjDoeY1idiCGTFSxJINmdGy|IHHzd4V{e2WmIHHzJJBz\X[nboTpc44hd2ZiTlTQOVIheHKxdHXpckBl\We{YXTheIlwdiCjdDCxJJRwKDFyIIXNJIlv[3WkYYTl[EBnd3JiMkSgbJJ{KGK7IGfld5Rmem5iYnzveEBidmGueYPpdy=> NIfubZc9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{NkixPVY3QSd-Mk[4NVk3Pjl:L3G+
DLD1 NUjTW3hyTnWwY4Tpc44h[XO|YYm= NIGzXHAyKHSxIEGwJJVO Mlj1NlQhcHK| M1vzfWlvcGmkaYTpc44hd2ZiVmDTN|QhcW5iaIXtZY4hTEyGMTDj[YxteyCjc4Pld5Nm\CCjczDwdoV3\W62aX;uJI9nKE[WSEGgdJJwfGWrbjDk[Ydz[WSjdHnvckBifCBzIITvJFExKHWPIHnuZ5Vj[XSnZDDmc5IhOjRiaILzJIJ6KFenc4Tldo4h[myxdDDhcoFtgXOrcx?= MVy8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zPjhzOU[2PUc,OjZ6MUm2Olk9N2F-
DLD1 NHjFNoVHfW6ldHnvckBie3OjeR?= NH7LNWgyKHSxIEGwJJVO NIrD[FQzPCCqcoO= NFjOPIZKdmirYnn0bY9vKG:oIG\QV|M1KGmwIHj1cYFvKESOREGgZ4VtdHNiYYPz[ZN{\WRiYYOgbY5kemWjc3WgbY4hVEN|LUGgdJJwfGWrbjDlfJBz\XO|aX;uJIF1KDFidH:gNVAhfU1iaX7jeYJifGWmIH\vdkAzPCCqcoOgZpkhX2W|dHXyckBjdG:2IHHuZYx6e2m| M2PGbFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ4OEG5OlY6Lz5{NkixPVY3QTxxYU6=
DLD1 Mm[ySpVv[3Srb36gZZN{[Xl? NIDIcnEyKHSxIEGwJJVO MlnzNlQhcHK| NHjBepNKdmirYnn0bY9vKG:oIG\QV|M1KGmwIHj1cYFvKESOREGgZ4VtdHNiYYPz[ZN{\WRiYYOgbY5kemWjc3WgbY4hVEN|LUKgdJJwfGWrbjDlfJBz\XO|aX;uJIF1KDFidH:gNVAhfU1iaX7jeYJifGWmIH\vdkAzPCCqcoOgZpkhX2W|dHXyckBjdG:2IHHuZYx6e2m| NHfTW3U9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{NkixPVY3QSd-Mk[4NVk3Pjl:L3G+
In vivo The pharmacokinetic profile of analogue 19 is determined in C57BL/6 mice. After oral administration at 10 mg/kg, the compound is rapidly absorbed and showed moderate mean systemic clearance (30 mL/min/kg, approximately 33% of hepatic blood flow), with good oral bioavailability (F% = 47). Based on these PK parameters and the cellular activity, compound 19 constitutes a suitable candidate for in vivo studies. Upon oral administration of compound 19 at 50 mg/kg twice a day (BID) for 7 days, LC3-II accumulates consistent with reduced autophagic capacity in time-dependent manner. It inhibits autophagy in vivo[1].

Protocol (from reference)

Cell Research:[1]
  • Cell lines: U2OS cells
  • Concentrations: 0, 1, 5, 10 μM
  • Incubation Time: 24 h
  • Method: For inhibitor assay, cells are plated and the following day when cells had reached 90%, are treated with dimethyl sulfoxide (DMSO, vehicle) or the indicated concentration of PIK-III or Compound 19, both dissolved in DMSO. 24 hours later, cells are lysed in RIPA supplemented with 1% SDS and mini-EDTA protease inhibitors, homogenized by passage through a Qiashredder column and the protein is quantified by DC Lowry protein assay.
Animal Research:[1]
  • Animal Models: C57BL/6 Mice
  • Dosages: 10 mg/kg(p.o.) or 2 mg/kg(I.V.)
  • Administration: oral administration or I.V.

Solubility (25°C)

In vitro

Chemical Information

Molecular Weight 391.47


CAS No. 1383716-46-8
Storage 3 years -20°C powder
2 years -80°C in solvent
Smiles CC(C)(CNC1=NC=C(C(=N1)CC2CC2)C3=NC(=NC=C3)NC4=CC=NC=C4)O

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