Catalog No.S1072

ZSTK474 Chemical Structure

Molecular Weight(MW): 417.41

ZSTK474 inhibits class I PI3K isoforms with IC50 of 37 nM in a cell-free assay, mostly PI3Kδ. Phase1/2.

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In DMSO USD 90 In stock
USD 70 In stock
USD 270 In stock
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8 Customer Reviews

  • j,k, Gene expression ofMYOCD (j) and ACTA2 ( SMA, k) after applying inhibitors of key components involved in the DDR2 downstream signalling pathway to HSCs cultured within 3D collagen matrix subjected to stretching (ST) (n=3, one-way ANOVA, **P=0.0036, ****P<0.0001). l,m, Expression of SMA was significantly reduced after treatment with related inhibitors in early-stage FμNs. (n=4, one-way ANOVA, ***P=0.001, ****P<0.0001). PI3K-i: ZSTK474

    Nature Materials, 2017, 16:1252-1261.. ZSTK474 purchased from Selleck.

    C. MCF-7 cells were transfected for 5 h with a plasmid containing GFP/mRFP-tagged LC3 (tfLC3) reporter gene by use of lipofectamine 2000, then treated with 2 μM of ZSTK for 0, 3, 6, 17, and 24 h, respectively. The treated cells were fixed to be available for microscopy. The GFP/mRFP images were acquired using Olympus FV1000 laser scanning confocal microscope. Arrows indicate autophagosomes. ZSTK: ZSTK474. Rapa: rapamycin.

    Oncotarget, 2016, 7(15):19897-909. ZSTK474 purchased from Selleck.

  • J Cell Physiol, 2018, 233(3):1796-1811. ZSTK474 purchased from Selleck.

    Representative Western blot of Erk1/2, phospho-Erk1/2, Akt, phospho-Akt antibodies in BCPAP, K1 and 8505C cells treated at 4 h using IC50 doses. 1, cells untreated; 2, cells treated with RAF265; 3, cells treated with ZSTK474; 4, cells treated with SB590885; 5, cells treated with RAF265+ZSTK474; 6, cells treated with SB590885+ZSTK474.

    Invest New Drugs 2014 32(4), 626-35. ZSTK474 purchased from Selleck.

  • Effects of Velcade and ZSTK474 on expression of proteins central to the PI3K/Akt pathway in GBM cell lines. U87 and U118 were cultured for 24 h with Velcade (100 nM), ZSTK474 (2.5 uM), or both simultaneously. Lysates were made and subjected to western blot analysis for P-Akt, P-mTOR, P-4EBP1 and cyclin D1 as well as GAPDH loading control.

    Int J Oncol 2014 44(2), 557-62. ZSTK474 purchased from Selleck.

    The proliferation of tachyzoites in ARPE-19 cells was examined by fluorescence microscopy. Cells were pre-incubated with PI3K inhibitors, 250 nM GDC-0941 and 10 nM ZSTK474 for 1 h. After washing, the cells were then infected with T. gondii at moi of 5 for 24 h. Cells were fixed and stained with Texas Red?X phalloidin for labeling F-actin (red), and nuclei were stained with DAPI (blue). Data are representative of three independent experiments. Scale bar = 100 uM.

    PLoS One 2013 8(6), e66306. ZSTK474 purchased from Selleck.

  • We treated all of drugs in T47D which has a PI3KCA H1044R mutation with the concentration shown below for 1 hour and performed western blot analysis using antibodies to phospho-AKT(SERINE 472), and total AKT.



    Saraswati Sukumar of Johns Hopkins University School of Medicine. ZSTK474 purchased from Selleck.

    Western blot analysis of Akt and p-Akt. 0-20μM ZSTK474 was added.

    Dr. Zhang of Tianjin Medical University . ZSTK474 purchased from Selleck.

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Biological Activity

Description ZSTK474 inhibits class I PI3K isoforms with IC50 of 37 nM in a cell-free assay, mostly PI3Kδ. Phase1/2.
Features First orally administered PI3K inhibitor used in vivo.
PI3Kδ [2]
(Cell-free assay)
PI3Kα [2]
(Cell-free assay)
PI3K [1]
(Cell-free assay)
PI3Kβ [2]
(Cell-free assay)
PI3Kγ [2]
(Cell-free assay)
4.6 nM 16 nM 37 nM 44 nM 49 nM
In vitro

ZSTK474 at 1 μM potently reduces PI3K activity to 4.7% of the control level, whereas LY2194002 only reduces the activity to 44.6% of the control. ZSTK474 inhibits the activities of recombinant p110β, -γ, and -δ with IC50 of 17 nM, 53 nM, and 6 nM, respectively. ZSTK474 shows potent antiproliferative activity against a panel of 39 human cancer cell lines with mean GI50 of 0.32 μM, more effectively than that of LY294002 or wortmannin with mean GI50 of 7.4 μM or 10 μM, respectively. ZSTK474 treatment at 1 μM blocks membrane ruffling and generation of PIP3 induced by platelet-derived growth factor in murine embryonic fibroblasts (MEFs). ZSTK474 at 10 μM induces apoptosis in OVCAR3 cells, and induces complete G1-phase arrest but not apoptosis in A549 cells. ZSTK474 treatment at 0.5 μM significantly decreases the level of phosphorylated Akt and GSK-3β, as well as the cyclin D1 protein expression. ZSTK474 also inhibits the phosphorylation of other downstream signaling components that are involved in regulating cell proliferation including FKHRL1, FKHR, TSC-2, mTOR, and p70S6K in a dose-dependent manner. [1] ZSTK474 does not inhibit mTOR at 0.1 μM, and even at a concentration of 100 μM, ZSTK474 inhibits mTOR activity less than 40%. [2] ZSTK474 blocks VEGF-induced cell migration and the tube formation in human umbilical vein endothelial cells (HUVECs), and inhibits the expression of HIF-1α and secretion of VEGF in RXF-631L cells, exhibiting potent in vitro antiangiogenic activity. [3] ZSTK474 treatment inhibits the production of IFNγ and IL-17 in concanavalin A-activated T cells, and inhibits the proliferation and PGE(2) production by fibroblast-like synovial cells (FLS). [6]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
Sf21 insect cells MmrWSpVv[3Srb36gZZN{[Xl? M3L0OVEhcA>? MmLvTY5pcWKrdHnvckBw\iCkb4\pcoUhemWlb33ibY5idnRiUFmzT{BxOTFyZHXseIEh\XiycnXzd4VlKGmwIGPmNlEhcW6|ZXP0JINmdGy|IIXzbY5oKHCqb4PwbIF1cWS7bHnuc5NqfG:uIHHzJJN2[nO2cnH0[UBi\nSncjCxJIhzKGK7IIDoc5NxcG:rbXHnbY5oNCCLQ{WwQVAvPyCwTR?= MVmyNVg5Ojh|Mh?=
human HCT116 cells M4q2VWZ2dmO2aX;uJIF{e2G7 MYexOUBucW6| NXO1WnptUW6qaXLpeIlwdiCxZjDQTWs{S0FiSEGwOFdTKG23dHHueE1u\WSrYYTl[EBk\WyuIIPp[45idGmwZzDpckBpfW2jbjDIR3QyOTZiY3XscJMh\XiycnXzd4lv\yCSVFXOJIF{e2W|c3XkJIF{KGmwaHnibZRqd25ib3[gbY5{fWyrbj3pcoR2[2WmIIDBb5QwWEuEIIDoc5NxcG:{eXzheIlwdiCjdDDUbJI{ODhidILlZZRm\CCob4KgNVUhdWmwczDi[YZwemViaX7zeYxqdiClaHHscIVv\2VibXXhd5Vz\WRiYX\0[ZIhPSCvaX7zJIJ6KGmvbYXuc4Jtd3S2aX7nMEBKSzVyPUe4JI5O NV3aTWE6OjF6OEK4N|I>
human LNCAP cells MkP1VJJwdGmoZYLheIlwdiCjc4PhfS=> NXLEPIlVOyCmYYnz NIfLZXVCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFzOR2FRKGOnbHzzJIFnfGW{IEOg[IF6eyCkeTDNWHMh[XO|YYmsJGlEPTB;MD6yNUDPxE1? M{jrNVIxOjJ5OEix
human NZB5 cells MYLQdo9tcW[ncnH0bY9vKGG|c3H5 M4HQ[|Uh\GG7cx?= NInBXmdCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF7aRlUh[2WubIOg[ZhxemW|c3nu[{B4cWymIIT5dIUheDFzMHHsdIhiKGG|c3Xzd4VlKGG|IHnuZ49zeG:{YYTpc44hd2ZiW{PIYZRpgW2rZHnu[UBi\nSncjC1JIRigXNuIFnDOVA:OC5{MjFOwG0> M1iwVlIyQDh{OEOy
human NZOV9 cells M{j3VnBzd2yrZnXyZZRqd25iYYPzZZk> MoftOUBl[Xm| M3SwRmFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTmrPWlkh[2WubIOg[ZhxemW|c3nu[{BxOTFyYXzwbIEhc2mwYYPlJHkyODJzQzDteZRidnRiYYPz[ZN{\WRiYYOgbY5kd3Kyb4LheIlwdiCxZjDbN2hefGi7bXnkbY5mKGGodHXyJFUh\GG7czygTWM2OD1yLkK5JO69VQ>? NWfj[IsxOjF6OEK4N|I>
human MDA-MB-468 cells NYHo[lFUS3m2b4TvfIlkyqCjc4PhfS=> MnvSOFghcA>? NFXyVYtEgXSxdH;4bYNqfHliYXfhbY5{fCCSVFXOMYRm\mmlaXXueEBpfW2jbjDNSGEuVUJvNE[4JINmdGy|IHHzd4V{e2WmIHHzJIlvcGmkaYTpc44hd2ZiY3XscEBoem:5dHigZYZ1\XJiNEigbJJ{KGK7IFPlcIwhXGm2ZYKgPVYh[XO|YYm= MVKyN|c6PTJ|OR?=
human A549 cells M{LmUWZ2dmO2aX;uJIF{e2G7 M3KxPFExKM7:TR?= MUKxJIg> M{LzNGlvcGmkaYTpc44hd2ZiUFmzT{BqdiCqdX3hckBCPTR7IHPlcIx{KGG|c3Xzd4VlKGG|IILl[JVkfGmxbjDpckBxSWu2IHzleoVtKGG2IEGwJJVOKGGodHXyJFEhcHJiYomgW4V{fGW{bjDicI91fGmwZzDhcoFtgXOrcx?= MmrqNlU4PjZ4M{O=
human DMS114 cells MlzTS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MnjTS5Jwf3SqIHnubIljcXSrb36gc4YhcHWvYX6gSG1UOTF2IHPlcIx{ MWeyNlM{PjJ2Nh?=
human MKN74 cells MYXHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NFHlbpBIem:5dHigbY5pcWKrdHnvckBw\iCqdX3hckBOU055NDDj[Yxtew>? MYCyNlM{PjJ2Nh?=
human SNB78 cells MVXHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? M{fWfGdzd3e2aDDpcohq[mm2aX;uJI9nKGi3bXHuJHNPSjd6IHPlcIx{ MlvBNlI{OzZ{NE[=
human St-4 cells M1KzNGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MWfHdo94fGhiaX7obYJqfGmxbjDv[kBpfW2jbjDTeE01KGOnbHzz NUL5O3BzOjJ|M{[yOFY>
human DU145 cells M{PLUmdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NYH5PZVXT3Kxd4ToJIlvcGmkaYTpc44hd2ZiaIXtZY4hTFVzNEWgZ4VtdHN? MWSyNlM{PjJ2Nh?=
human LOXIMVI cells M4nLdmdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MnH2S5Jwf3SqIHnubIljcXSrb36gc4YhcHWvYX6gUG9ZUU2YSTDj[Yxtew>? NXSxdHhsOjJ|M{[yOFY>
human PC3 cells NY\0dnhwT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MU\Hdo94fGhiaX7obYJqfGmxbjDv[kBpfW2jbjDQR|Mh[2WubIO= NHXhcGQzOjN|NkK0Oi=>
human LOXIMVI cells M4Pa[2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NVnseVdlT3Kxd4ToJIlvcGmkaYTpc44hd2ZiaIXtZY4hVE:[SV3WTUBk\Wyucx?= NFrrT2MzOjN|NkK0Oi=>
human OVCAR3 cells MYHHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MlnlS5Jwf3SqIHnubIljcXSrb36gc4YhcHWvYX6gU3ZESVJ|IHPlcIx{ MXmyNlM{PjJ2Nh?=
human SKOV3 cells Ml;NS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MoDBS5Jwf3SqIHnubIljcXSrb36gc4YhcHWvYX6gV2tQXjNiY3XscJM> NX\NXXljOjJ|M{[yOFY>
human KM12 cells NWHtNmpIT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NIXMb|dIem:5dHigbY5pcWKrdHnvckBw\iCqdX3hckBMVTF{IHPlcIx{ MWeyNlM{PjJ2Nh?=
human HT-29 cells M3HJOmdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NGrUcWtIem:5dHigbY5pcWKrdHnvckBw\iCqdX3hckBJXC1{OTDj[Yxtew>? MWqyNlM{PjJ2Nh?=
human HCT15 cells M4D5[Gdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MWnHdo94fGhiaX7obYJqfGmxbjDv[kBpfW2jbjDIR3QyPSClZXzsdy=> Mof5NlI{OzZ{NE[=
human NCI-H226 cells NFHCU4hIem:5dHigbY5pcWKrdHnvckBie3OjeR?= M4joWmdzd3e2aDDpcohq[mm2aX;uJI9nKGi3bXHuJG5EUS2KMkK2JINmdGy| NXLzVIQ6OjJ|M{[yOFY>
human NCI-H522 cells  Mle5S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NYTaWpd4T3Kxd4ToJIlvcGmkaYTpc44hd2ZiaIXtZY4hVkOLLVi1NlIh[2WubIRCpC=> M{PIT|IzOzN4MkS2
human A549 cells NXzzZ3ljT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NHXL[5NIem:5dHigbY5pcWKrdHnvckBw\iCqdX3hckBCPTR7IHPlcIx{ M4LCVlIzOzN4MkS2
human HCC2998 cells M{PGRWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 Mk\yS5Jwf3SqIHnubIljcXSrb36gc4YhcHWvYX6gTGNEOjl7ODDj[Yxtew>? M3XjUVIzOzN4MkS2
human SNB75 cells NHPXcZlIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MVrHdo94fGhiaX7obYJqfGmxbjDv[kBpfW2jbjDTUmI4PSClZXzsdy=> MV6yNlM{PjJ2Nh?=
human OVCAR4 cells MWXHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MlqxS5Jwf3SqIHnubIljcXSrb36gc4YhcHWvYX6gU3ZESVJ2IHPlcIx{ NUf5NVB3OjJ|M{[yOFY>
human OVCAR5 cells NYrL[lhPT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NGPhVFNIem:5dHigbY5pcWKrdHnvckBw\iCqdX3hckBQXkODUkWgZ4VtdHN? MkOwNlI{OzZ{NE[=
human OVCAR8 cells NGj3b2FIem:5dHigbY5pcWKrdHnvckBie3OjeR?= M3jCeGdzd3e2aDDpcohq[mm2aX;uJI9nKGi3bXHuJG9XS0GUODDj[Yxtew>? NXXZVnJNOjJ|M{[yOFY>
human SKOV3 cells MVvHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NVT4dlVMT3Kxd4ToJIlvcGmkaYTpc44hd2ZiaIXtZY4hW0uRVkOgZ4VtdHN? NH\sVnozOjN|NkK0Oi=>
human ACHN cells MnLBS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MnXJS5Jwf3SqIHnubIljcXSrb36gc4YhcHWvYX6gRWNJViClZXzsdy=> NX7wcWNQOjJ|M{[yOFY>

... Click to View More Cell Line Experimental Data

In vivo Oral administration of ZSTK474 inhibits the growth of subcutaneously implanted mouse B16F10 melanoma tumors in a dose-dependent manner, producing tumor regression of 28.5%, 7.1%, or 4.9% on day 14 at 100, 200, or 400 mg/kg, respectively, which is superior to that of the four major anticancer drugs irinotecan, cisplatin, doxorubicin, and 5-fluorouracil at their respective maximum tolerable doses with tumor regression of 96%, 35.7%, 24%, or 68.3%, respectively. ZSTK474 treatment at 400 mg/kg completely inhibits the growth of A549, PC-3, and WiDr xenografts in mice, and induces the regression of A549 xenograft tumors. [1] ZSTK474 significantly inhibits tumor growth in the RXF-631L xenograft model, correlated with a significantly reduced number of microvessels in the ZSTK474-treated mice. [3] Oral administration of ZSTK474 ameliorates the progression of adjuvant-induced arthritis (AIA) in rats. [6]


Kinase Assay:[1]
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Inhibition of PI3K activity:

A549 cells are lysed in a buffer containing 20 mM Tris-HCl (pH 7.5), 150 mM NaCl, 5 mM EDTA, and 1% Igepal CA-630, the lysates are centrifuged at 20,000 g and 4 °C for 10 minutes, and the supernatants are used as cell lysate (protein = 2-4 mg/mL). To immunoprecipitate PI3K, 200 μL of cell lysate are incubated with anti-p85 polyclonal antibody and protein G-agarose (5 μL). PI3Kα, PI3Kβ, and PI3Kδ can be immunoprecipitated by the anti-p85 polyclonal antibody. Agarose beads containing immunoprecipitates are washed twice with buffer A (20 mM Tris-HCl at pH 7.5, 150 mM NaCl, 5 mM EDTA, and 1% Igepal CA-630), once with buffer B (500 mM LiCl and 100 mM Tris-HCl at pH 7.5), once with distilled water, and once with buffer C (100 mM NaCl and 20 mM Tris-HCl at pH 7.5). Immunoprecipitates are suspended in 20 μL of buffer C containing phosphatidylinositol of 200 μg/mL. The mixture is preincubated with increasing concentrations of ZSTK474 at 25 °C for 5 minutes. [γ-32P]ATP (2 μCi per assay mixture; final concentration, 20 μM) and MgCl2 (final concentration, 20 mM) are added to start the reaction. The reaction mixture is incubated at 25 °C for 20 minutes. Phosphorylated products of phosphatidylinositol are separated by thin-layer chromatography and visualized by autoradiography. The phosphatidylinositol-3-phosphate region is scraped from the plate, and radioactivity is also measured with liquid scintillation spectroscopy. The level of inhibition for ZSTK474 is determined as the percentage of 32P counts per minute obtained without ZSTK474.
Cell Research:[1]
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  • Cell lines: MCF-7, HT-29, HCT-116, OVCAR3, A549, et al.
  • Concentrations: Dissolved in DMSO, final concentrations ~10 μM
  • Incubation Time: 48 hours
  • Method: Cells are exposed to increasing concentrations of ZSTK474 for 48 hours. The inhibition of cell proliferation is assessed by measuring changes in total cellular protein by use of a sulforhodamine B assay. Apoptosis is assessed by chromatin condensation or by flow cytometry. For chromatin condensation assay, cells are stained with Hoechst 33342 and examined by fluorescence microscopy. Morphologic changes induced by ZSTK474, such as the condensation of chromatin, are indicative of apoptosis. For flow cytometry analysis, cells are harvested, washed with ice-cold PBS, and fixed in 70% ethanol. Cells are then washed twice with ice-cold PBS again, treated with RNase A (500 μg/mL) at 37 °C for 1 hour, and stained with propidium iodide (25 μg/mL). The DNA content of the cells is analyzed with a flow cytometer.
    (Only for Reference)
Animal Research:[1]
+ Expand
  • Animal Models: Male BDF1 mice injected subcutaneously with B16F10 cells, and female BALB/c nude mice inoculated subcutaneously with A549, PC-3, or WiDr cells
  • Formulation: Suspended in 5% hydroxypropylcellulose in water as a solid dispersion form
  • Dosages: ~400 mg/kg/day
  • Administration: Orally
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 21 mg/mL (50.31 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
0.5% hydroxyethyl cellulose
For best results, use promptly after mixing.

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 417.41


CAS No. 475110-96-4
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01682473 Completed Neoplasms Zenyaku Kogyo Co. Ltd. September 20 2012 Phase 1
NCT01280487 Completed Neoplasms Zenyaku Kogyo Co. Ltd. January 2011 Phase 1

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID