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Fig. 1 · Structure
Cat. No.
A11089
CAS No.
1173204-81-3
Formula
C29H34N10O3
Mol. Weight
570.7

Documents & Downloads

PKI-402

Cat. No. A11089 CAS 1173204-81-3

PI3K inhibitor

PKI-402 is a dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor.

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Biological Activity

Target & Activity

Target Activity Value
PI3Kα IC50 2 nM
PI3Kα-H1047R IC50 3 nM
PI3Kα-E545K IC50 3 nM
PI3Kβ IC50 7 nM
PI3Kδ IC50 14 nM
PI3Kγ IC50 16 nM
mTOR IC50 3 nM

7 targets · Scroll to view more

Cellular Effect

Cell Line Activity Value Description Reference
MDA-MB-361 IC50 5 nM Inhibition of Akt T308 phosphorylation in human MDA-MB-361 cells after 4 hrs by Western blotting [PMID: 19968288]
MDA-MB-361 IC50 8 nM Growth inhibition of human MDA-MB-361 cells after 72 hrs [PMID: 21763134]
MDA-MB-361 IC50 8 nM Cytotoxicity against human MDA-MB-361 cells with Her2+/PI3KCA mutant after 72 hrs [PMID: 19968288]
PC-3 IC50 21 nM Growth inhibition of human PC3 cells after 72 hrs [PMID: 21763134]
PC-3 IC50 21 nM Cytotoxicity against human PC3 cells with PTEN mutant after 72 hrs [PMID: 19968288]
Sf9 IC50 1 nM Inhibition of human PI3Kalpha expressed in SF9 insect cells after 2 hrs by fluorescence polarization assay [PMID: 21763134]
Sf9 IC50 9 nM Inhibition of human PI3Kgamma expressed in SF9 insect cells after 2 hrs by fluorescence polarization assay [PMID: 21763134]

In Vitro Studies

PKI-402 increased phosphorylated eIF2α levels in A2780 cells. In QGP, PKI-402 completely inhibited pAkt expression at 4 h, although this effect was not prolonged. In KKU-213A cells, treatment for 72 h yielded a cell viability IC50 of 0.497 ± 0.01 μM. PKI-402 also decreased cell viability in SKOV3 cells. [1,2,3]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Increased eIF2α phosphorylation in A2780 cells

Cell-based study · A2780 cells [1]

A2780 cells treated with PKI-402 at 2.5 μM for 12 h showed increased phosphorylated eIF2α levels, measured by western blotting.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Levels of the proteins in B and D were measured by western blotting, respectively.Reported result PKI-402 increased the level of phosphorylated eIF2α in A2780[1]

Literature-Reported Treatment Conditions

Treatment concentration
2.5 μM
Exposure duration
12 h
Reported limits
Not stated in the sentences used: route, vehicle.
Methods and source locations

Compound reported in the paper: PKI-402

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Result > Stress granules formed in A2780 cells under the treatment of PKI-402 (S37); Fig. 1 legend (S69, S72, S73)

Levels of the proteins in B and D were measured by western blotting, respectively.: Levels of the proteins in B and D were measured by western blotting, respectively.; comparator: control — Result > Stress granules formed in A2780 cells under the treatment of PKI-402 (S37); Fig. 1 legend (S72)

Transient inhibition of pAkt expression in QGP

Cell-based study · QGP [2]

PKI-402 (500 and 10,000 nM) completely inhibited pAkt expression at 4 h in QGP. However, this effect was not prolonged.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
pAkt expressionReported result PKI-402 (500 and 10,000 nM) completely inhibited pAkt expression at 4 h in QGP. However, this effect was not prolonged.[2]

Literature-Reported Treatment Conditions

Treatment concentration
500 and 10,000 nM
Exposure duration
4 h
Vehicle
dimethyl sulfoxide (DMSO)
Reported limits
Not stated in the sentences used: route.
Methods and source locations

Compound reported in the paper: PKI-402

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

2. Materials and Methods > 2.1. Materials and Reagents (S5, S6); 3. Results > 3.2. Cellular Profiling of PI3K/mTOR Inhibitors, PF-04691502 and PKI-402, in GEP-NET Cancer Cell Lines (S79, S80)

pAkt expression: pAkt expression; comparator: A cell medium mixture with DMSO only — 3. Results > 3.2. Cellular Profiling of PI3K/mTOR Inhibitors, PF-04691502 and PKI-402, in GEP-NET Cancer Cell Lines (S79, S80)

Cell viability response in KKU-213A cells

Cell-based study · KKU-213A cells [3]

KKU-213A cells were treated with PKI-402 with wide concentration ranges for 72 h. IC50: 0.497 ± 0.01 μM.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cell viabilityIC50 72 h: IC50 0.497 ± 0.01 μM[3]

Literature-Reported Treatment Conditions

Treatment concentration
wide concentration ranges
Exposure duration
72 h
Vehicle
DMSO
Reported limits
Not stated in the sentences used: route.
Methods and source locations

Compound reported in the paper: PKI-402

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Materials and methods > Sulforhodamine B (SRB) assay (S5, S9, S10); Results > Combination of infigratinib with PKI-402 enhances cell cytotoxicity (S42); Fig. 1 legend (S88, S89)

Cell viability: Cell viability; comparator: full media with 0.05 % DMSO — Results > Combination of infigratinib with PKI-402 enhances cell cytotoxicity (S42); Fig. 1 legend (S88, S89)

Decreased viability in SKOV3 cells

Cell-based study · SKOV3 cells [1]

SKOV3 cells were treated with the tested compound at 1.25–10 μM for 24 h. Cell viability decreased, as assessed by MTT assays.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
cell viability was detected by MTT assaysReported result the viability of SKOV3 cells decreased[1]

Literature-Reported Treatment Conditions

Treatment concentration
1.25–10 μM
Exposure duration
24 h
Reported limits
Not stated in the sentences used: route, vehicle.
Methods and source locations

Compound reported in the paper: PKI-402

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Result > Adaptive stress response was activated in A2780 cells (S34); Fig. 1 legend (S67, S73)

cell viability was detected by MTT assays: cell viability was detected by MTT assays; comparator: control — Result > Adaptive stress response was activated in A2780 cells (S34); Fig. 1 legend (S67)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 1173204-81-3
Applications PI3K inhibitor
Formula C29H34N10O3
Molecular Weight 570.7
SMILES
CCN1C2=C(C(=NC(=N2)C3=CC=C(C=C3)NC(=O)NC4=CC=C(C=C4)C(=O)N5CCN(CC5)C)N6CCOCC6)N=N1

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 0.35 mg/mL (0.61 mM)
Water Insoluble
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
28 mg/mL
Vehicle
30% PEG400+0.5% Tween80+5% propylene glycol

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Lin N, Sun L, Chai J, et al. Stress granules affect the dual PI3K/mTOR inhibitor response by regulating the mitochondrial unfolded protein response. Cancer Cell Int (2024). PMID: 38238825 DOI: 10.1186/s12935-024-03210-x Source material
  2. [2] Chow Z, Johnson J, Chauhan A, et al. PI3K/mTOR Dual Inhibitor PF-04691502 Is a Schedule-Dependent Radiosensitizer for Gastroenteropancreatic Neuroendocrine Tumors. Cells (2021). PMID: 34065268 DOI: 10.3390/cells10051261 Source material
  3. [3] Mahaamnad N, Pocasap P, Kukongviriyapan V, et al. Dual blockage of PI3K-mTOR and FGFR induced autophagic cell death in cholangiocarcinoma cells. Heliyon (2024). PMID: 38799762 DOI: 10.1016/j.heliyon.2024.e31112 Source material

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