We use analytics and advertising cookies, which you can accept or reject; see our privacy policy.

Current choice:

Fig. 1 · Structure
Cat. No.
A10421
CAS No.
957054-30-7
Formula
C23H27N7O3S2
Mol. Weight
513.6

Documents & Downloads

Pictilisib (GDC-0941)

Cat. No. A10421 CAS 957054-30-7

PI3K inhibitor

GDC-0941 is a potent, selective, orally bioavailable inhibitor of class I PI3 kinase (PI3K) , with IC50 values (nM) of 3, 33, 3, 75, 1230 and 580 for p110 α, β, δ and γ isoforms, DNA-PK and mTOR respectively.

In Stock

Publications for Pictilisib

4 publications citing this product

  1. Kohei Maruyama, .et al. , NPJ Precis Oncol, 2025, Jan 6;9(1):4 PMID: 39762482
  2. Bopei Cui, .et al. , Signal Transduct Target Ther, 2023, Sep 25;8(1):366 PMID: 37743418
  3. Li T, .et al. , Oncogene, 2018, Nov;37(47):6180-6194 PMID: 30013190
  4. Joo Sang Lee, .et al. , Nat Commun, 2018, 9: 2546 PMID: 29959327
Notify me when the price drops

For laboratory research use only. We do not sell to patients.

Free Aliquoting for Your Order

Tell us your preferred amount per vial. We’ll confirm the options.

Biological Activity

Bioactivity / Mechanism

GDC-0941 inhibits class I PI3K enzymes, with greater potency against p110α/δ than p110β/γ in the reported recombinant-enzyme panel. Its mTOR and DNA-PK IC50 values were higher than its class I PI3K values. [1]

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

Target & Activity

Target Activity Value
p110α IC50 3nM
p110δ IC50 3nM
p110β IC50 33nM
p110γ IC50 75nM
mTOR Kiapp: 0.58μM
C2β IC50 0.67μM
DNA-PK IC50 1.23μM
Vps34 IC50 >10μM

8 targets · Scroll to view more

Cellular Effect

Cell Line Activity Value Description Reference
A2780 IC50 0.14 μM Antiproliferative activity against human A2780 cells with PIK3CA and PTEN mutation after 4 days by alamar blue assay [PMID: 18754654]
A549 IC50 1.03 μM Antiproliferative activity against human A549 cells assessed as inhibition of cell growth incubated for 72 hrs by MTT assay [PMID: 36599263]
A549 IC50 1.2 μM Cytotoxicity against human A549 cells assessed as reduction in cell viability after 72 hrs by MTT assay [PMID: 27043268]
A549 GI50 1217 nM Cytotoxicity against ALK-negative human A549 cells harboring wild type PI3KCA and CDKN2A and KRAS mutations assessed as cell growth inhibition measured after 72 hrs by MTT assay [PMID: 32184963]
A549 IC50 2.28 μM Antiproliferative activity against human A549 cells after 72 hrs by MTT assay [PMID: 25911625]
A549 IC50 2.48 μM Antiproliferative activity against human A549 cells assessed as reduction in cell viability after 72 hrs by sulforhodamine B assay [PMID: 33109399]
A549 IC50 6.9 μM Cytotoxicity against human A549 cells assessed as growth inhibition after 72 hrs by MTT assay [PMID: 23059545]
A549 IC50 6.99 μM Cytotoxicity against human A549 cells after 72 hrs by MTT assay [PMID: 27353887]
Calu-3 IC50 2.87 μM Antiproliferative activity against human Calu3 cells assessed as reduction in cell viability after 72 hrs by sulforhodamine B assay [PMID: 33109399]
HCC1954 IC50 1.3 μM Cytotoxicity against human HCC1954 cells by MTT assay [PMID: 28006668]
HCT-116 IC50 0.37 μM Antiproliferative activity against human HCT116 cells after 72 hrs by MTT assay [PMID: 25911625]
HeLa IC50 2.97 μM Antiproliferative activity against paclitaxel-resistant human HeLa cells assessed as inhibition of cell growth incubated for 72 hrs by MTT assay [PMID: 36599263]
HeLa IC50 3.15 μM Antiproliferative activity against human HeLa cells assessed as inhibition of cell growth incubated for 72 hrs by MTT assay [PMID: 36599263]
Hep 3B2 IC50 2.03 μM Antiproliferative activity against human Hep3B cells assessed as reduction in cell viability incubated for 72 hrs by sulforhodamine B assay/CellTiter Glo-luminescent assay [PMID: 29360358]
HepG2 IC50 1 μM Cytotoxicity against human HepG2 cells assessed as growth inhibition after 72 hrs by MTT assay [PMID: 23059545]
HepG2 IC50 6.22 μM Antiproliferative activity against human HepG2 cells assessed as reduction in cell viability incubated for 72 hrs by sulforhodamine B assay/CellTiter Glo-luminescent assay [PMID: 29360358]
HT-29 IC50 0.66 μM Cytotoxicity against human HT-29 cells assessed as growth inhibition after 72 hrs by MTT assay [PMID: 23059545]
HT-29 IC50 0.86 μM Cytotoxicity against human HT-29 cells assessed as reduction in cell viability after 72 hrs by MTT assay [PMID: 25440879]
HT-29 IC50 0.86 μM Cytotoxicity against human HT-29 cells after 72 hrs by MTT assay [PMID: 25086238]
Huh-7 IC50 1.72 μM Antiproliferative activity against human HuH-7 cells assessed as reduction in cell viability incubated for 72 hrs by sulforhodamine B assay/CellTiter Glo-luminescent assay

20 records · Scroll to view more

In Vitro Studies

In JC261 patient-derived colorectal cancer cells, GDC0941 alone suppressed pathway phosphorylation without inducing PARP cleavage. Combining GDC0941 with the mTOR inhibitor PP242 produced stronger viability suppression and PARP cleavage; adding sotorasib further reduced viability. These combination results are specific to this model and treatment context. [2]

Class I PI3K enzyme inhibition

Biochemical assay · Recombinant class I PI3K isoforms; mTOR and DNA-PK comparator enzymes [1]

The assay panel shows strongest inhibition of PI3K p110α and p110δ, with weaker inhibition of p110β and p110γ. Comparator inhibitors were assayed in the same panel.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
PI3K p110α inhibitionIC50 0.003 μM[1]
PI3K p110β inhibitionIC50 0.033 μM[1]
PI3K p110δ inhibitionIC50 0.003 μM[1]
PI3K p110γ inhibitionIC50 0.075 μM[1]
mTOR inhibitionIC50 0.58 μM[1]
DNA-PK inhibitionIC50 1.23 μM[1]

Literature-Reported Treatment Conditions

Method
Scintillation proximity PI3K assay with 1 μmol/L ATP; mTOR assessed by TR-FRET LanthaScreen.
Co-treatment
None; PI-103, PI-540 and PI-620 were separate comparator compounds.
Reported limits
Assay incubation duration and vehicle/control composition are not specified in the retrieved enzyme-method paragraph; no potency is presented as a treatment dose.
Methods and source locations

Compound reported in the paper: GDC-0941 (pictilisib); Compound label in the paper: GDC-0941

Literature results for the reported research material and model; no Adooq lot equivalence or salt conversion is established.

Fig. 1A/B; Materials and Methods, Compound Supply and following enzyme-assay paragraph

PI3K p110α inhibition: Scintillation proximity assay; ATP 1 μmol/L. — Fig. 1B, GDC-0941 row; enzyme-assay methods

PI3K p110β inhibition: Scintillation proximity assay; ATP 1 μmol/L. — Fig. 1B, GDC-0941 row; enzyme-assay methods

PI3K p110δ inhibition: Scintillation proximity assay; ATP 1 μmol/L. — Fig. 1B, GDC-0941 row; enzyme-assay methods

PI3K p110γ inhibition: Scintillation proximity assay; ATP 1 μmol/L. — Fig. 1B, GDC-0941 row; enzyme-assay methods

mTOR inhibition: TR-FRET LanthaScreen; ATP 1 μmol/L. — Fig. 1B, GDC-0941 row; enzyme-assay methods

DNA-PK inhibition: Enzyme panel; the retrieved paragraph does not separately describe the DNA-PK assay. — Fig. 1B, GDC-0941 row

PI3K/mTOR co-inhibition in patient-derived colorectal cells

Cell-based study · JC261 patient-derived colorectal cancer cells with KRAS G12C, HER2 amplification and PIK3CA K111E alteration [2]

GDC0941 plus PP242 suppressed viability more than either single agent; adding sotorasib further reduced viability. GDC0941 alone reduced AKT/S6 phosphorylation but did not induce PARP cleavage at the assessed time points. The combination increased PARP cleavage, separating pathway inhibition from apoptosis.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cell viability relative to DMSOQualitative comparison GDC0941 + PP242 reduced viability more than either single agent; addition of sotorasib further reduced viability.[2]
AKT/S6 phosphorylation and PARP cleavageQualitative immunoblot response Single GDC0941 or PP242 suppressed pathway phosphorylation but failed to induce PARP cleavage; dual treatment increased cleavage.[2]

Literature-Reported Treatment Conditions

Treatment concentration
GDC0941 1 μM; PP242 1 μM; sotorasib 1 μM when included.
Exposure duration
72 h viability; 3 and 24 h immunoblot.
Method
CellTiter-Glo viability and immunoblotting.
Vehicle
DMSO control for viability.
Co-treatment
PP242 (mTOR inhibitor), with or without sotorasib; separate single-agent and untreated/vehicle comparisons.
Reported limits
No catalog SKU, lot or salt form is given. The viability method specifies triplicate wells, without a panel-specific independent biological replicate count.
Methods and source locations

Compound reported in the paper: GDC-0941 (pictilisib); Compound label in the paper: GDC0941

Literature results for the reported research material and model; no Adooq lot equivalence or salt conversion is established.

Fig. 5a/c and caption; Results, PI3K/mTOR inhibition in JC261; Methods Reagents, Cell viability assay and immunoblot antibody methods

Cell viability relative to DMSO: CellTiter-Glo at 72 h; figure data mean ± SD. Shared viability method states triplicate wells; biological replicate number is not specified for this panel. — Fig. 5a and caption; Cell viability assay methods

AKT/S6 phosphorylation and PARP cleavage: Immunoblot at 3 and 24 h; total AKT, S6, PARP and GAPDH controls displayed. — Fig. 5c; associated Results paragraph; antibody methods

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 957054-30-7
Applications PI3K inhibitor
Formula C23H27N7O3S2
Molecular Weight 513.6
Synonyms GDC-0941
SMILES
CS(=O)(=O)N1CCN(CC1)CC2=CC3=C(S2)C(=NC(=N3)C4=C5C=NNC5=CC=C4)N6CCOCC6

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 40 mg/mL (77.87 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
4 mg/mL
Vehicle
2% DMSO+30% PEG 300+5% Tween 80+ddH2O

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] Raynaud FI, Eccles SA, Patel S, et al. Biological properties of potent inhibitors of class I phosphatidylinositide 3-kinases: from PI-103 through PI-540, PI-620 to the oral agent GDC-0941. Molecular cancer therapeutics (2009). PMID: 19584227 DOI: 10.1158/1535-7163.mct-08-1200 Source material
  2. [2] Maruyama K, Shimizu Y, Nomura Y, et al. Mechanisms of KRAS inhibitor resistance in KRAS-mutant colorectal cancer harboring Her2 amplification and aberrant KRAS localization. NPJ precision oncology (2025). PMID: 39762482 DOI: 10.1038/s41698-024-00793-6 Source material

Publications

4 publications citing this product

  1. Kohei Maruyama, .et al. , NPJ Precis Oncol, 2025, Jan 6;9(1):4 PMID: 39762482
  2. Bopei Cui, .et al. , Signal Transduct Target Ther, 2023, Sep 25;8(1):366 PMID: 37743418
  3. Li T, .et al. , Oncogene, 2018, Nov;37(47):6180-6194 PMID: 30013190
  4. Joo Sang Lee, .et al. , Nat Commun, 2018, 9: 2546 PMID: 29959327

Added to your cart

View Cart Checkout
Loading...