Pictilisib (GDC-0941)

Catalog No.S1065

Pictilisib (GDC-0941) is a potent inhibitor of PI3Kα/δ with IC50 of 3 nM in cell-free assays, with modest selectivity against p110β (11-fold) and p110γ (25-fold). Phase 2.

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Pictilisib (GDC-0941) Chemical Structure

Pictilisib (GDC-0941) Chemical Structure
Molecular Weight: 513.64

Validation & Quality Control

Cited by 56 publications:

7 customer reviews :

Quality Control & MSDS

Related Compound Libraries

Pictilisib (GDC-0941) is available in the following compound libraries:

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Product Information

  • Compare PI3K
    Compare PI3K Products
  • Research Area
  • Inhibition Profile
  • Pictilisib (GDC-0941) Mechanism
  • Combination Therapy
    Combination Therapy

Product Description

Biological Activity

Description Pictilisib (GDC-0941) is a potent inhibitor of PI3Kα/δ with IC50 of 3 nM in cell-free assays, with modest selectivity against p110β (11-fold) and p110γ (25-fold). Phase 2.
Targets p110α [1]
(Cell-free assay)
p110δ [1]
(Cell-free assay)
p110β [1]
(Cell-free assay)
p110γ [1]
(Cell-free assay)

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IC50 3 nM 3 nM 33 nM 75 nM
In vitro GDC-0941 is equipotent against PI3Kα and PI3Kδ as well as PI3Kα mutants E545-K and H1047-R, displaying modest levels of selectivity against PI3Kβ (10-fold) and PI3Kγ (25-fold), and greater levels of selectivity against members of PI3K class II, III, and IV, including C2β, Vps34, DNA-PK, and mTOR. GDC-0941 potently inhibits the phosphorylation of Akt in U87MG, PC3, and MDA-MB-361 cells with IC50 of 46 nM, 37 nM, and 28 nM, respectively. GDC-0941 inhibits the proliferation of U87MG, A2780, PC3, and MDA-MB-361 cells with IC50 of 0.95 μM, 0.14 μM, 0.28 μM, and 0.72 μM, respectively. [1] GDC-0941 treatment potently inhibits the proliferation of both trastuzumab-sensitive and -insensitive HER2-amplified cells with IC50 of 149-944 nM. GDC-0941 inhibits proliferation of HER2-amplified cells that harbor PIK3CA mutations with IC50 of <500 nM, and effectively inhibits both proliferation and viability of HER2-amplified breast cancer cells that are resistant to trastuzumab due to PTEN loss. [2] GDC-0941 significantly inhibits the growth of HCT116, DLD1 and HT29 cells with GI50 of 1081 nM, 1070 nM and 157 nM, respectively. [3] GDC-0941 inhibits tumor cell proliferation, induces apoptosis and suppresses centroblast population. [4]
Cell Data
Cell LinesAssay TypeConcentrationIncubation TimeFormulationActivity DescriptionPMID
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... Click to View More Cell Line Experimental Data

In vivo Administration of GDC-0941 at 75 mg/kg/day displays significant inhibitory effect against established human U87MG glioblastoma xenografts in female NCr athymic mice, with tumor growth inhibition of 83%. [1] Oral administration of GDC-0941 at 150 mg/kg/day inhibits the growth of HER2-amplified, trastuzumab-resistant MDA-MB-361.1 xenografts in mice, and significantly delays the tumor progression, in association with potent induced apoptosis in tumors. [2] GDC-0941 (75 mg/kg/day) treatment for 2 weeks induces ~40% reduction in tumor volume of spontaneous B-cell follicular lymphomas developed in PTEN+/-LKB1+/hypo mice, accompanied by ablation of phosphorylation of Akt, S6K and SGK (serum and glucocorticoid protein kinase) protein kinases. [4]
Features

Protocol(Only for Reference)

Kinase Assay: [1]

Scintillation proximity assay Recombinant human PI3Kα, PI3Kβ, and PI3Kδ are coexpressed in a Sf9 baculovirus system with the p85α regulatory subunit and purified as GST-fusion proteins using affinity chromatography on glutathione-sepharose. Recombinant human PI3Kγ is expressed as monomeric GST-fusions and purified similarly. GDC-0941 is dissolved in DMSO and added to 20 mM Tris-HCl (pH 7.5) containing 200 μg yttrium silicate (Ysi) polylysine SPA beads, 4 mM MgCl2, 1 mM dithiothreitol (DTT), 1 μM ATP, 0.125 μCi [γ-33P]-ATP, and 4% (v/v) DMSO in a total volume of 50 μL. The recombinant GST-fusion of PI3Kα (5 ng), PI3Kβ (5 ng), PI3Kδ (5 ng), or PI3Kγ (5 ng) is added to the assay mixture to initiate the kinase reaction. After incubation for 1 hour at room temperature, the kinase reaction is terminated with 150 μL PBS. The mixture is then centrifuged for 2 minutes at 2000 rpm and read using a Wallac Microbeta counter. The reported IC50 values are calculated using a sigmoidal, dose-response curve fit in MDL Assay Explorer.

Cell Assay: [2]

Cell lines SKBR-3, BT474-M1, AU-565, HCC-1419, ZR75-30, KPL-4, JIMT-1, BT474-EEI, HCC-1954, MCF-7, CALU-3, SKOV-3, and MKN-7 cells
Concentrations Dissolved in DMSO, final concentrations ~10 μM
Incubation Time 48 and 72 hours
Method Cells are exposed to various concentrations of GDC-0941 for 48, and 72 hours. Proliferation/viability of cells is detected by using the CellTiter-Glo Luminescent Cell Viability Assay. The pAkt (Ser473), cleaved caspase-3, and cleaved PARP are analyzed by western blot. The Caspase-Glo 3/7 assay and the Cell Death Detection ELISAplus assay are used to detect caspase 3/7 activity, and apoptosis, respectively.

Animal Study: [2]

Animal Models NCR nude mice implanted with MDA-MB-361.1 cells, and SCID, C.B-17/IcrHsd-Prkdcscid mice implanted subcutaneously with BT474-M1 cells
Formulation Dissolved in 10% DMSO, 5% Tween 20, 85% water
Dosages ~150 mg/kg/day
Administration Oral gavage

Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)

SpeciesMouseRatRabbitGuinea pigHamsterDog
Weight (kg)0.020.151.80.40.0810
Body Surface Area (m2)0.0070.0250.150.050.020.5
Km factor36128520
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.

Rat dose (mg/kg) = mouse dose (22.4 mg/kg) ×  mouse Km(3)  = 11.2 mg/kg
rat Km(6)
1

References

[1] Folkes AJ, et al. J Med Chem, 2008, 51(18), 5522-5532.

[2] Junttila TT, et al. Cancer Cell, 2009, 15(5), 429-440.

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Clinical Trial Information( data from http://clinicaltrials.gov, updated on 2016-06-18)

NCT Number Recruitment Conditions Sponsor
/Collaborators
Start Date Phases
NCT02092831 Completed Healthy Volunteer Genentech, Inc. April 2014 Phase 1
NCT01740336 Active, not recruiting Breast Cancer Genentech, Inc. February 2013 Phase 2
NCT01493843 Completed Non-Squamous Non-Small Cell Lung Cancer Genentech, Inc. January 2012 Phase 2
NCT01474668 Completed Healthy Volunteer Genentech, Inc. October 2011 Phase 1
NCT01437566 Active, not recruiting Breast Cancer Genentech, Inc. June 2011 Phase 2

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Chemical Information

Download Pictilisib (GDC-0941) SDF
Molecular Weight (MW) 513.64
Formula

C23H27N7O3S2

CAS No. 957054-30-7
Storage 3 years -20℃powder
6 months-80℃in solvent
Synonyms RG7321
Solubility (25°C) * In vitro DMSO 44 mg/mL (85.66 mM)
Water <1 mg/mL (<1 mM)
Ethanol <1 mg/mL (<1 mM)
In vivo 2% DMSO+30% PEG 300+5% Tween 80+ddH2O 5mg/mL
* <1 mg/ml means slightly soluble or insoluble.
* 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 Name 2-(1H-indazol-4-yl)-6-((4-(methylsulfonyl)piperazin-1-yl)methyl)-4-morpholinothieno[3,2-d]pyrimidine

Customer Product Validation(7)


Click to enlarge
Rating
Source Cancer Res 2011 71, 2750-2760. Pictilisib (GDC-0941) purchased from Selleck
Method Western blot, Immunofluorescence staining, flow cytometry
Cell Lines 1205Lu cells
Concentrations 3 µmol/L
Incubation Time 48 h
Results Combined PI3K and BRAF inhibition increased the level of BIM expression in both Western blot and immunofluorescence studies (Fig. A). Consistent with a role for increased AKT signaling suppressing BIM expression in PTEN- cells, dual BRAF and PI3K inhibition increased nuclear FOXO3a localization in the PTEN- cell lines (Fig. B) and enhanced the level of BIM mRNA (Fig. B). the combination of PLX4720 with the PI3K inhibitor GDC-0941 significantly enhanced the levels of apoptosis observed in PTEN melanoma cell lines compared to either the BRAF or PI3K inhibitor alone (Fig. C). Similar results were also observed in a 3D spheroid assay, where combined PLX4720 (3 µmol/L) and LY294002 (10 µmol/L) treatment prevented the recovery of cell growth observed when melanoma spheroids were treated with either drug alone (Fig. D).

Click to enlarge
Rating
Source J Inves Der 2010 131, 495-503. Pictilisib (GDC-0941) purchased from Selleck
Method Western blot
Cell Lines Mel-Juso cells, 518A2 cells
Concentrations 0.05–1 µmol/L
Incubation Time 24 h
Results In addition, GDC-0941 treatment blocked the phosphorylation of AKT protein (S473 and T308) at even lower concentrations than PI-103, and S6 protein phosphorylation was blocked at similar concentrations.

Click to enlarge
Rating
Source J Cell Sci 2012 125(Pt 5), 1259-73. Pictilisib (GDC-0941) purchased from Selleck
Method Western Blot
Cell Lines NMuMG cells
Concentrations 1 μM
Incubation Time 1 h
Results GDC-0941, a specific inhibitor of the class IA PI3K, similarly blocked the TGF-b-induced Akt(S473) phosphorylation, confirming the role of PI3K in the induction of mTORC2 kinase activity by TGF-β (Fig. C).

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Rating
Source Biochim Biophys Acta 2012 1823, 2210-6. Pictilisib (GDC-0941) purchased from Selleck
Method confocal laser-scanning microscopy
Cell Lines HEK293 cells
Concentrations 1 μM
Incubation Time 30 min
Results Both LY294002 and GDC-0941 markedly attenuated the high-glucose-dependent plasma membrane translocation of DGKδ1, indicating that the event is positively regulated by phosphatidylinositol 3-kinase.

Click to enlarge
Rating
Source Dr. Zhang of Tianjin Medical University. Pictilisib (GDC-0941) purchased from Selleck
Method Western blot
Cell Lines Breast cancer cells
Concentrations 0-10 nM
Incubation Time 3 h
Results

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Rating
Source Saraswati Sukumar of Johns Hopkins University School of Medicine. Pictilisib (GDC-0941) purchased from Selleck
Method Western blot
Cell Lines T47D cells
Concentrations
Incubation Time 1 h
Results

Click to enlarge
Rating
Source Pictilisib (GDC-0941) purchased from Selleck
Method Western blot analysis
Cell Lines MCF-7 cells
Concentrations 0 nM/50 nM/100 nM/400 nM
Incubation Time 24 h
Results GDC-0941 caused a surprising increase in phosphorylation of ERK proteins as well as AKT2 S474. GDC-0941 showed differences in its ability to suppr ess PI3K-dependent signaling across the genotypes. AKT1 mutant cells demonstrated greater residual AKT1 S473 phosphorylation and greater phosphorylation of downstream proteins FOXO 1/3, PRAS40, GSK3β , and p70S6K at equivalent doses of GDC-0941, compared to PIK3CA mutant cells.

Tech Support

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