Catalog No.S7008 Synonyms: AG 1879,AGL 1879

PP2 Chemical Structure

Molecular Weight(MW): 301.77

PP2, a Src family kinase inhibitor, potently inhibits Lck/Fyn with IC50 of 4 nM/5 nM in cell-free assays, ~100-fold less potent to EGFR, inactive for ZAP-70, JAK2 and PKA.

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In DMSO USD 180 In stock
USD 70 In stock
USD 147 In stock
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2 Customer Reviews

  • Inhibition of PLCG1 phosphorylation by the silencing of DopEcR, ErGPCR, and Gq and the addition of inhibitors of RTK and Src. 5 µM SU6668 (RTK inhibitor) and 20 µM PP2 (Src inhibitor) were added to the cells for 30 min treatment before the 20E stimulation.

    J Biol Chem, 2014, 289(19): 13026-41 . PP2 purchased from Selleck.

    D&E. Evaluation of fungal association and transcytosis activity in brain endothelial cells after PP2 treatment. *P < 0.05, **P < 0.01

    CNS Neurosci Ther, 2017, 23(4):291-300. PP2 purchased from Selleck.

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Biological Activity

Description PP2, a Src family kinase inhibitor, potently inhibits Lck/Fyn with IC50 of 4 nM/5 nM in cell-free assays, ~100-fold less potent to EGFR, inactive for ZAP-70, JAK2 and PKA.
LCK [1]
(Cell-free assay)
Fyn [1]
(Cell-free assay)
4 nM 5 nM
In vitro

PP2 inhibits Src by binding to an area of the molecule that does not overlap with the ATP binding domain. [2] PP2 (20 μM) induces 40-50% growth inhibition of HT29 cells, this concentration reduces the Src activity as early as 1 hour and maintains a 35% inhibition of Src activity for 2 days. PP2 (100 mM) decreases the Src activity of HT29 cells in a dose-dependent manner. PP2 (1 mM-100 mM) causes a dose-dependent growth inhibition of human colon cancer cells (HT29, SW480, and PMCO1), liver cancer cells (PLC/PRF/5, KYN-2, Li7, and HepG2), and breast cancer cells (MCF-7, MDA-MB-468, and BT-474). PP2 (20 μM) significantly increases aggregation in most of the cancer cells (HT29, SW480, PMCO1, PLC/PRF/5, KYN-2, Li7, MCF-7, and MDA-MB-468) in E-cadherin dependent manner. PP2 (20 μM) enhances E-cadherin expression and also strongly increases E-cadherin’s association with the actin cytoskeleton in cancer cells. PP2 (20 μM) increases the expression of α-catenin, β-catenin, and γ-catenin in HT29 cells, whereas in PLC/PRF/5 and MCF-7 cells, the total protein level of α-catenin does not change, but the levels of β- catenin and γ-catenin increases slightly. [3] PP2 inhibits proliferation of two cervical cancer cells (HeLa and SiHa) in a time- and dose-dependent manner. PP2 (10 μM) down-regulates pSrc-Y416, pEGFR-Y845, and -Y1173 expression levels in HeLa and SiHa cells. PP2 (10 μM) could modulate cell cycle arrest by up-regulating p21(Cip1) and p27(Kip1) in both HeLa and SiHa cells and down-regulating expression of cyclin A, and cyclin dependent kinase-2, -4 (Cdk-2, -4) in HeLa and of cyclin B and Cdk-2 in SiHa. [4]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human T cells NF6xSYhHfW6ldHnvckBie3OjeR?= NHzWZZFKdmirYnn0bY9vKG:oIHHkbIV{cW:wIHvpcoF{\SCrbjDoeY1idiCWIHPlcIx{NCCLQ{WwQVAvPiEQvF2u MlvNNVgxPzd|NkO=
human T cells MWLGeY5kfGmxbjDhd5NigQ>? NEHTe5JKdmirYnn0bY9vKG:oIIT5do9{cW6nIIDoc5NxcG:{eXzheIlwdiCrbjDoeY1idiCWIHPlcIx{NCCLQ{WwQVAvPiEQvF2u NUmw[nI6OThyN{ezOlM>
human Saos2 cells M37rWGN6fG:2b4jpZ:Kh[XO|YYm= NGDSTJU1QCCq NHHiSoZEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBU[W:|MjDj[YxteyCjZoTldkA1QCCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVgvODdizszN MnHqNlM6OzJyN{C=
human SaOS2 cells MmX1VJJwdGmoZYLheIlwdiCjc4PhfS=> NX64SWs6SW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDTZW9UOiClZXzsd{Bie3Onc4Pl[EBieyClZXzseYxieiC4aXHibYxqfHluIFnDOVA:QC5zIN88US=> Mn[wNVc6Ojl5OUK=
human MEG01 cells MkjGVJJwdGmoZYLheIlwdiCjc4PhfS=> M4DqTGFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTVXHNFEh[2WubIOsJGlEPTB;MUeg{txO NHrvPWsyQDJ3N{WxNy=>
A431 cells NUfTc|N3TnWwY4Tpc44h[XO|YYm= MkXqTY5pcWKrdH;yfUBm\m[nY4Sgc44heGixc4Doc{1UemNxbn;udIhwe3CqbzDh[pRmeiCHR1[gLFExOCC3TTmgd5RqdXWuYYTpc44hd2ZiQUSzNUBk\WyuczygTWM2OD1zNzFOwG0> NGqzTYkyPTFyOU[0Ni=>
human K562 cells NITzSG1Rem:uaX\ldoF1cW:wIHHzd4F6 NFnDXmxCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFu1OlIh[2WubIOsJGlEPTB;MkWg{txO NVK0O4RzOTh{NUe1NVM>
human KU812 cells NXLB[JJ{WHKxbHnm[ZJifGmxbjDhd5NigQ>? MkS4RY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCNVUixNkBk\WyuczygTWM2OD12NTFOwG0> NIHtNo4yQDJ3N{WxNy=>
8701-BC cells NVvjeWJNTnWwY4Tpc44h[XO|YYm= NGHBO5YyOCEQvF2= M2Pn[HBzd2Gyb4D0c5Rq[yCjY4Tpeol1gSCjZ3HpcpN1KDh5MEGtRmMh[2WubIOgZZQhOTBidV2gZpkhWEGUUDDhd5NigQ>? NEfkW3UyPjVyOUW3Ny=>
A431 cells M4K2ZWZ2dmO2aX;uJIF{e2G7 NFv3SpoyOCEQvF2= MmHlTY5pcWKrdHnvckBw\iCVcnOgZZV1d3Cqb4PwbI9zgWyjdHnvckBw\iC\NEG5JIlvKEF2M{GgZ4VtdHNiYYSgNVAhfU1? NXflVHN{OTZ3MEm1O|M>

... Click to View More Cell Line Experimental Data

In vivo PP2 (5 mg/kg/day) induces some slowing in the growth rate of the primary tumors relative to the control treated with vehicle in SCID mice inoculated HT29 cells in the spleen. PP2 (5 mg/kg/day) induces some slowing in the growth rate of the primary tumors relative to the control treated with vehicle in SCID mice inoculated HT29 cells in the spleen. PP2 (5 mg/kg/day) significantly reduces the relative liver weight and liver metastasis volume compared with the controls in SCID mice inoculated HT29 cells in the spleen. [3] PP2 (1.5 mg/kg i.p.) treated rats show approximately 50% reduction of infarct size on T2-weighted MRI and in TTC staining compared with controls in rats with focal ischemic brain injury. PP2 (1.5 mg/kg i.p.) results in better the neurological score than controls in rats with focal ischemic brain injury. [5]


Kinase Assay:[1]
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Immune complex enzyme assays:

The acid-treated enolase is diluted 1:20 with 1× PBS before aliquoting 100 mL/well into a Nunc 96-well high protein binding assay plate. Assay wells are then aspirated; blocked with 0.5% bovine serum, 1× PBS for 1 h at 37 ℃;and then washed five times with 300 mL of 1× PBS/well. The source of Lck is either LSTRA cells or Lck expressed in HeLa cells using a vaccinia expression system. FynT is expressed in HeLa cells using the vaccinia system. Cells (12.5× 106/mL) are lysed in lysis buffer (20 mM Tris, pH 8.0, 150 mM NaCl, 0.5% Nonidet P-40, and 23 trypsin inhibitory units/mL aprotinin), and the lysates are clarified by centrifugation at 14,000 cpm for 15 min at 4 ℃ in an Eppendorf tube. The clarified lysates are then incubated with the appropriate anti-kinase antibody at 10 μg/mL for 2 h at 4 ℃. Protein A-Sepharose beads are added to the antibody/lysate mixture at 250 μL/mL and allowed to incubate for 30 min at 4 ℃. The beads are then washed twice in 1 mL of lysis buffer and twice in 1 mL of kinase buffer (25 mM HEPES, 3 mM MnCl2, 5mM MgCl2, and 100 μM sodium orthovanadate) and resuspended to 50% (w/v) in kinase buffer. Twenty-five microliters of the bead suspension is added to each well of the enolase-coated 96-well high protein binding plate together with an appropriate concentration of compound and [γ-32P]ATP (25 μL/well of a 200 μCi/mL solution in kinase buffer). After incubation for 20 min at 20 ℃, 60 μLl of boiling 2× solubilization buffer containing 10 mM ATP is added to the assay wells to terminate the reactions. Thirty microliters of the samples is removed from the wells, boiled for 5 min, and run on a 7.5% SDS-polyacrylamide gel. The gels are subsequently dried and exposed to Kodak X-AR film. For quantitation, films are scanned using a Molecular Dynamics laser scanner, and the optical density of the major substrate band, enolase p46, is determined. In companion experiments for measuring the activity of compounds against Lck, the assay plate is washed with two wash cycles on a Skatron harvester using 50 mM EDTA, 1 mM ATP. Scintillation fluid (100 μL) is then added to the wells, and 32P incorporation is measured using a micro-β-counter.
Cell Research:[3]
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  • Cell lines: HT29, SW480, PMCO1, PLC/PRF/5, KYN-2, Li7, HepG2, MCF-7, MDA-MB-468 and BT-474 cell lines
  • Concentrations: ~100 μM
  • Incubation Time: 2 days
  • Method: Cell viability is determined using an in vitro toxicology assay kit following the manufacturer’s instructions. Cells are seeded in 96-well plates at day 0. Starting at day 1, cells are treated for 2 days with each of a series of increasing concentrations of PP2 (1 μM, 10 μM, and 100 μM). At the end of this period, cell proliferation is evaluated by a colorimetric assay based on the cleavage of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide by mitochondria dehydrogenase in viable cells, leading to formazan formation. This experiment is repeated three times with 10 determinations/tested concentration.
    (Only for Reference)
Animal Research:[3]
+ Expand
  • Animal Models: SCID mice inoculated HT29 cells in the spleen
  • Formulation: 1% DMSO
  • Dosages: 5 mg/kg/day
  • Administration: intraperitoneal injection
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 60 mg/mL (198.82 mM)
Ethanol 2 mg/mL (6.62 mM)
Water Insoluble
In vivo Add solvents individually and in order:
4% DMSO+corn oil

* 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 301.77


CAS No. 172889-27-9
Storage powder
Synonyms AG 1879,AGL 1879

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID