1. Protein Tyrosine Kinase/RTK
  2. Src
  3. PP2

PP2 (Synonyms: AGL 1879)

Cat. No.: HY-13805 Purity: 98.96%
Handling Instructions

PP2 is a reversible and ATP-competitive Src family kinases inhibitor with IC50s of 4 and 5 nM for Lck and Fyn, respectively.

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

PP2 Chemical Structure

PP2 Chemical Structure

CAS No. : 172889-27-9

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10 mM * 1 mL in DMSO USD 79 In-stock
Estimated Time of Arrival: December 31
5 mg USD 72 In-stock
Estimated Time of Arrival: December 31
10 mg USD 132 In-stock
Estimated Time of Arrival: December 31
50 mg USD 372 In-stock
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100 mg USD 588 In-stock
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Customer Review

Based on 19 publication(s) in Google Scholar

Top Publications Citing Use of Products

    PP2 purchased from MCE. Usage Cited in: Oncotarget. 2017 Nov 22;8(65):109135-109150.

    MCF-7 cells are pretreated with the indicated chemical inhibitors for 30min, followed by 15 min treatment with RA (20 μM) + EPA (80 μM).Cell extracts are prepared and subjected to western blotting analysis.

    PP2 purchased from MCE. Usage Cited in: Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2015 Jul;27(7):568-73.

    To determine whether the inhibition of caveolin-1 tyrosine residues 14 ( Cav-1-Y14 ) phosphorylation with protein tyrosine kinase inhibitors ( PP2 ) will upregulate heme oxygenase-1 ( HO-1 ) activity to protect against ventilation induced lung injury in vivo of an animal model. The group D1 or D2 receive high tidal volume ventilation for 1 hour or 2 hour respectively, but they are given PP2 1 hour before high tidal volume ventilation. The groups E1 and E2 also receive high tidal volume ventilat

    PP2 purchased from MCE. Usage Cited in: J Cell Mol Med. 2018 May 12;22(8):3768-3781.

    Prostate cancer cells are grown and treated with different concentrations of the Src inhibitor PP2 for 2 h and subjected to Western blot analysis. The data show that the inhibition of Src dose dependently decreases levels of p-Src527 but not p-Src426.

    PP2 purchased from MCE. Usage Cited in: Cancer Sci. 2018 May;109(5):1648-1659.

    Cells are treated with vehicle (0.1% DMSO) or PP2 (2.5 μM and 5 μM) for 48 h. Cell lysates are harvested. Total and phosphorylated c-Src are detected by western blotting.

    PP2 purchased from MCE. Usage Cited in: FASEB J. 2020 Jun 15.

    Cells are pretreated with PP2 (10 μM) for 24 hours and further treated with MMS, and GAPDH nuclear translocation is visualized by confocal microscopy. The immunofluorescence staining results directly show that inhibiting Src activity by PP2 decreases GAPDH nuclear distribution in response to MMS.
    • Biological Activity

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    PP2 is a reversible and ATP-competitive Src family kinases inhibitor with IC50s of 4 and 5 nM for Lck and Fyn, respectively.

    IC50 & Target

    IC50: 4 nM (Lck), 5 nM (Fyn)[1]

    In Vitro

    At 10 μM, the effect of PP2 on cellular proliferation is not significant, indicating that, at this low concentration, the effect of PP2 on Gemcitabine cytotoxicity does not simply reflect a direct antiproliferative effect, but rather a potentiation of Gemcitabine-induced cytotoxicity. Above 20 μM, growth is increasingly suppressed, a finding consistent with reports in other human cancer cell lines. Although 10 μM PP2 is used in our study, at higher concentrations PP2 is reported to inhibit other intracellular kinases[2]. PP2 is the most widely used commercially available Src family kinase inhibitor. PP2 inhibits Src family kinase activity with IC50 of ~5 nM in vitro, concentrations to 10 μM are often necessary to achieve complete Src family kinase inhibition in cell culture[3].

    In Vivo

    The tumor growth inhibition rate is 25% in the PP2 treatment group and 5% in the Gemcitabine treatment group (P>0.05). When administered in combination, PP2 and Gemcitabine produce a tumor growth inhibition rate of 98% (P<0.05). Hepatic metastasis occurred in 100% of control and Gemcitabine-treated groups; 88% of the PP2-treated group developed liver metastases. There are no detectable metastases in the group treated with PP2 and Gemcitabine in combination (P<0.05)[2].

    Molecular Weight




    CAS No.





    Room temperature in continental US; may vary elsewhere.

    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Solvent & Solubility
    In Vitro: 

    DMSO : 50 mg/mL (165.69 mM; Need ultrasonic)

    H2O : < 0.1 mg/mL (insoluble)

    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 3.3138 mL 16.5689 mL 33.1378 mL
    5 mM 0.6628 mL 3.3138 mL 6.6276 mL
    10 mM 0.3314 mL 1.6569 mL 3.3138 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  10% DMSO    90% corn oil

      Solubility: ≥ 3 mg/mL (9.94 mM); Clear solution

    *All of the co-solvents are provided by MCE.
    Cell Assay

    Cell growth is determined by MTT assay and confirmed by cell counting. Results of the MTT assay have been shown to correlate well with [3H]thymidine incorporation in pancreatic cancer cell lines. Logarithmically growing cells are plated at 5×103 cells/well in 96-well plates, allowed to adhere for 24 h, and cultured in the presence or absence of PP2 and Gemcitabine. Cell proliferation is determined after 96 h. Plates are read using a Vmax microplate spectrophotometer at a wavelength of 570 nm corrected to 650 nm and normalized to controls. Each independent experiment is performed three times, with 10 determinations for each condition tested. The IC50 of Gemcitabine is calculated from these results. At identical time points, cells are trypsinized to form a single cell suspension. Intact cells, determined by trypan blue exclusion, are counted using a Neubauer hemocytometer, and the number of cells per mL is calculated and compared with the control group to confirm the MTT results[2].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration

    Male athymic nu/nu mice (age, 5 weeks; weight, 20-22 g; specific pathogen free) are anesthetized with i.p. ketamine (200 mg/kg) and xylazine (10 mg/kg) and inoculated with 106 Gemcitabine-resistant PANC1GemRes cells in 20 μL of PBS by surgical orthotopic implantation into the pancreas. After inoculation, mice are randomized to three treatment groups: (a) treatment group 1 (n=8) receive 2 mg/kg PP2 in 1% DMSO by i.p. injection three times a week; (b) treatment group 2 (n=8) receive Gemcitabine (100 mg/kg) in the same volume of 1% DMSO vehicle as received by group 1, three times a week; and (c) treatment group 3 (n=8) receive 2 mg/kg PP2 and 100 mg/kg Gemcitabine in the same volume of DMSO as groups 1 and 2, three times a week. The control group receive the same volume of 1% DMSO vehicle as the other groups, three times a week. Treatment is commenced 1 day after implantation, and necropsy is performed 4 weeks after implantation. Primary tumors are identified, weighed, and normalized to total body mass. Tumor growth inhibition rate is calculated using the following formula: tumor growth inhibition rate (%)=(1−MT/MC)×100, where MT and MC are the mean normalized tumor masses of treatment and control groups, respectively. Liver metastases are counted and confirmed histologically.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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    PP2AGL 1879PP 2PP-2AGL1879AGL-1879SrcInhibitorinhibitorinhibit

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