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    Src I1
    Src I1

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V0093
    CAS #: 179248-59-0 Purity ≥98%

    Description: Src Inhibitor 1 (Src-I1) is a novel, potent and selective dual site inhibitor of Src tyrosine kinases with potential anticancer activity. It acts by competitively binding to both the ATP- and peptide-binding sites (IC50 = 44 nM for Src and 88nM for Lck, respectively). Src is a non-receptor tyrosine kinase that is deregulated in many types of cancer. Thus Src Inhibitor 1 (Src-I1) can be potentially used for cancer treatment.

    References:  2007 Dec 15;408(3):297-315;  2001 Jun 19;40(24):7084-91.

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    Molecular Weight (MW) 373.41
    Formula C22H19N3O3 
    CAS No. 179248-59-0 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: >6 mg/mL 
    Water: N/A
    Ethanol: N/A
    Chemical Name6,7-Dimethoxy-N-(4-phenoxyphenyl)-4-quinazolinamine
    SynonymsSrc I1; SrcI1; Src I-1 
    SMILES Code

    Chemical Name: 6,7-Dimethoxy-N-(4-phenoxyphenyl)-4-quinazolinamine


    InChi Code: InChI=1S/C22H19N3O3/c1-26-20-12-18-19(13-21(20)27-2)23-14-24-22(18)25-15-8-10-17(11-9-15)28-16-6-4-3-5-7-16/h3-14H,1-2H3,(H,23,24,25)


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    In Vitro

    In vitro activity: Src Inhibitor 1 ( Src-I1) is a novel, potent and selective dual site Src tyrosine kinase inhibitor which binds competitively to both the ATP- and peptide-binding sites with IC50 values of 44 nM for Src and 88nM for Lck. Src-I1, is found to be a potent inhibitor of Src (IC50=0.18 μM), but also inhibited other Src family members, such as Lck, Csk and Yes with similar potency to Src, and RIP2 (IC50=0.026 μM) with even greater potency. In addition, it inhibited CHK2 with similar potency to Src, and Aurora B with slightly lower potency. 

    Kinase Assay: All assays (25.5 μl volume) were carried out robotically at room temperature (21 °C) and were linear with respect to time and enzyme concentration under the conditions used. Assays were performed for 30 min using Multidrop Micro reagent dispensers (Thermo Electron Corporation, Waltham, MA, U.S.A.) in a 96-well format. The concentration of magnesium acetate in the assays was 10 mM and [γ-33P]ATP (800 c.p.m./pmol) was used at 5, 20 or 50 μM as indicated, in order to be at or below the Km for ATP for each enzyme. Protein kinases assayed at 5 μM ATP were: MKK1, ERK1, p38γ MAPK, p38δ MAPK, ERK8, PKBα, PKCζ, PRK2, GSK3β, CK2, MARK3, IKKβ, DYRK3, PIM2, EF2K, PLK1, Aurora C, HIPK2 and PAK4. Protein kinases assayed at 20 μM ATP were: JNK1, JNK2, p38β MAPK, PDK1, SGK1, S6K1, PKA, ROCK2, PKCα, MSK1, MAPKAP-K2, MAPKAP-K3, PRAK, CaMKKα, CaMKKβ, CHK1, CHK2, CDK2, Aurora B, CK1, PIM1, PIM3, NEK7, MST2, HIPK3, PAK5, PAK6, CSK, Yes and FGF-R1. Protein kinases assayed at 50 μM ATP were: Eph-A2 (Ephrin-A2 receptor), ERK2, JNK3, p38α MAPK, RSK1, RSK2, PKBβ, PKD1, MNK1, MNK2, AMPK, CaMK1, smMLCK, PHK, BRSK2, MELK, DYRK1a, DYRK2, NEK2a, NEK6, SRPK1, Src, Lck, IKKϵ and TBK1. Protein kinases assayed at 0.1 mM ATP were RIP2, GAK, c-Raf and B-Raf.

    In VivoN/A
    Animal modelN/A
    Formulation & DosageN/A
    References 2007 Dec 15;408(3):297-315;  2001 Jun 19;40(24):7084-91.

    These protocols are for reference only. InvivoChem does not independently validate these methods.


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