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Products are for research use only. Not for human use. We do not sell to patients.

Signaling Pathway



(PI 103; PI103)

PI-103 Chemical Structure

PI103 is a potent inhibitor with low IC50 values against recombinant PI3K isoforms p110alpha (IC50= 2 nM), p110beta (IC50= 3 nM), p110delta (IC50= 3 nM), and p110gamma (IC50= 15 nM), less potent to mTOR/DNA-PK with IC50 of 30 nM/23 nM.

Price and Availability of PI-103
Size Price Stock
10 mg $55 In-stock
25 mg $110 Backordered
50 mg $200 Backordered
200 mg $570 Backordered
500 mg $1100 Backordered
>1000 mg Get quote
For PI-103, please see related products: PI-103 Hydrochloride
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PI-103 Data Sheet

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Purity: 99.59%

Cell Cycle/DNA Damage

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Biological Activity of PI-103

PI-103 is inhibitor of DNA-PK, PI 3-kinase (p110α) and mTOR. (IC50 values are 2, 8, 20, 26, 48, 83, 88, 150, 850, 920, ~ 1000 and 2300 nM for DNA-PK, p110α, mTORC1, PI3KC2β, p110δ, mTORC2, p110β, p110γ, ATR, ATM, PI3KC2α and hsVPS34 respectively). PI-103 inhibits growth of human tumor xenografts in mice in vivo.

Clinical Information


References on PI-103

1 . Opel D, Naumann I, Schneider M, Bertele D, Debatin KM, Fulda S.Targeting aberrant PI3K/Akt activation by PI103 restores sensitivity to TRAIL-induced apoptosis in neuroblastoma.Clin Cancer Res. 2011 May 15;17(10):3233-47. Epub 2011 Feb 25.
PURPOSE: Because we recently identified Akt activation as a novel poor prognostic indicator in neuroblastoma, we investigated whether phosphoinositide 3'-kinase (PI3K) inhibition sensitizes neuroblastoma cells for TRAIL-induced apoptosis. EXPERIMENTAL DESIGN: The effect of pharmacological or genetic inhibition of PI3K or mTOR was analyzed on apoptosis induction, clonogenic survival, and activation of apoptosis signaling pathways in vitro and in a neuroblastoma in vivo model. The functional relevance of individual Bcl-2 family proteins was examined by knockdown or overexpression experiments.

2 . Gürsel DB, Connell-Albert YS, Tuskan RG, Anastassiadis T, Walrath JC, Hawes JJ, Amlin-Van Schaick JC, Reilly KM.Control of proliferation in astrocytoma cells by the receptor tyrosine kinase/PI3K/AKT signaling axis and the use of PI-103 and TCN as potential anti-astrocytoma therapies.Neuro Oncol. 2011 Jun;13(6):610-21.
A growing body of work suggests that astrocytomas and glioblastoma multiforme will require carefully tailored, molecularly targeted therapy for successful treatment. Recent efforts to comprehensively identify mutations and gene expression changes in glioblastoma have shown that mutation of NF1 is a common alteration in human glioblastoma. We have developed and characterized a panel of 14 tumor lines from grades II through IV astrocytomas developed from our Nf1-/+;Trp53-/+cis mouse model and have used this panel to characterize signal transduction pathways and inhibitors that are candidate therapeutic targets for astrocytoma and glioblastoma. We show that these tumors express platelet-derived growth factor receptor-α, epidermal growth factor receptor, and their respective ligands to varying degrees. We find that both the MEK and PI3K signaling pathways downstream of epidermal growth factor receptor and platelet-derived growth factor receptor-α are necessary for full proliferation of astrocytoma cells; however, inhibition of the PI3K pathway is more effective than inhibition of MEK at blocking cell growth. We have examined inhibitors of the PI3K/Akt/mTOR signaling pathway and find that PI-103 and TCN show particular promise for inhibiting growth in Nf1 and Trp53 mutant astrocytoma cells.

3 . Hong Z, Xiao M, Yang Y, Han Z, Cao Y, Li C, Wu Y, Gong Q, Zhou X, Xu D, Meng L, Ma D, Zhou J.Arsenic disulfide synergizes with the phosphoinositide 3-kinase inhibitor PI-103 to eradicate acute myeloid leukemia stem cells by inducing differentiation.Carcinogenesis. 2011 Oct;32(10):1550-8. Epub 2011 Jul 29.
Although dramatic clinical success has been achieved in acute promyelocytic leukemia (APL), the success of differentiating agents has not been reproduced in non-APL leukemia. A key barrier to the clinical success of arsenic is that it is not potent enough to achieve a clinical benefit at physiologically tolerable concentrations by targeting the leukemia cell differentiation pathway alone. We explored a novel combination approach to enhance the eradication of leukemia stem cells (LSCs) by arsenic in non-APL leukemia. In the present study, phosphatidylinositol 3-kinase /AKT/mammalian target of rapamycin (mTOR) phosphorylation was strengthened after As(2)S(2) exposure in leukemia cell lines and stem/progenitor cells, but not in cord blood mononuclear cells (CBMCs). propidium iodide-103, the dual PI3K/mTOR inhibitor, effectively inhibited the transient activation of the PI3K/AKT/mTOR pathway by As(2)S(2). The synergistic killing and differentiation induction effects on non-APL leukemia cells were examined both in vitro and in vivo. Eradication of non-APL LSCs was determined using the nonobese diabetic/severe combined immunodeficiency mouse model. We found that a combined As(2)S(2)/PI-103 treatment synergized strongly to kill non-APL leukemia cells and promote their differentiation in vitro. Furthermore, the combined As(2)S(2)/PI-103 treatment effectively reduced leukemia cell repopulation and eradicated non-APL LSCs partially via induction of differentiation while sparing normal hematopoietic stem cells. Taken together, these findings suggest that induction of the PI3K/AKT/mTOR pathway could provide a protective response to offset the antitumor efficacy of As(2)S(2). Targeting the PI3K/AKT/mTOR pathway in combination with As(2)S(2) could be exploited as a novel strategy to enhance the differentiation and killing of non-APL LSCs.

4 . Park, S.; Chapuis, N.; Bardet, V.; Tamburini, J.; Gallay, N.; Willems, L.; PI-103, a dual inhibitor of Class IA phosphatidylinositide 3-kinase and mTOR, has antileukemic activity in AML. Leukemia (2008), 22(9), 1698-1706.
The phosphatidylinositol 3-kinase (PI3K)/Akt and mammalian target of rapamycin complex 1 (mTORC1) signaling pathways are frequently activated in acute myelogenous leukemia (AML). mTORC1 inhibition with RAD001 induces PI3K/Akt activation and both pathways are activated independently, providing a rationale for dual inhibition of both pathways. PI-103 is a new potent PI3K/Akt and mTOR inhibitor. In human leukemic cell lines and in primary blast cells from AML patients, PI-103 inhibited constitutive and growth factor-induced PI3K/Akt and mTORC1 activation. PI-103 was essentially cytostatic for cell lines and induced cell cycle arrest in the G1 phase. In blast cells, PI-103 inhibited leukemic pro...

5 . Westhoff, M.-A.; Kandenwein, J. A.; Karl, S.; Vellanki, S. H. K.; Braun, V.; The pyridinylfuranopyrimidine inhibitor, PI-103, chemosensitizes glioblastoma cells for apoptosis by inhibiting DNA repair. Oncogene (2009), 28(40), 3586-3596.
The failure of conventional therapies in glioblastoma (GBM) is largely due to an aberrant activity of survival cascades, such as PI3 kinase (PI3K)/Akt-mediated signaling. This study is the first to show that the class I PI3K inhibitor, PI-103, enhances chemotherapy-induced cell death of GBM cells. Concurrent treatment with PI-103 and DNA-damaging drugs, in particular doxorubicin, significantly increases apoptosis and reduces colony formation compared with chemotherapy treatment alone. The underlying molecular mechanism for this chemosensitization was shown by two independent approaches, that is, pharmacological and genetic inhibition of PI3K, DNA-PK and mTOR, to involve inhibition of DNA-PK-...

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