PI-103

• Description:

  PI-103 is a potent PI3K and mTOR inhibitor with IC50s of 8 nM, 88 nM, 48 nM, 150 nM, 20 nM, and 83 nM for p110α, p110β, p110δ, p110γ, mTORC1, and mTORC2. PI-103 also inhibits DNA-PK with an IC50 of 2 nM. PI-103 induces autophagy[1][2][3][4].

• UNSPSC:

  12352005

• Hazard Statement:

  H302, H315, H319, H335

• Target:

  Apoptosis; Autophagy; DNA-PK; mTOR; PI3K

• Type:

  Reference compound

• Related Pathways:

  Apoptosis; Autophagy; Cell Cycle/DNA Damage; PI3K/Akt/mTOR

• Applications:

  Cancer-Kinase/protease

• Field of Research:

  Cancer

• Assay Protocol:

  https://www.medchemexpress.com/pi-103.html

• Purity:

  99.82

• Solubility:

  DMSO : 10 mg/mL (ultrasonic)

• Smiles:

  OC1=CC(C2=NC3=C(C(N4CCOCC4)=N2)OC5=C3C=CC=N5)=CC=C1

• Molecular Formula:

  C19H16N4O3

• Molecular Weight:

  348.36

• Precautions:

  H302, H315, H319, H335

• References & Citations:

  [1]Raynaud FI, et al. Biological properties of potent inhibitors of class I phosphatidylinositide 3-kinases: from PI-103through PI-540, PI-620 to the oral agent GDC-0941. Mol Cancer Ther. 2009 Jul;8 (7) :1725-39.|[2]Park S, et al. PI-103, a dual inhibitor of Class IA phosphatidylinositide 3-kinase anLeukemia. 2008 Sep;22 (9) :1698-706.d mTOR, has antileukemicactivity in AmL. Leukemia. 2008 Sep;22 (9) :1698-706.|[3]López-Fauqued M, et al. The dual PI3K/mTOR inhibitor PI-103 promotes immunosuppression, in vivo tumor growth and increases survival of melanoma cells. Int J Cancer. 2010 Apr 1;126 (7) :1549-61.|[4]Knight ZA, et al. A pharmacological map of the PI3-K family defines a role for p110 alpha. Cell. 2006 May 19;125 (4) :733-47.

• Shipping Conditions:

  Room Temperature

• Storage Conditions:

  -20°C, 3 years; 4°C, 2 years (Powder)

• Scientific Category:

  Reference compound1

• Clinical Information:

  No Development Reported

• Isoform:

  MTORC1; mTORC2; PI3KC2α; PI3KC2β; PI3Kα; PI3Kβ; PI3Kγ; PI3Kδ; Vps34

• Citation 01:

  Acta Biomater. 2021 Aug:130:409-422.|Adv Funct Mater. 2021 May 24.|Adv Healthc Mater. 2022 May;11 (9) :e2101944.|Am J Cancer Res. 2025 May 15;15 (5) :2097-2110.|Antimicrob Agents Chemother. 2020 Sep 21;64 (10) :e00608-20.|bioRxiv. 2024 May 31:2024.05.30.596676.|bioRxiv. 2025 Oct 31.|BMC Cancer. 2022 Nov 24;22 (1) :1211.|Cancer Lett. 2025 Apr 28:616:217532.|Cell Signal. 2024 Jun:118:111126.|Cell Syst. 2020 Jan 22;10 (1) :66-81.e11. |Cell Syst. 2025 Mar 19;16 (3) :101203.|ChemMedChem. 2019 Nov 20;14 (22) :1933-1939.|Clin Cancer Res. 2014 Nov 1;20 (21) :5483-95. |Clin Cancer Res. 2020 Apr 15;26 (8) :2011-2021. |Exp Eye Res. 2018 Jul:172:10-20.|Expert Rev Anticancer Ther. 2024 Sep 10:1-12.|Front Pharmacol. 2020 Nov 11;11:580407.|Harvard Medical School LINCS LIBRARY|Heliyon. 2024 May 6.|J Transl Med. 2021 Dec 7;19 (1) :497.|J Virol. 2022 Dec 14;96 (23) :e0145322.|Mol Cell. 2025 Apr 3;85 (7) :1411-1425.e8.|Molecules. 2020 Apr 23;25 (8) :1980.|Nat Commun. 2023 Mar 28;14 (1) :1726.|Nat Commun. 2025 May 15;16 (1) :4502.|Oncogenesis. 2025 Mar 1;14 (1) :4.|Princeton University. 2025.|Research Square Preprint. 2022 Jul.|cell rep methods. 2022 Jan 24;2 (2) :100155.|Harvard Medical School LINCS LIBRARY

• CAS Number:

  [371935-74-9]