API-1

API-1 is a potent selective Akt/PKB inhibitor that reduces the level of phosphorylated Akt (IC50 = 0.8 μM) . API-1 binds to the PH domain and inhibits Akt membrane translocation. API-1 induces c-FLIP degradation. API-1 reduces cell proliferation and induces apoptosis. API-1 decreases tumor growth in mouse xenograft model[1][2][3].

Product Specifications

CAS Number

[36707-00-3]

UNSPSC

12352005

Hazard Statement

H301

Target

Akt; Apoptosis; Caspase; PARP

Type

Reference compound

Related Pathways

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

Applications

Cancer-Kinase/protease

Field of Research

Cancer

Assay Protocol

https://www.medchemexpress.com/api-1.html

Purity

99.62

Solubility

DMSO : 50 mg/mL (ultrasonic; warming; heat to 60°C)

Smiles

O[C@H]1[C@@H](O[C@H](CO)[C@H]1O)N2C3=NC=NC(N)=C3C(C(C(N)=O)=C2)=O

Molecular Formula

C13H15N5O6

Molecular Weight

337.29

Precautions

H301

References & Citations

[1]Li B, et al. The novel Akt inhibitor API-1 induces c-FLIP degradation and synergizes with TRAIL to augment apoptosis independent of Akt inhibition. Cancer Prev Res (Phila) . 2012 Apr;5 (4) :612-20.|[2]Ren H, et al. The E3 ubiquitin ligases β-TrCP and FBXW7 cooperatively mediates GSK3-dependent Mcl-1 degradation induced by the Akt inhibitor API-1, resulting in apoptosis. Mol Cancer. 2013 Nov 22;12:146.|[3]Kim D, et al. A small molecule inhibits Akt through direct binding to Akt and preventing Akt membrane translocation. J Biol Chem. 2010 Mar 12;285 (11) :8383-94.