An inhibitor of Akt1 and Akt2
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3CAI

Item No. 14303

Product Insert (PDF)Safety Data Sheet (SDS) (PDF)
Technical Information
Formal Name
2-chloro-1-(1H-indol-3-yl)-ethanone
CAS Number
28755-03-5
Synonyms
  • 3-chloroacetyl Indole
Molecular Formula
C10H8ClNO
Formula Weight
193.6
Purity
≥95%
Formulation (Request formulation change)
A crystalline solid
Solubility(Learn about Variance in Solubility)
DMF: 50 mg/mlDMF:PBS (pH 7.2); (1:7): 0.125 mg/mlDMSO: 33 mg/mlEthanol: 17 mg/ml
λmax
244, 304 nm
SMILES
O=C(CCl)C1=CNC2=CC=CC=C21
InChi Code
InChI=1S/C10H8ClNO/c11-5-10(13)8-6-12-9-4-2-1-3-7(8)9/h1-4,6,12H,5H2
InChi Key
LLZQFAXTCYDVTR-UHFFFAOYSA-N
Shipping & Storage Information
Storage
-20°C
Shipping
Room temperature in continental US; may vary elsewhere
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    250 mg

    $103

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    500 mg

    $183

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    1 g

    $303

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    Product Description

    3CAI is an inhibitor of Akt1 and Akt2 with anticancer activity.1 It inhibits Akt1 and Akt2 in a kinase assay in a concentration-dependent manner, but has no effect on MEK1, JNK1, ERK1, or PDZ binding kinase (PBK) when used at a concentration of 1 µM. 3CAI (4 µM) increases apoptosis in HCT116 and HT-29 colon cancer cells and inhibits the growth of HCT116 cells in vitro in a concentration-dependent manner. Oral administration of 3CAI (30 mg/kg) reduces tumor growth in an HCT116 mouse xenograft model. It also decreases status epilepticus-induced vasogenic edema to 0.46-fold of vehicle control levels and reduces increases in endothelial nitric oxide synthase (eNOS) levels in the piriform cortex in rats when administered at a dose of 25 µM.2

    WARNING This product is not for human or veterinary use.

    References & Product Citations
    Product Description References

    1. Kim, D.J., Reddy, K., Kim, M.O., et al. (3-Chloroacetyl)-indole, a novel allosteric AKT inhibitor, suppresses colon cancer growth in vitro and in vivo. Cancer Prev. Res. (Phila.) 4(11), 1842-1851 (2011).

    2. Kim, J.-E., and Kang, T.-C. TRPC3- and ETB receptor-mediated PI3K/AKT activation induces vasogenic edema formation following status epilepticus. Brain Res. 1672, 58-64 (2017).