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Deguelin Akt inhibitor

Cat.No.S8132

Deguelin, a natural product isolated from plants in the Mundulea sericea family, is an PI3K/AKT Inhibitor.
Deguelin Akt inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 394.42

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Chemical Information, Storage & Stability

Molecular Weight 394.42 Formula

C23H22O6

 Storage (From the date of receipt)
CAS No. 522-17-8 Download SDF Storage of Stock Solutions

Synonyms (-)-Deguelin, (-)-cis-Deguelin Smiles CC1(C=CC2=C(O1)C=CC3=C2OC4COC5=CC(=C(C=C5C4C3=O)OC)OC)C

Solubility

In vitro
Batch:

DMSO : 78 mg/mL ( (197.75 mM) Moisture-absorbing DMSO reduces solubility. Please use fresh DMSO.)

Ethanol : 78 mg/mL

Water : Insoluble

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In vivo
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Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Mechanism of Action

Targets/IC50/Ki
PI3K [1]
Akt [1]
In vitro
Deguelin downregulates Akt phosphorylation in leukaemia cell lines with an active PI3K/Akt axis. At 10 or 100 nmol/l, this compound is effective in inhibiting Akt phosphorylation. Total Akt expression is unchanged by it. Moreover, it does not affect the expression or the phosphorylation levels of either p44/42 or p38 MAP kinases in U937 cells. It increases sensitivity of human leukaemia cells to chemotherapeutic drugs. This chemical dephosphorylates Akt and increases cytarabine sensitivity of AML blasts but not of CB CD34+. It, when employed for 24 h at 10 nmol/l, causes an S phase arrest of U937 cells, with interference of progression to G2/M phase. While employed alone up to a concentration of 10 nmol/l for 24 h, it does not significantly increase the apoptotic rate of U937 cells[1].
In vivo
Deguelin inhibits in vivo angiogenesis of chick chorioallantoic membrane (CAM) without cytotoxic effect and significantly reduces laser-induced CNV in a mouse model of AMD without significant retinal toxicity[2]. It exhibited significant anti-tumorigenesis and anti-proliferative activity in various types of cancer both in vitro and in vivo. In pre-clinical trials, this compound markedly decreased the tumor incidence. Topically-administered deguelin significantly suppressed the multiplicity of skin tumors with UVB-induction, indicating its effect as a potential cancer chemopreventive agent. In A/J mice, this chemical clearly reduced the tumor multiplicity and volume, as well as the overall tumor burden with exposure to the tobacco-specific carcinogen benzo(a)pyrene (Bap) and other carcinogens, with no detectable toxicity. Nevertheless, the toxicity of this compound over a certain dose should not be neglected. Treatment with deguelin, a potential mitochondria complex I inhibitor, reduced tyrosine hydroxylase-positive neurons, leading to Parkinson’s disease. Kim et al shows that this chemical promoted a PD-like syndrome, mainly by Src/STAT signaling, since α-synuclein (a key protein function in the pathogenesis of PD) was phosphorylated by deguelin-activated Src[3].
References

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