research use only

6AN (6-Aminonicotinamide) Dehydrogenase inhibitor

Cat.No.S9783

6-Aminonicotinamide (6AN) is an antimetabolite used to inhibit the NADPH-producing pentose phosphate pathway (PPP) in many cellular systems, making them more susceptible to oxidative stress. It is a competitive inhibitor of the NADP+-dependent enzyme glucose-6-phosphate dehydrogenase (G6PD) with Ki of 0.46 μM.
6AN (6-Aminonicotinamide) Dehydrogenase inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 137.14

Quality Control

Chemical Information, Storage & Stability

Molecular Weight 137.14 Formula

C6H7N3O

Storage (From the date of receipt) 3 years -20°C powder
CAS No. 329-89-5 -- Storage of Stock Solutions

Solubility

In vitro
Batch:

DMSO : 27 mg/mL (196.87 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Water : Insoluble

Ethanol : Insoluble

Molarity Calculator

Mass Concentration Volume Molecular Weight

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
G6PD [1]
(Cell-free assay)
0.46 μM(Ki)
In vitro

Blocking the pentose phosphate pathway (PPP) with 6-AN (6-Aminonicotinamide) significantly inhibits mES colony formation in the presence of a normal concentration of glucose. This compound effectively inhibits AKT phosphorylation and activation of its downstream effector S6, while having no effect on the ERK and PDK1 activities, suggesting an AKT-specific effect. It also inhibits cell growth.[2]

In vivo

PTEN null human cancer cells and in vivo murine models are sensitive to 6-AN (6-Aminonicotinamide, anti-PPP, anti pentose phosphate pathway) treatments, suggesting the importance of the PPP in maintaining AKT activation even in the presence of a constitutively activated PI3K pathway. The treatment of TALL models with this compound significantly increases the Phlda3 mRNA and protein levels, accompanied by substantial decreases in the levels of P-AKT and P-S6 as well as the PPP metabolic intermediates.[2]

References

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