AEG 3482inhibitor of Jun kinase (JNK)-dependent apoptosis CAS# 63735-71-7 |
Quality Control & MSDS
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| Cas No. | 63735-71-7 | SDF | Download SDF |
| PubChem ID | 698112 | Appearance | Powder |
| Formula | C10H8N4O2S2 | M.Wt | 280.33 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | AEG-3482,AEG3482 | ||
| Solubility | Soluble to 100 mM in DMSO and to 5 mM in ethanol | ||
| Chemical Name | 6-phenylimidazo[2,1-b][1,3,4]thiadiazole-2-sulfonamide | ||
| SMILES | C1=CC=C(C=C1)C2=CN3C(=N2)SC(=N3)S(=O)(=O)N | ||
| Standard InChIKey | MQUYTXDAVCOCMX-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C10H8N4O2S2/c11-18(15,16)10-13-14-6-8(12-9(14)17-10)7-4-2-1-3-5-7/h1-6H,(H2,11,15,16) | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Inhibitor of c-jun N-terminal kinase (JNK) signaling. Binds Hsp90 and facilitates HSF1 release, induces expression of Hsp70, which in turn blocks JNK activation and JNK-dependent apoptosis. Antiapoptotic; inhibits NGF withdrawal-induced death in SCG neurons (EC50 = 20 μM). |
AEG 3482 Dilution Calculator
AEG 3482 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.5672 mL | 17.8361 mL | 35.6722 mL | 71.3445 mL | 89.1806 mL |
| 5 mM | 0.7134 mL | 3.5672 mL | 7.1344 mL | 14.2689 mL | 17.8361 mL |
| 10 mM | 0.3567 mL | 1.7836 mL | 3.5672 mL | 7.1344 mL | 8.9181 mL |
| 50 mM | 0.0713 mL | 0.3567 mL | 0.7134 mL | 1.4269 mL | 1.7836 mL |
| 100 mM | 0.0357 mL | 0.1784 mL | 0.3567 mL | 0.7134 mL | 0.8918 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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AEG3482 is a small-molecule inhibitor of Jun kinase (JNK)-dependent apoptosis. [1,2]
Jun kinases, also called Jun N-terminal kinase stress-activated protein kinases. Activation of the JNK signaling pathway is a major event in neuronal apoptosis. This is proved by pathological specimens from Alzheimer’s disease, as well as samples from mouse models of Alzheimer’s and Huntington’s disease, reveal activated JNK. [2]
AEG3482 blocks apoptosis induced by the p75 neurotrophin receptor (p75NTR) or NRAGE, which is p75NTR’s cytosolic interactor,. AEG3482 inhibits proapoptotic JNK activity. AEG3482 induces production of heat shock protein 70 (HSP70) which is an endogenous inhibitor of JNK. HSP70 accumulation is required for the AEG3482-induced JNK blockade. [1]
As described, activation of C-jun N-terminal kinase (JNK) signaling is associated with neuronal cell death. AEG3482 interacts with heat shock protein 90 leading to inhibition of JNK and blockade of neuronal apoptosis. So AEG3482 can serve as useful tools for basic research, and it may have therapeutic potential for the treatment of acute and chronic neurological disorders. In the neuropathologicalstate, the chaperone-mediated stress response may be primed for response to Hsp90 inhibitors; and AEG3482, may be selective neuroprotective agents.[1,2]
References:
[1]Salehi AH, Morris SJ, Ho WC, etal. , AEG3482 is an antiapoptotic compound that inhibits Jun kinase activity and cell death through induced expression of heat shock protein 70. Chem Biol. 2006 Feb;13(2):213-23.
[2] Gallo KA. Targeting HSP90 to halt neurodegeneration. Chem Biol. 2006 Feb;13(2):115-6.
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Targeting HSP90 to halt neurodegeneration.[Pubmed:16492558]
Chem Biol. 2006 Feb;13(2):115-6.
Activation of c-jun N-terminal kinase (JNK) signaling is associated with neuronal cell death. As described in this issue of Chemistry & Biology, cell-based screening efforts yielded a compound, AEG3482, which interacts with heat shock protein 90 leading to inhibition of JNK and blockade of neuronal apoptosis .
AEG3482 is an antiapoptotic compound that inhibits Jun kinase activity and cell death through induced expression of heat shock protein 70.[Pubmed:16492569]
Chem Biol. 2006 Feb;13(2):213-23.
We describe a group of small-molecule inhibitors of Jun kinase (JNK)-dependent apoptosis. AEG3482, the parental compound, was identified in a screening effort designed to detect compounds that reduce apoptosis of neonatal sympathetic neurons after NGF withdrawal. We show that AEG3482 blocks apoptosis induced by the p75 neurotrophin receptor (p75NTR) or its cytosolic interactor, NRAGE, and demonstrate that AEG3482 blocks proapoptotic JNK activity. We show that AEG3482 induces production of heat shock protein 70 (HSP70), an endogenous inhibitor of JNK, and establish that HSP70 accumulation is required for the AEG3482-induced JNK blockade. We show that AEG3482 binds HSP90 and induces HSF1-dependent HSP70 mRNA expression and find that AEG3482 facilitates HSP70 production while retaining HSP90 chaperone activity. These studies establish that AEG3482 inhibits JNK activation and apoptosis by a mechanism involving induced expression of HSP proteins.
Neuron specific toxicity of oligomeric amyloid-beta: role for JUN-kinase and oxidative stress.[Pubmed:20858948]
J Alzheimers Dis. 2010;22(3):839-48.
Recent studies have demonstrated a potential role for oligomeric forms of amyloid-beta (Abeta) in the pathogenesis of Alzheimer's disease (AD), although it remains unclear which aspects of AD may be mediated by oligomeric Abeta. In the present study, we found that primary cultures of rat cortical neurons exhibit a dose-dependent increase in cell death following Abeta oligomer administration, while primary cultures of astrocytes exhibited no overt toxicity with even the highest concentrations of oligomer treatment. Neither cell type exhibited toxicity when treated by equal concentrations of monomeric Abeta. The neuron death induced by oligomer treatment was associated with an increase in reactive oxygen species (ROS), altered expression of mitochondrial fission and fusion proteins, and JUN kinase activation. Pharmacological inhibition of JUN kinase ameliorated oligomeric Abeta toxicity in neurons. These data indicate that oligomeric Abeta is sufficient to selectively induce toxicity in neurons, but not astrocytes, with neuron death occurring in a JUN kinase-dependent manner. Additionally, these observations implicate a role for oligomeric Abeta as a contributor to neuronal oxidative stress and mitochondrial disturbances in AD.
