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JSH-23

NF-κB inhibitor CAS# 749886-87-1

JSH-23

Catalog No. BCC4610----Order now to get a substantial discount!

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Chemical structure

JSH-23

3D structure

Chemical Properties of JSH-23

Cas No. 749886-87-1 SDF Download SDF
PubChem ID 16760588 Appearance Powder
Formula C16H20N2 M.Wt 240.34
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble in DMSO > 10 mM
Chemical Name 4-methyl-1-N-(3-phenylpropyl)benzene-1,2-diamine
SMILES CC1=CC(=C(C=C1)NCCCC2=CC=CC=C2)N
Standard InChIKey YMFNPBSZFWXMAD-UHFFFAOYSA-N
Standard InChI InChI=1S/C16H20N2/c1-13-9-10-16(15(17)12-13)18-11-5-8-14-6-3-2-4-7-14/h2-4,6-7,9-10,12,18H,5,8,11,17H2,1H3
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.
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.
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.

Biological Activity of JSH-23

DescriptionJSH-23 is an inhibitor of NF-κB transcriptional activity with an IC50 value of 7.1 μM.
TargetsNF-κB    
IC507.1 μM     

Protocol

Cell Assay [1]
Apoptosis is analyzed by 4',6-diamidino-2-phenylindole (DAPI) staining. Macrophages RAW 264.7 incubated with JSH-23 are treated with 1 μg/mL LPS and/or sample for 24 h. The cells are stained with 1 μg/mL DAPI for 30 min at 37°C and then analyzed using fluorescence microscopy with excitation at 300-500 nm. Cells with nuclei containing clearly condensed chromatin or cells with fragmented nuclei are scored as an apoptosis index.

Animal Administration [4]
Male Sprague Dawley rats (250-270 g) are used and fed on standard rat diet and water ad libitum. Diabetes is induced by single dose of streptozotocin (STZ, 55 mg/kg, intraperitoneally) in citrate buffer. Blood samples are collected 48 h after STZ administration. Rats with plasma glucose level more than 250 mg/dL are considered as diabetics and are further considered for study. The experimental groups comprised of non-diabetic control rats (ND), diabetic control rats (STZ-D) and diabetic rats treated with two doses of JSH-23 (STZ-D + JSH 1 and STZ-D + JSH 3, respectively, for 1 and 3 mg/kg, orally in 0.5% sodium carboxymethyl cellulose). After 6 weeks of diabetes induction, the drug is administered daily for a period of 2 weeks. The functional, behavioural and biochemical experiments are performed 24 h after the administration of last dose.

References:
[1]. Shin, H.M., et al. Inhibitory action of novel aromatic diamine compound on lipopolysaccharide-induced nuclear translocation of NF-kappaB without affecting IkappaB degradation. FEBS Lett, 2004. 571(1-3): p. 50-4. [2]. Arias-Salvatierra, D., et al. Role of nitric oxide produced by iNOS through NF-kappaB pathway in migration of cerebellar granule neurons induced by Lipopolysaccharide. Cell Signal, 2011. 23(2): p. 425-35. [3]. Kasparkova, J., et al. Different affinity of nuclear factor-kappa B proteins to DNA modified by antitumor cisplatin and its clinically ineffective trans isomer. FEBS J, 2014. 281(5): p. 1393-408. [4]. Kumar, A., et al. JSH-23 targets nuclear factor-kappa B and reverses various deficits in experimental diabetic neuropathy: effect on neuroinflammation and antioxidant defence. Diabetes Obes Metab, 2011. 13(8): p. 750-8.

JSH-23 Dilution Calculator

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Preparing Stock Solutions of JSH-23

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 4.1608 mL 20.8039 mL 41.6077 mL 83.2154 mL 104.0193 mL
5 mM 0.8322 mL 4.1608 mL 8.3215 mL 16.6431 mL 20.8039 mL
10 mM 0.4161 mL 2.0804 mL 4.1608 mL 8.3215 mL 10.4019 mL
50 mM 0.0832 mL 0.4161 mL 0.8322 mL 1.6643 mL 2.0804 mL
100 mM 0.0416 mL 0.208 mL 0.4161 mL 0.8322 mL 1.0402 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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Background on JSH-23

JSH-23 is an inhibitor of NF-κB transcriptional activity with IC50 value of 7.1μM [1].

JSH-23 is developed to inhibit NF-κB transcriptional activity in LPS-stimulated macrophages RAW 264.7. It shows a dose-dependent inhibition. This effect is not due to its cytotoxicity. In the same condition, JSH-23 is found to significantly decrease the LPS-induced DNA binding activity of NF-κB while decrease nuclear amount of NF-κB p65. JSH-23 plays these roles without affecting IκB degradation. In addition, JSH-23 also shows inhibition effects on the expression of the pro-inflammatory transcripts and enzymes, including IL-6, IL-1β, COX-2 and TNF-α. Furthermore, JSH-23 inhibits LPS-induced apoptotic chromatin condensation [1].

References:
[1] Shin HM, Kim MH, Kim BH, Jung SH, Kim YS, Park HJ, Hong JT, Min KR, Kim Y. Inhibitory action of novel aromatic diamine compound on lipopolysaccharide-induced nuclear translocation of NF-kappaB without affecting IkappaB degradation. FEBS Lett. 2004 Jul 30;571(1-3):50-4.

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References on JSH-23

JSH-23 targets nuclear factor-kappa B and reverses various deficits in experimental diabetic neuropathy: effect on neuroinflammation and antioxidant defence.[Pubmed:21447040]

Diabetes Obes Metab. 2011 Aug;13(8):750-8.

AIM: Nuclear factor-kappa B (NF-kappaB) being reported to play an important role in the pathogenesis of diabetic neuropathy is believed to be a central mechanism involved in the genesis and promulgation of inflammatory insult. Here we have targeted the nuclear translocation of NF-kappaB using JSH-23 to elucidate its role in diabetic neuropathy. METHODS: JSH-23 (1 and 3 mg/kg) was administered for 2 weeks in diabetic rats, after 6 weeks of diabetes induction using streptozotocin (55 mg/kg) as diabetogenic agent. Functional (motor nerve conduction velocity and blood flow), behavioural (mechanical hyperalgesia), biochemical [malondialdehyde, glutathione, tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels] and NF-kappaB translocation studies (western blot technique) were then undertaken. RESULTS: JSH-23 treatment significantly reversed the nerve conduction and nerve blood flow deficits seen in diabetic animals. Reduction in mechanical pain threshold was also partially corrected by the treatment. Protein expression studies showed that nuclear translocation of p65/p50 subunit was inhibited by JSH-23 treatment in the sciatic nerve. The treatment also lowered the elevated IL-6, TNF-alpha, cyclo-oxygenase (COX-2) and inducible nitric oxide synthase (iNOS) levels/expression, indicating reduction in the inflammatory damage of the sciatic nerve. Apart from these effects, JSH-23 also increased Nrf2 and hemeoxygenase-1 (HO-1) levels which could imply its potential in increasing the strength of antioxidant defence. CONCLUSION: We observed that NF-kappaB inhibition partially reversed functional, behavioural and biochemical deficits with JSH-23 treatment. This study substantiates the role of NF-kappaB activation in the aetiology of diabetic neuropathy and protection afforded by inhibition of NF-kappaB by JSH-23, which can be attributed to its effect on neuroinflammation and oxidative stress.

Description

JSH-23 is an inhibitor of NF-κB transcriptional activity with IC50 of 7.1 μM in RAW 264.7 cell line.

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