NH125
NH125 Basic information
- Product Name:
- NH125
- Synonyms:
-
- eEF-2 Kinase Inhibitor, NH125 - CAS 278603-08-0 - Calbiochem
- EEF-2 KINASE INHIBITOR
- 1-Hexadecyl-2-methyl-3-(phenylmethyl)-1H-imidazoliumiodide
- eEF-2 Kinase Inhibitor, NH125
- NH125 USP/EP/BP
- 3-Benzyl-1-hexadecyl-2-methyl-1H-imidazol-3-ium iodide
- NH 125,Calmodulin-dependent protein kinases,NH-125,Calmodulin-dependent kinases,NH125,Inhibitor,Autophagy,inhibit,Fungal,Virus Protease,Bacterial,CaMK
- CAS:
- 278603-08-0
- MF:
- C27H45N2.I
- MW:
- 524.567
- Product Categories:
-
- Inhibitors
- Mol File:
- 278603-08-0.mol
NH125 Chemical Properties
- Melting point:
- 88.2-94.9 °C
- storage temp.
- -20°C
- solubility
- DMSO: 20 mg/mL
- form
- solid
- color
- white to off-white
NH125 Usage And Synthesis
Uses
NH125 is an inhibitor of multiple kinases. It kills methicillin-resistant Staphylococcus.
Biological Activity
Histidine protein kinase and eukaryotic elongation factor 2 (eEF-2) kinase (CaMK III) inhibitor (IC 50 = 60 nM) that displays 125-fold, > 1300-fold and > 1500-fold selectivity over PKC, PKA and CaMK II respectively. Exhibits anticancer activity in a variety of malignant cell lines (IC 50 values are 0.7 - 4.8 μ M) and blocks G 1 /S cell cycle progression. Also is an effective antibacterial agent in vitro (IC 50 = 6.6 μ M) and in vivo .
Biochem/physiol Actions
NH125 exhibits anti-proliferation activity against many cancer cells. It also exhibits antibacterial effects by inhibiting bacterial histidine protein kinase.
storage
Desiccate at -20°C
References
[1]. arora, s., et al., identification and characterization of an inhibitor of eukaryotic elongation factor 2 kinase against human cancer cell lines. cancer res, 2003. 63(20): p. 6894-9.
[2]. cheng, y., et al., integrated regulation of autophagy and apoptosis by eef2k controls cellular fate and modulates the efficacy of curcumin and velcade against tumor cells. autophagy, 2013. 9(2): p. 208-19.
[3]. usui, t., et al., eukaryotic elongation factor 2 kinase regulates the development of hypertension through oxidative stress-dependent vascular inflammation. am j physiol heart circ physiol, 2013. 305(5): p. h756-68.
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