| Identification | Back Directory | [Name]
Benzeneacetamide, N-cycloheptyl-α-[(4,5-dihydro-1-methyl-1H-imidazol-2-yl)thio]- | [CAS]
2559703-06-7 | [Synonyms]
Benzeneacetamide, N-cycloheptyl-α-[(4,5-dihydro-1-methyl-1H-imidazol-2-yl)thio]-
N-Cycloheptyl-2-[(1-methyl-4,5-dihydro-1H-imidazol-2-yl)sulfanyl]-2-phenylacetamide | [Molecular Formula]
C19H27N3OS | [MDL Number]
MFCD32899498 | [MOL File]
2559703-06-7.mol | [Molecular Weight]
345.51 |
| Chemical Properties | Back Directory | [density ]
1.21±0.1 g/cm3(Predicted) | [storage temp. ]
Store at -20°C | [solubility ]
DMSO : 83.33 mg/mL (241.19 mM; ultrasonic and warming and adjust pH to 4 with HCl and heat to 80°C) | [form ]
Solid | [pka]
13.99±0.20(Predicted) | [color ]
White to off-white |
| Hazard Information | Back Directory | [Biological Activity]
Apostatin-1 (Apt-1) is a potent TRADD inhibitor. Apostatin-1 can bind with TRADD-N (KD=2.17 μM), disrupting its binding to both TRADD-C and TRAF2. Apostatin-1 modulates the ubiquitination of RIPK1 and beclin 1. Apostatin-1 blocks apoptosis and restores cellular homeostasis by activating autophagy in cells with accumulated mutant tau, α-synuclein, or huntingtin[1].
Apostatin-1 inhibits Velcade (Bortezomib, 0)-induced apoptosis and RIPK1-dependent apoptosis (RDA) and necroptosis, with an IC50 of 0.97 μM[1].Apostatin-1 (10 μM, 6 h) effectively induces autophagy and the degradation of long-lived proteins[1].
Apostatin-1 (20 mg/kg, IP, once) inhibits inflammatory responses, and increases survival of systemic inflammation mouse model[1]. | [References]
[1]. Xu D, et al. Modulating TRADD to restore cellular homeostasis and inhibit apoptosis. Nature. 2020 Nov;587(7832):133-138. |
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