product name Aloxistatin
Description: Aloxistatin, also known as E-64d, is a potent, selective, irreversible and membrane-permeable cysteine protease inhibitor. Aloxistatin prevents in vitro cerulein- induced trypsinogen activation. Aloxistatin can enter the intact cell and inhibit calpain. E-64d has been shown safe for the treatment of Alzheimers disease in human. Aloxistatin is potentially useful in the treatment of developmental seizure-induced brain damage both by regulating abnormal zinc signal transduction and through the modulation of altered lipid metabolism via ApoE/clusterin pathway in hippocampus.
References: J Pharmacobiodyn. 1986 Aug;9(8):672-7; Biochem Biophys Res Commun. 1989 Jan 31;158(2):432-5.
342.43
Formula
C17H30N2O5
CAS No.
88321-09-9
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 68 mg/mL (198.6 mM)
Water: <1 mg/mL
Ethanol: 68 mg/mL (198.6 mM)
Solubility (In vivo)
2% DMSO+corn oil: 5 mg/mL
Synonyms
E-64d
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19409607
| In Vitro |
In vitro activity: Aloxistatin can enter the intact platelet and inhibit proteolysis by inhibiting calpain. Aloxistatin blunts Parathyroid hormone (PTH)-induced cell proliferation and inhibits differentiation osteoblasts in vitro. Kinase Assay: Cell Assay: Platelets were activated with A23187 plus calcium, a condition known to lead to calpain-catalyzed proteolysis of ABP and talin. In the absence of inhibitor, A23187 led to complete degradation of ABP and talin. E 64d, the permeant inhibitor, did inhibit intracellular proteolysis. Some inhibition was observed at the lowest concentration tested, 20 μg/ml, and essentially complete inhibition was obtained with 50 μg/ml. |
|---|---|
| In Vivo | After E-64d treatment, mice were treated with penicillin to induce recurrent seizures. The result showed that E-64d remarkably reduced the aberrant mossy fiber sprouting in the supragranular region of dentate gyrus and CA3 subfield of hippocampus. In rats without E-64d treatment, there was prominent aggregation of mossy fiber terminals in the dentate gyrus and in the stratum pyramidale of CA3 subfield. In rats treated with E-64d, the aggregation of mossy fiber terminals was remarkably decreased in both the supragranular region of dentate gyrus and CA3 subfield. |
| Animal model | Male Sprague–Dawley rats |
| Formulation & Dosage | 4 μg; i.p. injection |
| References | J Pharmacobiodyn. 1986 Aug;9(8):672-7; Biochem Biophys Res Commun. 1989 Jan 31;158(2):432-5; Toxicol Lett. 2013 Feb 27;217(2):162-9. |
