Amifostine thiol dihydrochlorideAmifostine thiol dihydrochloride
MedChemExpress (MCE)
HY-103640
14653-77-1
WR-1065 dihydrochloride
97.0%
-20°C, sealed storage, away from moisture *In solvent : -80°C, 6 months
-20°C, 1 month (sealed storage, away from moisture)
Room temperature in continental US
may vary elsewhere.
Amifostine thiol (WR-1065) dihydrochloride can protect normal tissues from the toxic effects of certain cancer agents and activate p53 through a JNK-dependent signaling pathway.
The DNA-binding activity is increased in a Amifostine thiol dihydrochloride (Amifostine thiol) concentration-dependent manner. Cells treated with 1 mM Amifostine thiol dihydrochloride for 24 h reveal that all of the p53-induced genes analyzed are transactivated following Amifostine thiol dihydrochloride treatment, in a p53-dependent manner. Significantly, treatment with Amifostine thiol dihydrochloride leads to a 3-fold increase in luciferase expression driven by AP-1, and a 5-fold increase when this reporter gene is driven by NF-κB, when these values are normalized to the level of the cotransfected β-galactosidase gene[2].
The results show that Amifostine thiol dihydrochloride (Amifostine thiol) attenuates the severity of 6-OHDA-induced catalepsy (PSOD activity and restores it to normal range compare with 6-OHDA lesioned rats[3].
Seventy two rats are divided randomly into 9 equal groups: 1) Control group receives no injection and is left untreated for the entire period of the experiment as intact animals
2) Sham operated group is subjected only to surgical procedure
3) Vehicle (saline)-treated group receives 2 μL saline (intra-SNc)
4) Lesioned group receives 6-hydroxydopamine
5) Vehicle+6OHDA group receives saline as a vehicle 3 days once daily (2 μL/rat) before 6-OHDA injection
6 to 8) Rats in these groups are pretreated with intra-SNc injection of WR-1065 dihydrochloride (WR-1065) (20, 40 and 80 μg/2 μL/rat) 3 days before 6-OHDA injection
9) Non-lesioned animals receive intra-SNc injection of WR-1065 dihydrochloride (80 μg/2 μL/rat) for three days[3].
To test the effects of paclitaxel in the presence or absence of WR-1065 dihydrochloride (WR-1065) on cell growth, cells are seeded in 96-well tissue culture dishes at 20% confluence and allowed to attach and recover for at least 24 h. Varying combinations of paclitaxel alone or in combination with a 60 min pretreatment with 1 mM WR-1065 dihydrochloride are then added to each well, and the plates are incubated for an additional 48 h or 72 h. The number of surviving cells is determined by staining. The percentage of cells killed by paclitaxel and/or WR-1065 dihydrochloride is calculated as the percentage decrease in sulforhodamine B binding compare with control cells[2].
For Western analysis, cells are treated with 1 mM WR-1065 dihydrochloride (WR-1065) for 24 h, and subconfluent cultures of cells are harvested and lysed in RIPA buffer supplemented with protease inhibitors. Protein concentrations are determined by a detergent-compatible assay. Western blots are blocked and incubated in antibody in PBS/0.2% Tween 20/5% nonfat dry milk. Blots are incubated with 1 μg/mL antibody for 1 h at room temperature, followed by washing in PBS/0.2% Tween 20 and incubation in peroxidase-conjugated secondary antibody and chemiluminescence detection[2].
p53[1] In Vitro The DNA-binding activity is increased in a Amifostine thiol dihydrochloride (Amifostine thiol) concentration-dependent manner. Cells treated with 1 mM Amifostine thiol dihydrochloride for 24 h reveal that all of the p53-induced genes analyzed are transactivated following Amifostine thiol dihydrochloride treatment, in a p53-dependent manner. Significantly, treatment with Amifostine thiol dihydrochloride leads to a 3-fold increase in luciferase expression driven by AP-1, and a 5-fold increase when this reporter gene is driven by NF-κB, when these values are normalized to the level of the cotransfected β-galactosidase gene[2]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> Amifostine thiol dihydrochloride Related Antibodies
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[1]. Pluquet O, et al. The cytoprotective aminothiol WR1065 activates p53 through a non-genotoxic signaling pathway involving c-Jun N-terminal kinase. J Biol Chem. 2003 Apr 4
278(14):11879-87. [Content Brief]
[2]. Shen H, et al. Binding of the aminothiol WR-1065 to transcription factors influences cellular response to anticancer drugs. J Pharmacol Exp Ther. 2001 Jun
297(3):1067-73. [Content Brief]
[3]. Afshin Kheradmand, et al. Effect of WR-1065 on 6-hydroxydopamine-induced catalepsy and IL-6 level in rats. Iran J Basic Med Sci. 2016 May
19(5): 490-496. [Content Brief]
