Amifostine thiol dihydrochloride

Research use only, not for human use.

WR-1065 dihydrochloride can activate p53 through a JNK-dependent signaling pathway. It also protects normal tissues from the toxic effects of certain cancer drugs.

WR-1065 dihydrochloride can activate p53 through a JNK-dependent signaling pathway. It also protects normal tissues from the toxic effects of certain cancer drugs.(In Vitro):The DNA-binding activity is increased in a WR-1065 concentration-dependent manner. Cells treated with 1 mM WR-1065 dihydrochloride for 24 h revealed that all of the p53-induced genes analyzed are transactivated following WR-1065 dihydrochloride treatment, in a p53-dependent manner. Significantly, treatment with WR-1065 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 .(In Vivo):WR-1065 attenuates the severity of 6-OHDA-induced catalepsy when compared with 6-OHDA-lesioned rats. Also, it has been observed that WR-1065 dihydrochloride improves catalepsy in a dose-dependent manner. Pretreatment with three different doses of WR-1065 dihydrochloride (20, 40, and 80 μg/2 μL/rat) for 3 days before 6-OHDA administration, significantly elevates SOD activity and restores it to normal range compare with 6-OHDA lesioned rats .

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WR-1065 dihydrochloride | Amifostine thiol dihydrochloride

Apoptosis

p53

p53

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14653-77-1

207.16

C5H16Cl2N2S

>98% (HPLC)

In Vitro:?H2O : 125 mg/mL (603.40 mM)

Cl.Cl.NCCCNCCS

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(-20℃)

With Ice Pack

≥ 2 years