CAS No. : 149003-01-0
(Synonyms: ICRF-187 (hydrochloride); ADR-529 (hydrochloride); NSC-169780 (hydrochloride))
| Size | Price | Stock |
|---|---|---|
| 5mg | $38 | In-stock |
| 10mg | $60 | In-stock |
| 50mg | $114 | In-stock |
| 100mg | $156 | In-stock |
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| Cat. No. : | HY-76201 |
| M.Wt: | 341.19 |
| Formula: | C11H18Cl2N4O4 |
| Purity: | >98 % |
| Solubility: | H2O : 20 mg/mL (ultrasonic);DMSO : 50 mg/mL (ultrasonic) |
Dexrazoxane hydrochloride (ICRF-187 hydrochloride) is a heart protectant that can help preserve ovarian function and fertility. Dexrazoxane hydrochloride has antioxidant and anti-inflammatory properties, can cross the blood-brain barrier, improves motor function disorders, and offers neuroprotective effects, making it useful in the study of neurodegenerative diseases[1][2][3][4].
IC50 & Target:As a derivative of EDTA, dexrazoxane chelates iron, thus reduce the number of metal ions complexed with anthracycline and, consequently, decrease the formation of superoxide radicals. This agent is used to protect the heart against the cardiotoxic side effects of anthracyclines, such as doxorubicin. It was speculated that dexrazoxane could be used for further investigation to synthesize new antimalarial drugs.
In Vitro:Dexrazoxane (0-500 μM; 0-24 h) induces DNA breaks, ATF3 accumulation, DNA damage response and apoptosis in human fibrosarcoma cell line[1].
Dexrazoxane hydrochloride protects ovarian cells from DXR-induced DNA damage (neutral comet assay)[2].
In Vivo:Dexrazoxane hydrochloride (20 mg/kg, intraperitoneal injection, single dose) reduces acute ovarian toxicity induced by DXR (HY-121259) in mice, improving long-term fertility[2].
Dexrazoxane hydrochloride (0-120 mg/kg, intravenous injection, once a week for 13 weeks) dose-dependently reduces DOX-induced heart toxicity in rats, mice, and dogs, but the efficacy decreases at higher doses of DOX[3].
Dexrazoxane hydrochloride (1.5-15 mg/kg, intraperitoneal injection, single dose) improves motor dysfunction in mice, protects dopaminergic neurons from neurotoxin-induced SNc degeneration, along with reduced activation of glial cells, and inhibits oxidative stress and endoplasmic reticulum stress[4].
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