Hydroxyurea | Anticancer agent
NMR (Conforms)
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 g | $54.00 | ||
| 25 g | $185.00 |
Readily oxidized in vivo to free radical forms, which destroy the stable tyrosyl free radical of the metalloenzyme ribonucleotide reductase, suppressing deoxyribonucleotide production and blocking DNA synthesis and repair.1,2 Reduces cell proliferation, and causes S-phase arrest and death.3 Induces p53-dependent NF-κB target gene expression in U2OS cells expressing HA-RelA.4 Stimulates fetal hemoglobin production in vitro and in vivo.5 Allows for S phase enrichment of CHO cells with maintenance of viability for enhanced site-specific genome engineering.6 Anticancer and antiviral agent.
References:
- Gräsland et al. (1985), The tyrosyl free radical in ribonucleotide reductase; Health Perspect., 64 139
- Yarbro (1992), Mechanism of action of hydroxyurea; Oncol., 3 (Suppl 9) 1
- Singh and Xu (2016), The Cell Killing Mechanisms of Hydroxyurea; Genes (Basel), 7 99
- Campbell et al. (2021), Temporal modulation of the NF-kB Re1A network in response to different types of DNA damage; J., 478 533
- Baliga et al. (2000), Mechanism for fetal hemoglobin induction by hydroxyurea in sickle cell erythroid progenitors; J. Hematol., 65 227
- Kwak et al. (2021), Hydroxyurea selection for enhancement of homology-directed targets integration of transgenes in CHO cells; Biotechnol, 62 26
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
Readily oxidized in vivo to free radical forms, which destroy the stable tyrosyl free radical of the metalloenzyme ribonucleotide reductase, suppressing deoxyribonucleotide production and blocking DNA synthesis and repair.1,2 Reduces cell proliferation, and causes S-phase arrest and death.3 Induces p53-dependent NF-κB target gene expression in U2OS cells expressing HA-RelA.4 Stimulates fetal hemoglobin production in vitro and in vivo.5 Allows for S phase enrichment of CHO cells with maintenance of viability for enhanced site-specific genome engineering.6 Anticancer and antiviral agent.
References:
- Gräsland et al. (1985), The tyrosyl free radical in ribonucleotide reductase; Health Perspect., 64 139
- Yarbro (1992), Mechanism of action of hydroxyurea; Oncol., 3 (Suppl 9) 1
- Singh and Xu (2016), The Cell Killing Mechanisms of Hydroxyurea; Genes (Basel), 7 99
- Campbell et al. (2021), Temporal modulation of the NF-kB Re1A network in response to different types of DNA damage; J., 478 533
- Baliga et al. (2000), Mechanism for fetal hemoglobin induction by hydroxyurea in sickle cell erythroid progenitors; J. Hematol., 65 227
- Kwak et al. (2021), Hydroxyurea selection for enhancement of homology-directed targets integration of transgenes in CHO cells; Biotechnol, 62 26
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