Hydralazine
CAS No. : 86-54-4
Price and Availability of
CAS No. : 86-54-4
| Size | Price | Stock |
|---|---|---|
| 5mg | $62 | In-stock |
| 10mg | $100 | In-stock |
| 25mg | $203 | In-stock |
| 50mg | $325 | In-stock |
| 100mg | $520 | In-stock |
| 200 mg | Get quote | |
| 500 mg | Get quote | |
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| Cat. No. : | HY-B0464A |
| M.Wt: | 160.18 |
| Formula: | C8H8N4 |
| Purity: | >98 % |
| Solubility: | DMSO : 20 mg/mL (ultrasonic;warming;heat to 60°C) |
Introduction of
86-54-4
:
Hydralazine (10 μM; 24 hours) reduces DNMT1 and DNMT3a mRNA expression in MCF-7 breast cancer cells[1].
Hydralazine (0.1-10.0 mM) does not impair phagocytic function or viability of thioglycollate-prestimulated rat peritoneal macrophages[2].
Hydralazine (0.1-10.0 mM) significantly inhibits nitrite production by LPS/IFN-γ-stimulated thioglycollate-prestimulated rat peritoneal macrophages, with an IC50 of 0.43 ± 0.03 mM[2].
Hydralazine (1.0-10.0 mM) inhibits both NOS-2 and COX-2 protein synthesis in LPS/IFNγ-stimulated thioglycollate-prestimulated rat peritoneal macrophages[2].
Hydralazine (3.1-50 nmol, plate incorporation test without S-9 mix; 1 mg per plate, spot test with/without S-9 mix) is a direct-acting, low-potency mutagen that induces mixed genetic mutation mechanisms in Salmonella typhimurium strains TA1535, TA100, TA1537, TA97, and TA98, with highest potency in strain TA97[3].
Hydralazine (5 mg per spot, spot test; serial twofold dilutions, micromethod assay with/without S-9 mix; 16 h incubation at 37°C) is a direct-acting genotoxin that is preferentially lethal to repair-deficient Escherichia coli strains WP67 and CM871, indicating involvement of recA recombination repair, lexA post-replication repair, and polA repair mechanisms, with no dependence on excision repair systems[3].
Hydralazine (≤25 μM) significantly mitigates acrolein-mediated cell death in PC12 cells[4]. In Vivo:Hydralazine (i.p.; daily; 7 d) promotes demethylation of the estrogen receptor gene promoter and reactivates estrogen receptor expression in MDA-MB-231 breast cancer xenografts in nude mice[1].
Hydralazine (used in combination with valproic acid (HY-10585)) eliminates tumor recurrence of HT1080 fibrosarcoma xenografts in nude mice[1].
Hydralazine (83 mg/kg; i.p.; once daily; 5 days) induces DNA fragmentation in the liver, kidney and spleen (but not the lung) of mice at 6 hours after the last administration, and the damage is completely repaired at 12 hours post-administration; meanwhile, it moderately increases the sister chromatid exchange rate of mouse bone marrow cells by 33%[3].
Hydralazine (5 mg/kg; i.p.; twice; 14 d) reduces acrolein levels by 50-70% in the injured spinal cord of rats, decreases post-injury cyst formation by 70%, improves motor function recovery, and alleviates mechanical hyperalgesia in rat models of spinal cord injury[4].
Hydralazine (0.1-10 mg/kg; i.p.; single dose) dose-dependently alleviates formalin-induced somatic and emotional inflammatory pain in male C57BL/6 mice, with a ED50 of 0.239-1.0160 mg/kg, while inhibiting excessive acrolein production and neuronal activation in the spinal cord[5].
Hydralazine (10 mg/kg; i.p.; single dose) does not impair central nervous system function in male C57BL/6 mice[5].
Hydralazine is an orally active, blood-brain barrier-permeable DNA methyltransferase inhibitor with vasodilatory, arterial smooth muscle relaxant and hypotensive activities. Hydralazine reactivates silenced tumor suppressor genes via mediating DNA demethylation, while exerting neuroprotective and anti-inflammatory properties. Hydralazine inhibits NOS-2 (iNOS) and COX-2, and reduces the production of NO and PGEE2; meanwhile, Hydralazine scavenges reactive oxygen species and inhibits macrophage activation. Hydralazine alleviates motor dysfunction, neuropathic inflammatory pain, and formalin-induced somatic and emotional pain responses. In addition, Hydralazine directly induces DNA strand breaks and sister chromatid exchange, exhibiting certain mutagenic characteristics. Hydralazine has been widely used in studies on hypertension, various cancers (such as cervical cancer, leukemia), spinal cord injury and the mechanisms of inflammatory pain[1][2][3][4][5].
IC50 & Target:IC50: 9.53 mM (ROS), 1.19 mM (O2·-)[1]
In Vitro:Hydralazine (10 μM; 5 days) demethylates and reactivates expression of silenced tumor suppressor genes (ER, RARβ, p16) in MDA-231, MCF-7, and T24 cancer cell lines, respectively[1].Hydralazine (10 μM; 24 hours) reduces DNMT1 and DNMT3a mRNA expression in MCF-7 breast cancer cells[1].
Hydralazine (0.1-10.0 mM) does not impair phagocytic function or viability of thioglycollate-prestimulated rat peritoneal macrophages[2].
Hydralazine (0.1-10.0 mM) significantly inhibits nitrite production by LPS/IFN-γ-stimulated thioglycollate-prestimulated rat peritoneal macrophages, with an IC50 of 0.43 ± 0.03 mM[2].
Hydralazine (1.0-10.0 mM) inhibits both NOS-2 and COX-2 protein synthesis in LPS/IFNγ-stimulated thioglycollate-prestimulated rat peritoneal macrophages[2].
Hydralazine (3.1-50 nmol, plate incorporation test without S-9 mix; 1 mg per plate, spot test with/without S-9 mix) is a direct-acting, low-potency mutagen that induces mixed genetic mutation mechanisms in Salmonella typhimurium strains TA1535, TA100, TA1537, TA97, and TA98, with highest potency in strain TA97[3].
Hydralazine (5 mg per spot, spot test; serial twofold dilutions, micromethod assay with/without S-9 mix; 16 h incubation at 37°C) is a direct-acting genotoxin that is preferentially lethal to repair-deficient Escherichia coli strains WP67 and CM871, indicating involvement of recA recombination repair, lexA post-replication repair, and polA repair mechanisms, with no dependence on excision repair systems[3].
Hydralazine (≤25 μM) significantly mitigates acrolein-mediated cell death in PC12 cells[4]. In Vivo:Hydralazine (i.p.; daily; 7 d) promotes demethylation of the estrogen receptor gene promoter and reactivates estrogen receptor expression in MDA-MB-231 breast cancer xenografts in nude mice[1].
Hydralazine (used in combination with valproic acid (HY-10585)) eliminates tumor recurrence of HT1080 fibrosarcoma xenografts in nude mice[1].
Hydralazine (83 mg/kg; i.p.; once daily; 5 days) induces DNA fragmentation in the liver, kidney and spleen (but not the lung) of mice at 6 hours after the last administration, and the damage is completely repaired at 12 hours post-administration; meanwhile, it moderately increases the sister chromatid exchange rate of mouse bone marrow cells by 33%[3].
Hydralazine (5 mg/kg; i.p.; twice; 14 d) reduces acrolein levels by 50-70% in the injured spinal cord of rats, decreases post-injury cyst formation by 70%, improves motor function recovery, and alleviates mechanical hyperalgesia in rat models of spinal cord injury[4].
Hydralazine (0.1-10 mg/kg; i.p.; single dose) dose-dependently alleviates formalin-induced somatic and emotional inflammatory pain in male C57BL/6 mice, with a ED50 of 0.239-1.0160 mg/kg, while inhibiting excessive acrolein production and neuronal activation in the spinal cord[5].
Hydralazine (10 mg/kg; i.p.; single dose) does not impair central nervous system function in male C57BL/6 mice[5].
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