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1-ヒドラジノフタラジン 化学構造式
MOL File:

1-ヒドラジノフタラジン 物理性質

融点 :
沸点 :
276.07°C (rough estimate)
比重(密度) :
1.2583 (rough estimate)
屈折率 :
1.5872 (estimate)
pKa 6.820± 0.005(H2O,t = 25.0,Iundefined) (Uncertain)
水溶解度 :
4.8mg/L(22.5 ºC)
CAS データベース:
1(2H)-phthalazinone, hydrazone(86-54-4)
Hydralazine (86-54-4)


毒性 LD50 in mice, rats (mg/kg): 122, 90 orally; 101, 40 i.p. (Dorigotti)

1-ヒドラジノフタラジン 価格

メーカー 製品番号 製品説明 CAS番号 包装 価格 更新時間 購入

1-ヒドラジノフタラジン MSDS


1-ヒドラジノフタラジン 化学特性,用途語,生産方法


血管拡張薬 降圧薬


血圧降下薬, 血管拡張薬


Yiellow Solid


Inhibits DNA methyltransferase and modulates epigenetic regulation of gene expression. Non-selective MAO-A/B inhibitor; semicarbazide-sensitive amine oxidase inhibitor. Antihypertensive


Hydralazine is a non-nucleoside analog that inhibits DNA methylation and reactivates the expression of tumor suppressor genes. Non-selective MAO-A/B inhibitor; semicarbazide-sensitive amine oxidase inhibitor. Antihypertensive.


ChEBI: The 1-hydrazino derivative of phthalazine; a direct-acting vasodilator that is used as an antihypertensive agent.

brand name

Apresoline (Novartis); Dralzine (Teva).


The vasodilation produced by hydralazine (Apresoline) depends in part on the presence of an intact blood vessel endothelium. This implies that hydralazine causes the release of nitric oxide, which acts on the vascular smooth muscle to cause relaxation. In addition, hydralazine may produce vasodilation by activating K+ channels.


Hydralazine is a hydrazine derivative used as a antihypertensive drug. Skin rashes have been described during treatment. Exposure occurs mainly in the pharmaceutical industry. Cross-sensitivity is frequent with hydrazine, which is considered to be a potent sensitizer.


Hydralazine produces widespread but apparently not uniform vasodilation; that is, vascular resistance is decreased more in cerebral, coronary, renal, and splanchnic beds than in skeletal muscle and skin. Renal blood flow and ultimately glomerular filtration rate may be slightly increased after acute treatment with hydralazine. However, after several days of therapy, the renal blood flow is usually no different from that before drug use.
In therapeutic doses, hydralazine produces little effect on nonvascular smooth muscle or on the heart. Its pharmacological actions are largely confined to vascular smooth muscle and occur predominantly on the arterial side of the circulation; venous capacitance is much less affected. Because cardiovascular reflexes and venous capacitance are not affected by hydralazine, postural hypotension is not a clinical concern. Hydralazine treatment does, however, result in an increase in cardiac output.This action is brought about by the combined effects of a reflex increase in sympathetic stimulation of the heart, an increase in plasma renin, and salt and water retention. These effects limit the hypotensive usefulness of hydralazine to such an extent that it is rarely used alone.


Hydralazine is generally reserved for moderately hypertensive ambulatory patients whose blood pressure is not well controlled either by diuretics or by drugs that interfere with the sympathetic nervous system. It is almost always administered in combination with a diuretic (to prevent Na+ retention) and a β-blocker, such as propranolol (to attenuate the effects of reflex cardiac stimulation and hyperreninemia). The triple combination of a diuretic, β-blocker, and hydralazine constitutes a unique hemodynamic approach to the treatment of hypertension, since three of the chief determinants of blood pressure are affected: cardiac output (β-blocker),plasma volume (diuretic), and peripheral vascular resistance (hydralazine).
Although hydralazine is available for intravenous administration and has been used in the past for hypertensive emergencies, it is not generally employed for this purpose. The onset of action after intravenous injection is relatively slow, and its actions are somewhat unpredictable in comparison with those of several other vasodilators.


Most side effects associated with hydralazine administration are due to vasodilation and the reflex hemodynamic changes that occur in response to vasodilation. These side effects include headache, flushing, nasal congestion, tachycardia, and palpitations. More serious manifestations include myocardial ischemia and heart failure. These untoward effects of hydralazine are greatly attenuated when the drug is administered in conjunction with a β-blocker.
When administered chronically in high doses, hydralazine may produce a rheumatoidlike state that when fully developed, resembles disseminated lupus erythematosus.


Hydralazine is well absorbed (65–90%) after oral administration. Its peak antihypertensive effect occurs in about 1 hour, and its duration of action is about 6 hours.
The major pathways for its metabolism include ring hydroxylation, with subsequent glucuronide conjugation and N-acetylation. Hydralazine exhibits a first-pass effect in that a large part of an orally administered dose is metabolized before the drug reaches the systemic circulation. The first-pass metabolism occurs in the intestinal mucosa (mostly N-acetylation) and the liver. The primary excretory route is through renal elimination, and about 80% of an oral dose appears in the urine within 48 hours. About 10% is excreted unchanged in the feces.
Approximately 85% of the hydralazine in plasma is bound to plasma proteins. Although this does not appear to be a major therapeutic concern, the potential for interactions with other drugs that also bind to plasma proteins does exist. The plasma half-life of hydralazine in patients with normal renal function is 1.5 to 3 hours.
Interestingly, the half-life of the antihypertensive effect is somewhat longer than the plasma half-life. This may occur because hydralazine is specifically accumulated in artery walls, where it may continue to exert a vasodilator action even though plasma concentrations are low.
The plasma half-life of hydralazine may be increased fourfold or fivefold in patients with renal failure. If renal failure is present, therefore, both the antihypertensive and toxic effects of hydralazine may be enhanced. Since N-acetylation of hydralazine is an important metabolic pathway and depends on the activity of the enzyme N-acetyltransferase, genetically determined differences in the activity of this enzyme in certain individuals (known as slow acetylators) will result in higher plasma levels of hydralazine; therefore, the drug’s therapeutic or toxic effects may be increased.


It crystallises from MeOH. UV: max 656nm at pH ~11. It complexes with Bi3+ , Zn2+ , Fe2+ and Co2+ .

1-ヒドラジノフタラジン 上流と下流の製品情報



1-ヒドラジノフタラジン 生産企業

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  • 86-54-4
  • Dihydralazine Impurity 2(Dihydralazine EP Impurity B)
  • Dihydralazine Impurity 2
  • 1-hydrazino-phthalazin
  • 1-hydrazinophthalazine
  • apresolin
  • Dihydralazine EP Impurity B
  • apressin
  • aprezolin
  • ba5968
  • c-5068
  • c5968
  • ciba5968
  • hidralazin
  • hidralazina
  • hipoftalin
  • hydralazin
  • hydrallazine
  • hydrazinophthalazine
  • hypophthalin
  • phthalazin-1-ylhydrazine
  • 1-Hydrazinylphthalazine
  • 1-HydrazinophthalazineDiscontinued See: H716531
  • 1-Phthalazinylhydrazine
  • Hydralazine Discontinued See: H716531
  • NSC 126699
  • Phthalazine,1-hydrazinyl-
  • hydralazine
  • apresoline
  • 1(2h)-phthalazinonehydrazone
  • アプレソリン
  • アプレゾリン
  • アプレッシン
  • (フタラジン-1-イル)ヒドラジン
  • ヒドララジン
  • 1-(フタラジン-1-イル)ヒドラジン
  • フタラジン-1(2H)-オンヒドラゾン
  • 1-ヒドラジノフタラジン
  • 降圧薬
  • 血管拡張薬
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