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Captopril Basic information

Product Name:
Mol File:

Captopril Chemical Properties

Melting point:
104-108 °C(lit.)
-129.5 º (c=1, EtOH)
Boiling point:
427.0±40.0 °C(Predicted)
1.2447 (rough estimate)
refractive index 
-127.5 ° (C=1.7, EtOH)
storage temp. 
-20°C Freezer
H2O: 0.1 g/mL, very slightly hazy, colorless
3.7, 9.8(at 25℃)
Crystalline Powder
white to off-white
Water Solubility 
Stable. Incompatible with strong oxidizing agents.
CAS DataBase Reference
62571-86-2(CAS DataBase Reference)
NIST Chemistry Reference

Safety Information

Hazard Codes 
Risk Statements 
Safety Statements 
WGK Germany 
HS Code 
Hazardous Substances Data
62571-86-2(Hazardous Substances Data)
LD50 in mice (mg/kg): 1040 i.v.; 6000 orally (Keim)



Captopril Usage And Synthesis

Chemical Properties

White or almost white, crystalline powder.




angiotensin-converting enzyme (ACE) inhibitor,anti-hypertensive


Orally active angiotensin-converting enzyme (ACE) inhibitor


ChEBI: A L-proline derivative in which L-proline is substituted on nitrogen with a (2S)-2-methyl-3-sulfanylpropanoyl group. It is used as an anti-hypertensive ACE inhibitor drug.

brand name

Capoten (Par).

Biological Functions

Captopril (Capoten) is an orally effective ACE inhibitor with a sulfhydryl moiety that is used in binding to the active site of the enzyme. Captopril blocks the blood pressure responses caused by the administration of angiotensin I and decreases plasma and tissue levels of angiotensin II.

General Description

Captopril, 1-[(2S)-3-mercapto-2-methyl-1-oxopropionyl]proline (Capoten), blocks the conversion of angiotensinI to angiotensin II by inhibiting the convertingenzyme. The rational development of captopril as an inhibitorof ACE was based on the hypothesis that ACE and carboxypeptidaseA functioned by similar mechanisms. It wasnoted that d-2-benzylsuccinic acid was a potent inhibitor ofcarboxypeptidase A, but not ACE. By use of this small molecule as a prototype, captopril was designed with a carboxylgroup on a proline and a thiol group was introduced toenhance the binding to the zinc ion of ACE. The importantbinding points at the active site of ACE are thought to be anarginine residue, which provides a cationic site that attracts acarboxylate ion, and a zinc ion, which can polarize a carbonylgroup of an amide function to make it more susceptible to hydrolysis.Hydrophobic pockets lie between these groups in theactive site, as does a functional group that forms a hydrogenbond with an amide carbonyl.


Treatment with captopril reduces blood pressure in patients with renovascular disease and in patients with essential hypertension.The decrease in arterial pressure is related to a reduction in total peripheral resistance. Most studies demonstrate a good correlation between the hypotensive effect of inhibitors and the degree of blockade of the renin–angiotensin system.Many of the pharmacological effects of captopril are attributable to the inhibition of angiotensin II synthesis. However, ACE is a relatively nonselective enzyme that also catabolizes a family of kinins to inactive products. Bradykinin, one of the major kinins, acts as a vasodilator through mechanisms related to the production of nitric oxide and prostacyclin by the vascular endothelium. Thus, administration of the ACE inhibitor captopril not only inhibits angiotensin II production but also prevents the breakdown of bradykinin. Increases in bradykinin concentrations after administration of ACE inhibitors contribute to the therapeutic efficacy of these compounds in the treatment of hypertension and congestive heart failure. However, alterations in bradykinin concentrations are also thought to contribute to cough and angioedema sometimes seen after ACE inhibition. The hypotensive response to captopril is accompanied by a fall in plasma aldosterone and angiotensin II levels and an increase in plasma renin activity. Serum potassium levels are not affected unless potassium supplements or potassium-sparing diuretics are used concomitantly; this can result in severe hyperkalemia.
There is no baroreflex-associated increase in heart rate, cardiac output, or myocardial contractility in response to the decrease in pressure, presumably because captopril decreases the sensitivity of the baroreceptor reflex.
Captopril enhances cardiac output in patients with congestive heart failure by inducing a reduction in ventricular afterload and preload. Converting enzyme inhibitors have been shown to decrease the mass and wall thickness of the left ventricle in both normal and hypertrophied myocardium. ACE inhibitors lack metabolic side effects and do not alter serum lipids.

Clinical Use

Captopril, as well as other ACE inhibitors, is indicated in the treatment of hypertension, congestive heart failure, left ventricular dysfunction after a myocardial infarction, and diabetic nephropathy. In the treatment of essential hypertension, captopril is considered firstchoice therapy, either alone or in combination with a thiazide diuretic. Decreases in blood pressure are primarily attributed to decreased total peripheral resistance or afterload. An advantage of combining captopril therapy with a conventional thiazide diuretic is that the thiazide-induced hypokalemia is minimized in the presence of ACE inhibition, since there is a marked decrease in angiotensin II–induced aldosterone release.
If the patient is asymptomatic, captopril can be used as monotherapy in the treatment of congestive heart failure. The use of ACE inhibitors in the treatment of congestive heart failure is supported by results from large-scale clinical trials demonstrating a general reduction in the relative risk of death. In symptomatic patients captopril should be used in conjunction with a diuretic because of the weak natriuretic properties of ACE inhibitors. In combination, captopril will reduce afterload and preload and prevent diuretic-induced activation of the renin–angiotensin system. Finally, ACE inhibitors may slow the progression of congestive heart failure by limiting left ventricular hypertrophy.
In the treatment of diabetic nephropathy associated with type I insulin-dependent diabetes mellitus, captopril decreases the rate of progression of renal insufficiency and retards the worsening of renal function.

Side effects

Approximately 10% of the patients treated with captopril report a dose-related maculopapular rash that often disappears when the dosage of captopril is reduced. Other common adverse effects are fever, a persistent dry cough (incidence as high as 39%), initial dose hypotension, and a loss of taste that may result in anorexia. These effects are reversed when drug therapy is discontinued. More serious toxicities include a 1% incidence of proteinuria and glomerulonephritis; less common are leukopenia and agranulocytosis. Since food reduces the bioavailability of captopril by 30 to 40%, administration of the drug an hour before meals is recommended. All converting enzyme inhibitors are contraindicated in patients with bilateral renal artery disease or with unilateral renal artery disease and one kidney. Use under these circumstances may result in renal failure or paradoxical malignant hypertension.

Veterinary Drugs and Treatments

The principle uses of captopril in veterinary medicine, at present, are as a vasodilator in the treatment of CHF and in the treatment of hypertension. Because of fewer adverse effects, enalapril and benazepril have largely supplanted the use of this drug in veterinary medicine.


The onset of action following oral administration of captopril is about 15 minutes, with peak blood levels achieved in 30 to 60 minutes. Its apparent biological half-life is approximately 2 hours, with its antihypertensive effects observed for 6 to 10 hours. The kidneys appear to play a major role in the inactivation of captopril.

Purification Methods

Purify it by recrystallisation from EtOAc/hexane. It is also purified by dissolving in EtOAc and chromatographed on a column of Wakogel C200 using a linear gradient of MeOH in EtOAc (0-100o) and fractions which give a positive nitroprusside test (for SH), are combined, evaporated and recrystallised from EtOAc/hexane (1:1), to give white crystals with [] D -128.2o (c 2.0, EtOH). [Nam J Pharm Sci 73 1843 1984]. Alternatively, dissolve it in H2O, apply to a column of AG-50Wx2 (BioRad) and elute with H2O. The free acid is converted to the dicyclohexylamine salt in MeCN by addition of the amine until the pH is 8-9. The salt is converted to the free acid by shaking with EtOAc and 10% aqueous KHSO4 or passage through an AG50Wx2 column. The EtOAc solution is dried (MgSO4), evaporated to dryness and the residue is recrystallised as above from EtOAc/hexane [Cushman et al. Biochemistry 16 5484 1977, NMR and IR: Horii & Watanabe Yakugaku Zasshi (J Pharm Soc Japan) 81 1786 1961]. It is an antihypertensive because it is a potent competitive inhibitor of the angiotensive convertive enzyme (ACE-inhibitor) with a Ki value of 0.0017\M [Shimazaki et al. Chem Pharm Bull Jpn 30 3139 1982].



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