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SML0148

Sigma-Aldrich

Imidapril hydrochloride

≥98% (HPLC)

Synonym(s):

(4S)-3-[(2S)-2-[[(1S)-1-(ethoxycarbonyl)-3-phenylpropyl]amino]-1-oxopropyl]-1-methyl-2-oxo-4-imidazolidinecarboxylic acid hydrochloride, Novaloc, TA 6366, Tanapril

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About This Item

Empirical Formula (Hill Notation):
C20H27N3O6 · HCl
CAS Number:
Molecular Weight:
441.91
MDL number:
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77

Assay

≥98% (HPLC)

form

powder

optical activity

[α]/D -50 to -70° in ethanol (c=0.5)

color

white to tan

solubility

H2O: ≥5 mg/mL

originator

Trinity Pharma Solutions

storage temp.

−20°C

SMILES string

Cl.CCOC(=O)[C@H](CCc1ccccc1)N[C@@H](C)C(=O)N2[C@@H](CN(C)C2=O)C(O)=O

InChI

1S/C20H27N3O6.ClH/c1-4-29-19(27)15(11-10-14-8-6-5-7-9-14)21-13(2)17(24)23-16(18(25)26)12-22(3)20(23)28;/h5-9,13,15-16,21H,4,10-12H2,1-3H3,(H,25,26);1H/t13-,15-,16-;/m0./s1

InChI key

LSLQGMMMRMDXHN-GEUPQXMHSA-N

General description

Imidapril comprises large acyl moiety and is hydrolyzed by carboxylesterase (CES) 1.

Application

Imidapril hydrochloride may be used to test its effect on pharyngeal and laryngeal muscle to treat impaired swallowing.
Imidapril hydrochloride was used as a standard in bioequivalence test by LC/MS method.

Biochem/physiol Actions

Imidapril hydrochloride is a long-acting inhibitor of angiotensin converting enzyme used in the treatment of hypertension, congestive heart failure and diabetic nephropathy. It restores decreased airway sensation and bladder sensation in patients with multiple sclerosis.
Imidapril is a potent angiotensin converting enzyme inhibitor and anti-hypertensive.

Features and Benefits

This compound is featured on the Angiotensin Receptors page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.
This compound was developed by Trinity Pharma Solutions. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

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Yosuke Takeda et al.
Hypertension research : official journal of the Japanese Society of Hypertension, 33(9), 965-973 (2010-07-29)
We and others recently reported that long-term Rho-kinase inhibition has renoprotective effects. This study was designed to compare the effects of an angiotensin-converting enzyme (ACE) inhibitor (imidapril), a Rho-kinase inhibitor (fasudil) and a combination of them both on renal interstitial
Kazuhide Ogino et al.
Circulation journal : official journal of the Japanese Circulation Society, 74(11), 2346-2352 (2010-09-10)
Angiotensin II and insulin resistance (IR) have clinical implications in the pathophysiology of chronic heart failure (CHF). However, it is still unclear whether the combination of an angiotensin-receptor blocker and angiotensin-converting enzyme inhibitor (ACEI) improves IR in CHF patients who
Ryo Watanabe et al.
Journal of cardiovascular pharmacology, 59(4), 323-330 (2011-12-02)
Angiotensin converting enzyme inhibitors have been used clinically to prevent myocardial infarction (MI). The angiotensin converting enzyme inhibitors attenuated ventricular remodeling and improved cardiac function by inhibition of matrix metalloproteinases after MI. Although the effect is thought to be a
Hiromichi Yoshida et al.
Respiration; international review of thoracic diseases, 72(4), 423-426 (2005-08-10)
We describe an unusual case of a patient with eosinophilic pleurisy associated with long-term administration of imidapril, an angiotensin-converting enzyme inhibitor (ACEI). An 81-year-old woman who had been given imidapril for the treatment of essential hypertension was admitted to our
Tetsuya Matsumoto et al.
Hypertension (Dallas, Tex. : 1979), 56(3), 364-368 (2010-07-08)
The renin-angiotensin system regulates the vascular fibrinolytic balance. In the human forearm vasculature, angiotensin-converting enzyme (ACE) inhibitors (ACE-Is) increase the release of t-PA through endogenous bradykinin. We tested the hypothesis that ACE inhibition and sex modulate the endogenous coronary release

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