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Merck

SML0148

Sigma-Aldrich

Imidapril hydrochloride

≥98% (HPLC)

Synonym(e):

(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

Empirische Formel (Hill-System):
C20H27N3O6 · HCl
CAS-Nummer:
Molekulargewicht:
441.91
MDL-Nummer:
UNSPSC-Code:
12352200
PubChem Substanz-ID:
NACRES:
NA.77

Qualitätsniveau

Assay

≥98% (HPLC)

Form

powder

Optische Aktivität

[α]/D -50 to -70° in ethanol (c=0.5)

Farbe

white to tan

Löslichkeit

H2O: ≥5 mg/mL

Ersteller

Trinity Pharma Solutions

Lagertemp.

−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

InChIKey

LSLQGMMMRMDXHN-GEUPQXMHSA-N

Allgemeine Beschreibung

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

Anwendung

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. Wirkung

Angiotensin Converting Enzyme (ACE) inhibitor
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.

Leistungsmerkmale und Vorteile

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.

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


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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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