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Chemical Compound Review

LIBENZAPRIL     (2S)-6-amino-2-[[(4S)-6- (carboxymethyl)-5...

Synonyms: CHEMBL430554, SureCN295229, AG-J-96996, CGS-16617, CHEBI:161463, ...
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Disease relevance of LIBENZAPRIL

  • The present study was designed to examine the effects of two new angiotensin-converting enzyme (ACE) inhibitors, CGS 14831 and CGS 16617 (3 mg/kg i. v. 1 min prior to occlusion and 4 and 24 h after occlusion), on myocardial ischemic (MI) damage and left-ventricular hypertrophy in rats [1].

High impact information on LIBENZAPRIL

  • Oral administration of the angiotensin converting enzyme inhibitor CGS 16617 significantly lowered mean arterial pressure [2].
  • In contrast, however, responses to norepinephrine were decreased in carotid arteries obtained from CGS 16617-treated SHR.(ABSTRACT TRUNCATED AT 250 WORDS)[3]
  • Similarly, normal responsiveness to the contractile effects of ANG I were observed with carotid arteries removed from SHR with decreased blood pressure and plasma ACE activity after 5 weeks exposure to CGS 16617 [3].
  • The antihypertensive actions of CGS 16617 also were potentiated by the cyclooxygenase inhibitor indomethacin, a result suggesting that CGS 12970 may enhance the action of CGS 16617 by inhibiting the action of vasoconstrictor prostaglandins produced after administration of an ACEI [4].
  • Colonic coadministration of the poorly-absorbed CGS 16617 with 2 mL of Intralipid (within dietary range for fecal fat content) enhanced Cmax and AUC 2.5- and 3.5-fold, respectively, in the dog and AUC 1.5-fold in the rat.(ABSTRACT TRUNCATED AT 250 WORDS)[5]

Chemical compound and disease context of LIBENZAPRIL


Biological context of LIBENZAPRIL


Associations of LIBENZAPRIL with other chemical compounds

  • Except for the absence of a significant change in urinary osmolality, the changes in MAP and renal function produced by saralasin were essentially identical to those produced by CGS 16617 [7].

Gene context of LIBENZAPRIL


Analytical, diagnostic and therapeutic context of LIBENZAPRIL


  1. Effects of two nonsulfhydryl angiotensin-converting enzyme inhibitors, CGS 14831 and CGS 16617, on myocardial damage and left-ventricular hypertrophy following coronary artery occlusion in the rat. Smith, E.F., Egan, J.W., Goodman, F.R., Zimmerman, M.B., Webb, R.L., Ribeiro, L.G. Pharmacology (1988) [Pubmed]
  2. Thromboxane synthase inhibition enhances action of converting enzyme inhibitors. Levens, N.R., Ksander, G.M., Zimmerman, M.B., Mullane, K.M. Hypertension (1989) [Pubmed]
  3. Rapid reversal of angiotensin I-induced contractions in rat carotid arteries after acute and chronic treatment with the angiotensin-converting enzyme inhibitor, 3-[(5-amino-1-carboxy-1S-pentyl)amino]2,3,4,5-tetrahydro-2-oxo- 3S-1H-1-benzazepena-1-acetic acid (CGS 16617). Weiss, G.B., Sturm, B., Levens, N.R. J. Pharmacol. Exp. Ther. (1993) [Pubmed]
  4. Inhibition of thromboxane synthetase potentiates the antihypertensive action of an angiotensin-converting enzyme inhibitor by a prostaglandin-dependent but kinin-independent mechanism. Levens, N.R., Cóte, D., Ksander, G. J. Pharmacol. Exp. Ther. (1991) [Pubmed]
  5. Absorption of ACE inhibitors from small intestine and colon. Kim, J.S., Oberle, R.L., Krummel, D.A., Dressman, J.B., Fleisher, D. Journal of pharmaceutical sciences. (1994) [Pubmed]
  6. Effects of food on the bioavailability of CGS 16617, an angiotensin-converting enzyme inhibitor, in healthy subjects. Choi, R.L., Kochak, G.M., Reydel-Bax, P., Nelson, E.B. Journal of clinical pharmacology. (1988) [Pubmed]
  7. Renal actions of the new angiotensin converting enzyme inhibitor CGS 16617. Levens, N.R. Archives internationales de pharmacodynamie et de thérapie. (1988) [Pubmed]
  8. Effects of prolonged administration of the angiotensin converting enzyme inhibitor CGS 16617 in normotensive volunteers. Waeber, G., Burnier, M., Porchet, M., Nussberger, J., Waeber, B., Brunner, H.R. Eur. J. Clin. Pharmacol. (1989) [Pubmed]
  9. Determination of CGS 16617 and stable isotope-labeled CGS 16617, an angiotensin-converting enzyme inhibitor, in human plasma by gas chromatography/mass spectrometry. Gaudry, D., Hayes, M., Khemani, L., Miotto, J., Alkalay, D. Biol. Mass Spectrom. (1991) [Pubmed]
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