The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
Chemical Compound Review

Moexiprilat     (3S)-2-[(2S)-2-[[(1S)-1- carboxy-3-phenyl...

Synonyms: SureCN616776, CHEMBL1201405, AC1L1IVG, CTK8E8826, FT-0672451, ...
 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of RS 10029

  • The inhibition of oestrone-stimulated cardiac fibroblast growth by moexiprilat may contribute to the beneficial effects seen in postmenopausal women with hypertensive heart disease treated with ACE inhibitors [1].
 

High impact information on RS 10029

  • The IGF-I induced overexpression of the IGF-IR was reduced by ACE inhibition with moexiprilat (10(-7) M) by 79+/-7% and by AT(1) receptor blockade with CV11974 (10(-7) M) by 79+/-5% [2].
  • These data show that the ACE inhibitors moexiprilat and enalaprilat inhibit Ang II induced proliferation of cardiac fibroblasts according to their relative potency of ACE inhibition in vitro [3].
  • To assess the efficacy and time-dependent effects of once-daily moexipril, a nonsulfhydryl ester prodrug of the angiotensin-converting enzyme (ACE) inhibitor, moexiprilat, we conducted a multicenter, double-blind, placebo-controlled trial in 51 hypertensive patients using both clinic and ambulatory blood pressure (BP) recordings [4].
  • Compared to fasting, the postprandial moexiprilat Cmax and AUC (ratio fed/fasted 58.0%; 90% CI 52.2-64.5%) were distinctly reduced (ANOVA p = 0.0001) [5].
  • OBJECTIVE: To characterize the lipophilic ACE inhibitor moexipril and its active metabolite moexiprilat regarding the duration of action, the susceptibility of the pharmacokinetics and pharmacodynamics to food intake and the concentration-dependent effect [5].
 

Biological context of RS 10029

 

Anatomical context of RS 10029

 

Associations of RS 10029 with other chemical compounds

 

Analytical, diagnostic and therapeutic context of RS 10029

  • Moexipril is a prodrug which is hydrolysed after oral administration to its active metabolite moexiprilat, an inhibitor of the angiotensin converting enzyme (ACE) [8].
  • Monitoring the metabolism of moexipril to moexiprilat using high-performance liquid chromatography- electrospray ionization mass spectrometry [9].
  • Preclinical development of an intravenous dosage form for the ACE inhibitor RS-10029 involved the formulation and characterization of the drug's chemical/physical stability in two prototype formulations (injectable solution and lyophilized powder) [10].
  • High-performance liquid chromatography combined with a UV absorbance detector and electrospray ionization mass spectrometer is used for the simultaneous analysis of moexipril and moexiprilat in biological samples [9].
  • Similar results were obtained in vivo in experiments investigating the blood pressure increasing response to intravenous injection of ANG I or ANG II in conscious normotensive rats and dogs after oral or intravenous application of moexipril or moexiprilat, respectively [7].

References

  1. Effects of moexiprilat on oestrogen-stimulated cardiac fibroblast growth. Grohé, C., Kahlert, S., Lóbbert, K., van Eickels, M., Stimpel, M., Vetter, H., Neyses, L. Br. J. Pharmacol. (1997) [Pubmed]
  2. Angiotensin-converting enzyme (ACE) inhibition attenuates insulin-like growth factor-I (IGF-I) induced cardiac fibroblast proliferation. van Eickels, M., Vetter, H., Grohé, C. Br. J. Pharmacol. (2000) [Pubmed]
  3. Angiotensin converting enzyme inhibitors block mitogenic signalling pathways in rat cardiac fibroblasts. van Eickels, M., Grohé, C., Löbbert, K., Stimpel, M., Vetter, H. Naunyn Schmiedebergs Arch. Pharmacol. (1999) [Pubmed]
  4. Tricenter assessment of the efficacy of the ACE inhibitor, moexipril, by ambulatory blood pressure monitoring. White, W.B., Whelton, A., Fox, A.A., Stimpel, M., Kaihlanen, P.M. Journal of clinical pharmacology. (1995) [Pubmed]
  5. Moexipril shows a long duration of action related to an extended pharmacokinetic half-life and prolonged ACE inhibition. Cawello, W., Boekens, H., Waitzinger, J., Miller, U. International journal of clinical pharmacology and therapeutics. (2002) [Pubmed]
  6. Metabolism of Moexipril to Moexiprilat: Determination of In Vitro Metabolism Using HPLC-ES-MS. Kalász, H., Petroianu, G., Tekes, K., Klebovich, I., Ludányi, K., G Ulyás, Z. Medicinal chemistry (Sh⁻ariqah, United Arab Emirates) (2007) [Pubmed]
  7. Pharmacological and toxicological studies of the new angiotensin converting enzyme inhibitor moexipril hydrochloride. Friehe, H., Ney, P. Arzneimittel-Forschung. (1997) [Pubmed]
  8. Moexipril. A review of its use in the management of essential hypertension. Brogden, R.N., Wiseman, L.R. Drugs (1998) [Pubmed]
  9. Monitoring the metabolism of moexipril to moexiprilat using high-performance liquid chromatography- electrospray ionization mass spectrometry. Kóti, J., Háda, V., Petroianu, G., Hasan, M.Y., Tekes, K., Szücs, Z., Kalász, H. Journal of chromatographic science. (2006) [Pubmed]
  10. Preclinical development and characterization of an intravenous dosage form for the ACE inhibitor RS-10029. Visor, G.C., Lin, L.H., Henry, P., Singer, L. Journal of parenteral science and technology : a publication of the Parenteral Drug Association. (1989) [Pubmed]
 
WikiGenes - Universities