Last update 21 Nov 2024

Ornoprostil

Last update 21 Nov 2024

Overview

R&D Status

Clinical Result

Translational Medicine

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Ornoprostil (JAN/INN), Alloca

+ [1]

Target

EP1

Mechanism

EP1 agonists(Prostanoid EP1 receptor agonists)

Therapeutic Areas-

Active Indication-

Inactive Indication-

Originator Organization-

Active Organization-

Inactive Organization-

Drug Highest Phase-

First Approval Date-

Regulation-

Structure

Molecular FormulaC23H38O6

InChIKeyBBRBUTFBTUFFBU-LHACABTQSA-N

CAS Registry70667-26-4

100 Clinical Results associated with Ornoprostil

100 Translational Medicine associated with Ornoprostil

100 Patents (Medical) associated with Ornoprostil

Literatures (Medical) associated with Ornoprostil

01 Jul 2013·Digestive Diseases and SciencesQ3 · MEDICINE

The Mechanism of the Down-Regulation of Hepatic Transporters in Rats with Indomethacin-Induced Intestinal Injury

Q3 · MEDICINE

Article

Author: Toshiharu Horie ; Nobuhiro Fujiyama ; Yoshihisa Shitara

BACKGROUNDPreviously, we reported that hepatic transporters were down-regulated consistent with intestinal injury in indomethacin (IDM)-treated rats.AIMThe purpose of this study was to characterize this mechanism of the down-regulation of hepatic transporters in IDM-treated rats.METHODSHepatic nuclear receptor expressions, oxidative stress condition and the expression of hepatic transporters were evaluated in rats with IDM-induced intestinal injury with or without the administration of mucosal protectant ornoprostil, a prostaglandin E1 analogue, or aminoguanidine (AG), an iNOS inhibitor.RESULTSAll the nuclear receptors examined in the present study, which regulates hepatic transporters, were decreased by the administration of IDM. Hepatic glutathione, an indicator of oxidative stress, was significantly reduced compared with control. We then determined the expression of hepatic transporters by semi-quantitative real-time RT-PCR and Western blot analysis in IDM-treated rats with or without the administration of ornoprostil or AG. Ornoprostil recovered the gene expression of Oatp1a1, Oatp1b2 and Mrp2 and protein expression of Mrp2 while it had no effect on Oatp1a1 and Oatp1b2 proteins. These results indicated that the gene expression of hepatic transporters was down-regulated in association with the intestinal injury. On the other hand, there is no effect of AG on the reduced gene expression of hepatic Oatp1a1, Oatp1b2 and Mrp2. In protein expression, AG slightly recovered Mrp2 expression accompanied by a partial decrease in portal NO levels.CONCLUSIONSWe suggest that the transcriptional process influenced by a dysfunction of hepatic nuclear receptors as well as the effect of NO on the post-transcriptional process due to intestinal injury are partially involved in the down-regulation of hepatic transporters.

01 Feb 2006·Rinsho byori. The Japanese journal of clinical pathology

Studies of serum and feces bile acids determination by gas chromatography-mass spectrometry.

Article

Author: Tadano, Tomoaki ; Kanoh, Motonari ; Sakamoto, Kazuhiro ; Kamano, Toshiki ; Matsumoto, Masaru

Both radioimmunoassay (RIA) and enzyme-linked immunosorbent assay (ELISA) methods are utilized in the clinical laboratory to measure bile acids in human body fluids. For a more detailed analysis, we attempted simultaneous analysis of serum and feces bile acids using gas chromatography-mass spectrometry (GC-MS) and also investigated the dynamics of bile acids. Serum bile acid composition was examined in 22 healthy adults (79.9 +/- 6.0 years) and 20 colon cancer patients (65.1 +/- 9.5 years). Feces bile acid composition was examined in 20 healthy adults (50.7 +/- 7.6 years) and 20 colon cancer patients (63.6 +/- 8.5 years). The significance of differences was examined by Student's t-test. In both healthy adults and colon cancer patients, the bile acids detected in serum were cholic acid (CA), chenodeoxycholic acid (CDCA), deoxycholic acid (DCA), lithocholic acid (LCA), ursodeoxycholic acid (UDCA), and hyocholic acid (HCA). The following 12 bile acids were detected in feces: CA, allo CA, CDCA, allo CDCA, DCA, allo DCA, LCA, allo LCA, UDCA, HCA, UCA, and CA-6alpha-ol. For allo CA and allo CDCA, no significant differences were observed between the control group and the colon cancer patients. On the other hand, the concentration of allo LCA tended to be higher in the patients (p < 0.05), and the concentration of allo DCA was distinctly higher (p < 0.001) in the colon cancer group, particularly in men. The GC-MS method demonstrated bile acids undetectable by conventional RIA and ELISA. The dynamics suggested association of allo bile acids (DCA and LCA) with colon cancer.

01 Jul 1997·Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology

[Effects of NSAIDs and PGE1 analogue on the permeability of human small intestine].

Article

Author: Noguchi, M ; Kinouchi, Y ; Nagase, K ; Hiwatashi, N ; Maekawa, H ; Toyota, T ; Ito, K

We studied permeability of human small intestine to clarify the following questions. 1) Does indomethacin increase intestinal permeability (IP)? 2) Does ornoprostil (PGE1 analogue) prevent the increased IP due to indomethacin? 3) Does acemetacin (pro-drug) increase IP? Eleven healthy volunteers were studied before and after ingestion of indomethacin, acemetacin, ornoprostil. After an overnight fast, they drank an isotonic solution containing 1.5 g rhamnose and 10.5 g lactulose. IP was estimated with lactulose/rhamnose percentage excretion in urine for 5 hours. An administration of indomethacin (75 mg) for one day increased IP significantly, and the coadministration of indomethacin and ornoprostil showed no significant change in IP compared with those of controls. Pro-drug administration did not increase IP. It is suggested that simultaneous administration of ornoprostil prevent the mucosal damage caused by indomethacin clinically, and that the mechanism of this increase IP is due to lack of mucosal prostaglandins on the small intestine.

100 Deals associated with Ornoprostil

External Link

KEGG	Wiki	ATC	Drug Bank
D01869	-	-	-

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