Disease relevance of ONO 1206

• Rapid effect of oral limaprost in Raynaud's disease in childhood [1].
• A synthetic analog of prostaglandin E(1), OP-1206 (17S,20-dimethyl-trans-Delta(2)-prostaglandin E(1); 0.5 microg/kg body weight) was orally administered to rats twice a day for 5 days [2].
• Rats were treated orally with 300 micrograms/kg/day OP-1206 alpha-cyclodextrin clathrate (OP-1206), a stable PGE1 analogue, for 14 days after photodynamic retinal vascular thrombosis by rose Bengal [3].
• Six hours after the sixth-administration of OP-1206, the level of the thermal hyperesthesia was attenuated in a dose-dependent manner, and this effect lasted more than 1 day after the last drug administration [4].
• These data show that oral treatment with OP-1206 alpha-CD is effective in improving walking dysfunction induced by spinal canal stenosis, and this therapeutic effect is likely mediated by improved SCBF at the territory of spinal stenosis [5].

Psychiatry related information on ONO 1206

• CONCLUSION: Limaprost was more effective for mild erectile dysfunction than was gosyajinki-gan [6].

High impact information on ONO 1206

• In a morphometric analysis of myelinated nerve fibers (MNFs) in long-term diabetes, the mean diameter of the largest 10% of MNFs was significantly reduced in untreated diabetic compared with control rats, but OP-1206 completely reversed this reduction [7].
• OP-1206 increased phosphorylation of the 50,000 mol. wt vasodilator-stimulated phosphoprotein, at concentrations of 7.9-79 nM, which inhibited aggregation induced by STA2 [8].
• (8R*, 9S*, 11S*)-(-)-9-Hydroxy-9-n-hexyloxy-8-methyl-2,3,9,10- tetrahydro-8,11-epoxy-1H, 8H, 11H-2, 7b, 11a-triazadibenzo(a,g)-cycloocta(c,d,e)trinden-1-one (KT-5720), a specific inhibitor of A kinase, not only reversed the inhibition by OP-1206 of STA2-induced platelet aggregation, but also inhibited the OP-1206-induced protein phosphorylation [8].
• We have recently reported that coadministration of 17 S,20-dimethyl- trans- lower right triangle (2)-prostaglandin E(1) (OP-1206), a stable synthetic analogue of prostaglandin E(1), with 5-FU to rats protects the small intestine from 5-FU-induced damage [9].
• The present study provides evidence that oral treatment with the prostaglandin E1 analog (OP-1206 alpha-CD) is effective in improving motor dysfunction and spinal cord blood flow in rats with spinal compression [5].

Chemical compound and disease context of ONO 1206

• Effect of a prostaglandin E1 derivative (OP-1206) and acetylsalicylic acid on electrically induced thrombosis in guinea-pig mesenteric artery and its modification by an inhibitor of prostaglandin I2 synthetase, tranylcypromine [10].
• Platelet aggregation, adhesiveness, bleeding time, and thrombocytopenia induced by ADP and collagen infusion in guinea-pigs were inhibited by oral administration of OP 1206 at the same doses or doses less than those relieving vasopressin-induced ST depression of ECG [11].

Biological context of ONO 1206

• Inhibition of the STA2-induced aggregation by OP-1206 may be associated with cAMP-dependent protein phosphorylation, while cilostamide may have inhibitory effects on STA2-induced platelet activation through mechanisms other than the activation of A kinase [8].
• After the 3-day administration of limaprost, the peripheral and renal blood flows, and the glomerular filtration rate (GFR) were observed to rise, but the filtration fraction (FF) and urinary protein output were elevated [12].
• Effects of OP-1206 (prostaglandin E1) on nerve-conduction velocity in the dog cauda equina subjected to acute experimental compression [13].
• These findings indicate that vasopressin is a suitable agent for the induction of coronary vasoconstriction in primates and that ONO 1206 is able to reverse this effect [14].
• Intra-coronary injection of OP 1206 (1-100 ng/kg) in dogs resulted in a remarkable increase of coronary blood flow without any influence on heart rate, blood pressure, myocardial oxygen consumption and redox potential [11].

Anatomical context of ONO 1206

• In parallel with the histological change, after 14 days following thrombosis ADF immunoreactivity was preserved on retinal pigment epithelial cells in the OP-1206-treated rats, whereas it was diminished in the non-treated rats [3].
• The MTX treatment decreased the incorporation of 3H-thymidine into DNA in the jejunal mucosa, while the coadministration of OP-1206 with MTX prevented it [15].
• These results indicated that OP-1206 could protect the intestinal mucosa against the biochemical effects of MTX through a trophic action on intestinal villi [15].
• The treatment of OP-1206 with methotrexate showed significantly lower chemiluminescence of both the jejunum and mucosal scrapings than those of the methotrexate-treated rats [16].
• The effect of OP-1206, a prostaglandin E1 derivative, on cauda equina function was analyzed in a model for acute cauda equina compression in the dog [13].

Associations of ONO 1206 with other chemical compounds

• Thus, it was shown histologically and biochemically that OP-1206 was effective in protecting the small intestine from methotrexate-induced damage [17].
• These observations indicate that OP-1206 reduced the leukocyte infiltration and the change in epithelial permeability of rat small intestine induced by 5-FU [18].
• The potent relaxant effect of ONO 1206 on human respiratory tract smooth muscle in vitro suggests that this compound may be a bronchodilator in man [19].

Gene context of ONO 1206

• OP-1206 cyclodextrin clathrate (OP-1206 CD: prostaglandin E1 derivate) and ONO-4819 CD (a highly selective EP4 agonist) were intravenously administrated [20].
• These findings suggest an important role for ADF in the OP-1206-dependent suppression of retinal tissue damage caused by oxidative insult [3].
• We also observed a short-term effect of limaprost on renal hemodynamics in three cases with diabetic nephropathy [12].

Analytical, diagnostic and therapeutic context of ONO 1206

• In the OP-1206-treated rats, minimal retinal atrophy due to ischemia/reperfusion was observed histologically up to 14 days, whereas in the non-treated rats the inner layer of the retina became markedly atrophic [3].
• In the present study, the authors examine the role of nerve ischemia in the maintenance of the thermal hyperesthesia induced by nerve constriction injury by orally administering OP-1206, a prostaglandin E1 derivative [4].
• Thus, OP-1206 may possibly help the anticancer chemotherapy by protecting the small intestine from the methotrexate-induced damage [16].
• Oral administration of PGE(1), limaprost alfadex, was followed at doses of 30 microg/day for 2 weeks [21].
• Intravenous infusion of ONO 1206 in baboon also produced ex-vivo inhibition of ADP-induced platelet aggregation [19].

References