[Translation] A Phase III multicenter, randomized, single-blind (evaluator-blind), parallel, positive-controlled clinical trial to evaluate the efficacy and safety of OPC-1085EL eye drops in the treatment of primary open-angle glaucoma or ocular hypertension in Chinese subjects

主要目的以原发性开角型青光眼或高眼压症中国受试者为对象，评价OPC-1085EL 滴眼液与0.005％拉坦前列素滴眼液相比的降眼压作用的优效性。次要目的比较OPC-1085EL滴眼液与0.005％拉坦前列素滴眼液使用的安全性。

[Translation]

Primary objective To evaluate the superiority of OPC-1085EL eye drops in lowering intraocular pressure compared with 0.005% latanoprost eye drops in Chinese subjects with primary open-angle glaucoma or ocular hypertension. Secondary objective To compare the safety of OPC-1085EL eye drops and 0.005% latanoprost eye drops.

Start Date27 Sep 2022

Sponsor / Collaborator

Teika Pharmaceutical Co., Ltd.

[+2]

NCT05583474 / RecruitingPhase 3

A Phase III, Multi-center, Randomized, Single-blind (to Evaluator), Parallel, and Positive-controlled Clinical Trial Evaluating the Efficacy and Safety of OPC-1085EL Ophthalmic Solution in the Treatment of Primary Open Angle Glaucoma or Ocular Hypertension in Chinese Subjects

It is a phase III, multi-center, randomized, single-blind (to evaluator), parallel, and positive-controlled clinical trial evaluating the efficacy and safety of OPC-1085EL in the treatment of primary open angle glaucoma or ocular hypertension in Chinese subjects. It is planned that 240 subjects (120 in each group) will be randomly assigned to receive OPC-1085EL or 0.005% latanoprost ophthalmic solution (latanoprost) at a ratio of 1:1.

Start Date27 Sep 2022

Sponsor / Collaborator

Otsuka Beijing Research Institute

NCT04828057 / CompletedNot Applicable

Preservative-free Fixed-dose Combination of Tafluprost 0.0015% / Timolol 0.5% in Patients With Open-angle Glaucoma or Ocular Hypertension: Clinical Effectiveness, Tolerability and Safety in a Real World Setting

The primary objective of this study is to assess the effectiveness of Tafluprost / Timolol in controlling ocular hypertension, as measured by mean change in intra-ocular pressure (IOP) from baseline to after 6 months of treatment from initiation, in patients with open angle glaucoma (OAG) or ocular hypertension (OHT), who do not respond sufficiently to initial topical treatment, in routine clinical practice.

Start Date01 Sep 2021

Sponsor / Collaborator

Santen Pharmaceutical Co., Ltd.

100 Clinical Results associated with β-adrenoceptors x PTGFR

100 Translational Medicine associated with β-adrenoceptors x PTGFR

0 Patents (Medical) associated with β-adrenoceptors x PTGFR

107

Literatures (Medical) associated with β-adrenoceptors x PTGFR

01 Aug 2010·Emergency Medicine JournalQ3 · MEDICINE

Effects of a -blocker on the cardiovascular response to MDMA (Ecstasy)

Q3 · MEDICINE

Article

Author: C M Hysek ; F X Vollenweider ; M E Liechti

BACKGROUNDMDMA (3,4-methylenedioxymethamphetamine, 'Ecstasy') produces tachycardia and hypertension and is rarely associated with cardiovascular and cerebrovascular complications. In clinical practice, beta-blockers are often withheld in patients with stimulant intoxication because they may increase hypertension and coronary artery vasospasm due to loss of beta(2)-mediated vasodilation and unopposed alpha-receptor activation. However, it is unknown whether beta-blockers affect the cardiovascular response to MDMA.METHODSThe effects of the non-selective beta-blocker pindolol (20 mg) on the cardiovascular effects of MDMA (1.6 mg/kg) were investigated in a double-blind placebo-controlled crossover study in 16 healthy subjects.RESULTSPindolol prevented MDMA-induced increases in heart rate. Peak values (mean+/-SD) for heart rate were 84+/-13 beats/min after MDMA vs 69+/-7 beats/min after pindolol-MDMA. In contrast, pindolol pretreatment had no effect on increases in mean arterial blood pressure (MAP) after MDMA. Peak MAP values were 115+/-11 mm Hg after MDMA vs 114+/-11 mm Hg after pindolol-MDMA. Pindolol did not change adverse effects of MDMA.CONCLUSIONThe results of this study indicate that beta-blockers may prevent increases in heart rate but not hypertensive and adverse effects of MDMA.

01 Oct 2007·UrologyQ3 · MEDICINE

Doxazosin Relaxes Ureteral Smooth Muscle and Inhibits Epinephrine-Induced Ureteral Contractility In Vitro

Q3 · MEDICINE

Article

Author: Travis J. Jerde ; Tawnya L. Cary Coyle ; Murali K. Ankem ; Timothy D. Moon ; Stephen Y. Nakada

OBJECTIVESAlthough recent evidence has supported increased ureteral stone passage with selective alpha(1)-adrenergic receptor antagonists, no mechanistic study evaluating ureteral relaxation by alpha(1) antagonism has been reported to date. We evaluated whether the alpha-blocker doxazosin reduces spontaneous, and inhibits alpha(1)-agonist-induced ureteral contractility. Additionally, alpha-receptor subtypes in normal and obstructed human ureter were analyzed.METHODSWe exposed porcine ureters in organ tissue baths with 0.1, 1.0, or 10 microM doxazosin and recorded the tension for 90 minutes. After the initial treatment, a concentration-response curve of epinephrine or phenylephrine (1 nM to 10 microM) was generated. The experiment was repeated with the proximal, mid-, and distal ureter. The relative expression of the alpha 1A, 1B, and 1D receptor subtypes in normal and obstructed human ureters was analyzed using immunoblotting.RESULTSDoxazosin reduced the spontaneous ureteral contractility rates in a concentration-dependent fashion by 23% to 34%. A more pronounced relaxation effect by doxazosin was evident when epinephrine was introduced to the tissues. In 1 and 10-microM doxazosin-pretreated tissues, epinephrine caused 89% and 100% relaxation, respectively. Phenylephrine-induced contractions were antagonized by doxazosin but not reversed to any relaxant function. No differential expression of alpha(1)-receptor subtypes was identified in the obstructed versus normal ureters.CONCLUSIONSThe results of our study have shown that alpha(1)-receptor blockade decreases ureteral contractility and inverses the effect of epinephrine, providing even greater relaxation. We hypothesize that alpha receptor blockade might relax the ureter and induce stone passage by way of epinephrine activation of beta receptors. Additional studies should be performed to validate this hypothesis and to compare various alpha(1)-receptor subtype antagonists.

01 Jan 2004·Journal of Pharmacological SciencesQ3 · MEDICINE

Effects of Norepinephrine and Cardiotrophin-1 on Phospholipase D Activity and Incorporation of Myristic Acid Into Phosphatidylcholine in Rat Heart

Q3 · MEDICINE

ArticleOA

Author: Jochen Klein ; Tobias Weismüller ; Konrad Löffelholz

The present study is part of a project on phospholipase D (PLD) in cardiac hypertrophy and analyzed effects on PLD activity of two growth stimuli, norepinephrine (NE) and cardiotrophin-1 (CT-1), in incubated rat heart. Phosphatidylcholine (PC) was labeled by (3)H-myristic acid. PLD produced (3)H-phosphatidylethanol ((3)H-PEth) from (3)H-PC in the presence of ethanol and maintained a basal formation of (3)H-PEth. Short-term and long-term exposure to NE for 2 or 13 h, respectively, enhanced the formation of (3)H-PEth, which was blocked by prazosin. Long-term pretreatment with NE or CT-1 increased the incorporation of (3)H-myristic acid into PC, which was blocked by atenolol. When the (3)H-PEth formation was expressed as a fraction of (3)H-PC, PLD activity seemingly was unchanged (NE) or markedly reduced (CT-1); the true effects, namely, stimulation by NE and nonresponsiveness towards CT-1, were unraveled by atenolol (NE) or when PLD activity was expressed as (3)H-PEth per ng protein. In conclusion, alpha-adrenoceptor activation increased PLD activity. Long-term treatment with NE (via beta-receptors) or CT-1 enhanced the (3)H-myristic acid incorporation into a PC compartment, that was not available for the alpha-receptor-mediated PLD activation. These results were discussed in regard to cellular mechanisms of cardiac hypertrophy and to the transphosphatidylation assay of PLD.

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