Kyoto Pharmaceutical University

www.kyoto-phu.ac.jp
Kyoto, Japan

京都薬科大学 Kyoto Pharmaceutical University is a private university in Kyoto, Kyoto, Japan. The predecessor of the school was founded in 1884. It was chartered as a university in 1949. As a university that trains Pharmacist-Scientists -- pharmacists that also possess research skills -- Kyoto Pharmaceutical University has laboratories in a wide range of fields. Each laboratory offers the optimal environment for enhancing skills, with about 10 members that each focus on their own research.Students devote themselves to around-the-clock research in order to master their own specialization and develop reformed medical care and a new vitality in the field of pharmaceuticals. Wikipedia.

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Patent
Kyoto Pharmaceutical University | Date: 2015-06-09

The problem of the present invention is to provide a useful prodrug compound of a naphthofuran compound. The present invention relates to a compound represented by the formula (IA): [wherein each symbol is as described in the DESCRIPTION] or a pharmaceutically acceptable salt thereof.


Patent
Kyoto Pharmaceutical University | Date: 2017-04-12

The problem of the present invention is to provide a useful prodrug compound of a naphthofuran compound. The present invention relates to a compound represented by the formula (IA):


Motohashi H.,Kyoto Pharmaceutical University | Inui K.-I.,Kyoto Pharmaceutical University
AAPS Journal | Year: 2013

In the kidney, human organic cation transporters (OCTs) and multidrug and toxin extrusion proteins (MATEs) are the major transporters for the secretion of cationic drugs into the urine. In the human kidney, OCT2 mediates the uptake of drugs from the blood at the basolateral membrane of tubular epithelial cells, and MATE1 and MATE2-K secrete drugs from cells into the lumen of proximal tubules. However, the expression of these transporters depends on the species of the animal. In the rodent kidney, OCT1 and OCT2 are expressed at the basolateral membrane, and MATE1 localizes at the brush-border membrane. Together, these transporters recognize various compounds and have overlapping, but somewhat different, substrate specificities. OCTs and MATEs can transport important drugs, such as metformin and cisplatin. Therefore, functional variation in OCTs and MATEs, including genetic polymorphisms or inter-individual variation, may seriously affect the pharmacokinetics and/or pharmacodynamics of cationic drugs. In this review, we summarize the recent findings and clinical importance of these transporters. © 2013 American Association of Pharmaceutical Scientists.


Satoh H.,Kyoto Pharmaceutical University
Current Pharmaceutical Design | Year: 2013

The proton pump inhibitors (PPIs) lansoprazole (LPZ) and omeprazole (OPZ) have been widely used for more than 20 years in the treatment of acid-related diseases such as gastro-duodenal ulcers and reflux esophagitis. Both LPZ and OPZ are derivatives of 2-[(2- pyridylmethyl)sulfinyl]-1H-benzimidazole, but LPZ has a trifluoroethoxy group in the molecule which seems to provide unique pharmacological properties in addition to its anti-secretory effect. For example, the anti-secretory effect of LPZ in rats was roughly 2 times greater than that of OPZ but the anti-ulcer effects were more than 10 times stronger than those of OPZ in rat models of reflux esophagitis, indomethacin-induced gastric antral ulcers and mepirizole-induced duodenal ulcers. It has also been reported that LPZ has acidindependent protective effects on the gastrointestinal mucosa, anti-inflammatory effects, and anti-bacterial effects on Helicobacter pylori. In contrast, recent advances in endoscopy have revealed that non-steroidal anti-inflammatory drugs (NSAIDs) often cause ulcers not only in the stomach and duodenum, but also in the small intestine in humans. Anti-secretory drugs such as PPIs and histamine H2-receptor antagonists (H2-RAs) are commonly used for the treatment of upper gastrointestinal mucosal lesions induced by NSAIDs. However, the effects of these drugs on NSAID-induced small intestinal lesions are still not fully understood. In this article, both a brief history of the discovery of LPZ and the unique pharmacological properties of LPZ independent from its anti-secretory action are reviewed, and the effects of PPIs and H2-RAs on NSAID-induced small intestinal lesions are discussed. © 2013 Bentham Science Publishers.


Kato S.,Kyoto Pharmaceutical University
Biological and Pharmaceutical Bulletin | Year: 2013

Serotonin (5-hydroxytryptamine; 5-HT), a well-characterized neurotransmitter in the central nervous system, plays a crucial role in regulating mood, body temperature, sleep, appetite, and metabolism. Serotonin is synthesized in the serotonergic neuron of the central nervous system; however, approximately 90% of serotonin is synthesized and localized in the gastrointestinal (GI) tract, especially in the enterochromaffin (EC) cells. In the GI tract, serotonin mediates control over a variety of physiological functions such as contraction/relaxation of smooth muscle, and peristaltic and secretory reflexes, directly or indirectly through intrinsic primary afferent neurons. The receptors mediating the action of serotonin are mainly classified into 7 major groups known as the 5-HT1 to 5-HT7 receptors. The 5-HT3 receptor is distinguished from among the other 5-HT receptor subtypes because it is only a ligand-gated ion channel, whereas the other subtypes serve as G protein-coupled receptors. The 5-HT3 receptor, which is generally considered to be localized in the central and peripheral nervous systems, is involved in processes associated with emotion, cognition, memory, pain perception, and GI functions including secretion and motility. Recently, an increasing number of findings have provided evidence of the important role of the 5-HT3 receptor in the regulation of inflammatory and immune responses. In fact, several 5-HT3 receptor antagonists have been reported to ameliorate intestinal inflammation. Therefore, this review focuses on the role of 5-HT3 receptors in the pathogenesis of intestinal inflammation. © 2013 The Pharmaceutical Society of Japan.


Takeuchi K.,Kyoto Pharmaceutical University
World journal of gastroenterology : WJG | Year: 2012

This article reviews the pathogenic mechanism of non-steroidal anti-inflammatory drug (NSAID)-induced gastric damage, focusing on the relation between cyclooxygenase (COX) inhibition and various functional events. NSAIDs, such as indomethacin, at a dose that inhibits prostaglandin (PG) production, enhance gastric motility, resulting in an increase in mucosal permeability, neutrophil infiltration and oxyradical production, and eventually producing gastric lesions. These lesions are prevented by pretreatment with PGE 2 and antisecretory drugs, and also via an atropine-sensitive mechanism, not related to antisecretory action. Although neither rofecoxib (a selective COX-2 inhibitor) nor SC-560 (a selective COX-1 inhibitor) alone damages the stomach, the combined administration of these drugs provokes gastric lesions. SC-560, but not rofecoxib, decreases prostaglandin E 2 (PGE 2) production and causes gastric hypermotility and an increase in mucosal permeability. COX-2 mRNA is expressed in the stomach after administration of indomethacin and SC-560 but not rofecoxib. The up-regulation of indomethacin-induced COX-2 expression is prevented by atropine at a dose that inhibits gastric hypermotility. In addition, selective COX-2 inhibitors have deleterious influences on the stomach when COX-2 is overexpressed under various conditions, including adrenalectomy, arthritis, and Helicobacter pylori-infection. In summary, gastric hypermotility plays a primary role in the pathogenesis of NSAID-induced gastric damage, and the response, causally related with PG deficiency due to COX-1 inhibition, occurs prior to other pathogenic events such as increased mucosal permeability; and the ulcerogenic properties of NSAIDs require the inhibition of both COX-1 and COX-2, the inhibition of COX-1 upregulates COX-2 expression in association with gastric hypermotility, and PGs produced by COX-2 counteract the deleterious effect of COX-1 inhibition.


Toba H.,Kyoto Pharmaceutical University
Current atherosclerosis reports | Year: 2014

MicroRNAs (miRNAs) are a class of post-transcriptional regulators that provide a mechanism of gene silencing by translational repression or degradation of the targeted gene. Gene expression regulation by miRNAs is involved in most if not all physiological and pathophysiological processes. Atherosclerosis is a major cardiovascular disease pathology regulated by miRNAs. Recent miRNA profiling studies have implicated the potential use of miRNAs as biomarkers in patients with atherosclerosis, as both diagnostic and prognostic indicators. This review will discuss the clinical and basic science research information that has been gleaned regarding miRNA roles in dyslipidemia, diabetes, obesity, and insulin resistance which are the major stimulators for the development of atherosclerosis.


Motohashi H.,Kyoto Pharmaceutical University | Inui K.-I.,Kyoto Pharmaceutical University
Molecular Aspects of Medicine | Year: 2013

The kidney plays an important role in the secretion of organic compounds including drugs, toxins and endogeneous metabolites. The renal elimination process of organic cations is mediated by two distinct transport systems expressed on the apical and basolateral membrane of proximal epithelial cells. In 2005, mammalian multidrug and toxin extrusion 1 (MATE1)/SLC47A1 was identified as an orthologue of bacterial NorM. MATE1 is the H +/organic cation antiporter at the apical membrane, which mediates the secretion of organic cations. Kidney-specific MATE2-K was isolated from human kidney and localized at the brush-border membrane of proximal tubules. Like MATE1, MATE2-K mediates the secretion of organic cations into urine. MATE1 and MATE2-K are involved in the excretion of important medications and the disruption of these transporters can cause severe pharmacological problems. Recent findings regarding the MATE/SLC47 family are summarized in this review. © 2012 Elsevier Ltd. All rights reserved.


Patent
Kyoto Pharmaceutical University | Date: 2016-07-06

Provided is a compound showing a bone formation promoting action (and/or bone resorption suppressive action). A compound of the formula (I) or a pharmacologically acceptable salt:


Patent
Kyoto Pharmaceutical University | Date: 2014-08-29

Provided is a compound showing a bone formation promoting action (and/or bone resorption suppressive action). A compound of the formula (I) or a pharmacologically acceptable salt: [wherein each substituent is as defined in the DESCRIPTION], has low toxicity, shows good pharmacokinetics, has an action to promote bone formation, and is useful for the prophylaxis or To treatment of metabolic bone diseases (osteoporosis, fibrous osteitis (hyperparathyroidism), osteomalacia, Pagets disease that influences the systemic bone metabolism parameter etc.) associated with a decrease in the bone formation ability as compared to the bone resorption capacity.

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