Last update 21 Nov 2024

Traxanox

Last update 21 Nov 2024

Overview

R&D Status

Clinical Result

Translational Medicine

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms-

Target-

Mechanism-

Therapeutic Areas-

Active Indication-

Inactive Indication-

Originator Organization

Mitsubishi Pharma Corp.

Active Organization-

Inactive Organization-

Drug Highest Phase-

First Approval Date-

Regulation-

Structure

Molecular FormulaC13H6ClN5O2

InChIKeyMLCGWPUVZKTVLO-UHFFFAOYSA-N

CAS Registry58712-69-9

100 Clinical Results associated with Traxanox

100 Translational Medicine associated with Traxanox

100 Patents (Medical) associated with Traxanox

Literatures (Medical) associated with Traxanox

01 Apr 1989·The Journal of Clinical PharmacologyQ3 · MEDICINE

Effects of Traxanox Sodium on Blood Pressure and Serum Uric Acid in Hypertensive Patients: A Preliminary Study

Q3 · MEDICINE

Article

Author: Yuichi Koike ; Akio Fujimura ; Naoko Hino ; Akio Ebihara

The effects of chronic administration of traxanox sodium (traxanox) on blood pressure and serum uric acid level were investigated in 15 patients who had mild to moderate hypertension. Traxanox or its placebo was orally administered in a single‐blind protocol. Blood pressure was significantly reduced from baseline after treatment with traxanox. The serum uric acid level after drug administration was significantly lower than with placebo whereas urinary uric acid excretion was significantly greater and uric acid clearance tended to be greater. These results indicate that chronic administration of traxanox reduces serum uric acid level as well as blood pressure in patients with mild to moderate hypertension. This reduction in serum uric acid is due in part to a traxanox‐induced elevation of urinary uric acid excretion.

01 Jan 1989·The Japanese Journal of Pharmacology

Stimulation of phagocytic activity of leukocytes and macrophages by traxanox sodium in mice and rats.

Article

Author: Michio Terasawa ; Takeki Okumoto ; Masao Hisadome ; Kazuhiro Goto ; Yasushi Kawazoe

Phagocytosis of yeast particles by mouse peritoneal macrophages or rat peritoneal polymorphonuclear leukocytes was enhanced by traxanox sodium in vitro. Traxanox sodium (30 and 100 mg/kg, p.o.) enhanced phagocytosis of yeast particles by leukocytes and macrophages in vivo or ex vivo. On the other hand, prednisolone, isoproterenol and theophylline inhibited phagocytosis by leukocytes and macrophages under the same conditions. Traxanox sodium (30 mg/kg, p.o.) prevented the suppression of phagocytosis by the above drugs. Combined with theophylline, isoproterenol synergistically inhibited phagocytosis by leukocytes in vivo. Traxanox sodium (100 mg/kg, p.o.) administered alone had no influence on carbon clearance in normal mice. However, traxanox sodium (1-30 mg/kg, p.o.) prevented the suppression of carbon clearance by the treatment with carrageenan, but not by the treatment with ethyl palmitate. These results suggest that traxanox sodium stimulates the phagocytic activity of leukocytes or macrophages and prevents the drug-induced suppression of the phagocytic activity of these cells.

01 Jan 1989·International Journal of Immunopharmacology

Different inhibitory actions of immunomodulating agents and immunosuppressive agents on bone resorption of mouse calvaria

Article

Author: Kazuko Sasagawa ; Kazuhiko Someya ; Shigeru Fujibayashi ; Yukio Yamada ; Kazutoshi Okano ; Chieko Nawa ; Shosei Kou ; Satoshi Suzuki

In this study, we have investigated the in vitro effects of the immunomodulators lobenzarit and traxanox and a newly synthesized immunosuppressant, mizoribine, as well as cyclosporin A, on bone resorption using neonatal mouse calvariae labelled with 45Ca. As stimulators of bone resorption, bovine parathyroid hormone (PTH), lipopolysaccharide (LPS), interleukin 1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) were used. Lobenzarit, traxanox, mizoribine and cyclosporin A inhibited or tended to inhibit bone resorption stimulated by PTH, LPS, IL-1 beta or TNF-alpha in a dose-dependent manner. Basal bone resorption was inhibited by immunosuppressant cyclosporin A or mizoribine, while immunomodulators lobenzarit and traxanox failed to inhibit basal bone resorption. Removal of lobenzarit from the culture medium resulted in the recovery of bone resorptive activity. These results suggest that the inhibitory effect of immunomodulators on bone resorption is reversible and nonselective. Also, it raises the possibility that immunomodulators and immunosuppressants may affect bone resorption by different mechanisms.

100 Deals associated with Traxanox

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Traxanox

Overview

Basic Info

Structure

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R&D Status

Clinical Result

Translational Medicine

Deal

Core Patent

Clinical Trial

Approval

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