Pharmaceutical Raw Materials Pirfenidonefor Anti-Fibrosis Piresupa 53179-13-8

Pharmaceutical Raw Materials Pirfenidonefor Anti-Fibrosis Piresupa 53179-13-8

Abstract

CAS:53179-13-8
MF:C12H11NO
MW:185.22
EINECS:1806241-263-5
Melting point:96-97°C
storage temp. Store at RT
solubility DMSO: ≥10 mg/mL, soluble
form solid
InChIKeyISWRGOKTTBVCFA-UHFFFAOYSA-N

Description

Pirfenidone is used to treat a lung disease called idiopathic pulmonary fibrosis (IPF). IPF causes scar tissue to form deep in the lungs. As time goes on, the scar tissue becomes thicker and becomes stiffer or thicker, which makes the work of the lungs more difficult. A decrease in lung function can make you breathless. When your brain, heart, and other organs don’t get enough oxygen, other medical problems can occur.

This is a drug developed by a number of companies around the world, including InterMune Inc. (now part of Roche), Shionogi Ltd. and GNI Group Ltd.
In October 2010, the Indian company Cipla launched the product under the name Pirfenex.
China’s State Food and Drug Administration has approved the approval of the new Chinese drug pirfenidone to GNI Group Co., Ltd., and approved production in 2013 with the Etuary trademark.

Applicant

In vitro, pirfenidone inhibits the proliferation of uterine fibroid cells and leiomyoma cells. Pirfenidone inhibits TGF-1 -induced collagen formation in fibroblasts. Inhibition of PDGF, FGF, and TGF-1 induces fibroblast proliferation. In the hamster model, oral pirfenidone prevents and treats bleomycin-induced pulmonary fibrosis. Pirfenidone prevents chemically induced sclerosing peritonitis in rats and can also be used in the treatment of keloid transplantation in nude mice. Pirfenidone 0.01 1 mg/ml inhibited maternal and dose-dependent serum stimulation of DNA synthesis in uterine fibroids and leiomyoma cells. The compound had no cytotoxic effects and had no effect on collagen mRNA levels. In the hamster pulmonary fibrosis model, pirfenidone reduced the level of procollagen I mRNA, reduced the levels of lung hydroxyproline and malondialdehyde, and retained the aminoacyl hydroxylase activity in the lung.

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