Shionogi partner Ildong gains South Korean approval for Pirespa Article | 14 August 2012 Japanese drug major Shionogi (TYO: 4507) says that its South Korean partner Ildong Pharma has received marketing and manufacturing approval for idiopathic pulmonary fibrosis (IPF) treatment of Pirespa (pirfenidone) 200mg tablets, and Ildong plans to launch the drug as soon as possible. Shionogi in-licensed pirfenidone from the USA-based Marnac and KDL of Japan and received marketing and manufacturing approval for IPF in October and launched it as Pirespa in December 2008 in Japan for the first time in the world. Pirfenidone is a promising therapeutic agent which is expected to inhibit the progression of IPF through a new mechanism of action inhibiting fibrosis directly and offering a new option for IPF treatment. Shionogi entered into licensing agreement for the sale of pirfenidone in South Korea with Ildong last year, the financial terms of which were not disclosed (The Pharma Letter July 14, 2011). Following the execution of deal, Ildong has developed it and submitted a New Drug Application of pirfenidone for the treatment of IPF to Ministry of Health and Welfare in April 2012 and received the approval after a fast track procedure as an orphan drug.Shionogi will provide the product to Ildong and receive the royalty payment based on the net sales of the drug. The royalty will not impact Shionogi's consolidated earnings forecast for fiscal 2012, the Japanese drugmaker said.
Wikipedia for Pirfenidone
Pirfenidone is a drug developed by InterMune Inc. for the treatment of idiopathic pulmonary fibrosis (IPF). In 2011 it was approved for use in Europe for IPF under the trade name Esbriet.[2] The proposed trade name in the US is also Esbriet.
In Japan it is marketed as Pirespa by Shionogi & Co. In October 2010, the Indian Company Cipla launched it as Pirfenex. In September 2011, the Chinese State Food and Drug Administration provided GNI Group Ltd with approval of pirfenidone in China.[3]
Pirfenidone has well-established antifibrotic and anti-inflammatory properties in various in vitro systems and animal models of fibrosis.[4] A number of cell-based studies have shown that pirfenidone reduces fibroblast proliferation,[5][6][7][8] inhibits TGF-β stimulated collagen production[5][6][9][10][11] and reduces the production of fibrogenic mediators such as TGF-β.[7][10] Pirfenidone has also been shown to reduce production of inflammatory mediators such as TNF-α and IL-1β in both cultured cells and isolated human peripheral blood mononuclear cells.[12][13] These activities are consistent with the broader antifibrotic and anti-inflammatory activities observed in animal models of fibrosis.
The clinical efficacy of pirfenidone has been studied in three Phase III, randomized, double-blind, placebo-controlled studies in patients with IPF.[31][32] The first Phase III clinical trial to evaluate the efficacy and safety of pirfenidone for the treatment of patients with IPF was conducted in Japan. This was a multicentre, randomised, double-blind, trial, in which 275 patients with IPF were randomly assigned to receive pirfenidone 1800 mg/day (110 patients), pirfenidone 1200 mg/day (56 patients), or placebo (109 patients), for 52 weeks. Pirfenidone 1800 or 1200 mg/day reduced the mean decline in vital capacity from baseline to week 52 compared with placebo. Progression-free survival was also improved with pirfenidone compared with placebo.[31] The CAPACITY (004 & 006) studies were randomized, double-blind, placebo-controlled Phase III trials in eleven countries across Europe, North America, and Australia.[32] Patients with IPF were randomly assigned to treatment with oral pirfenidone or placebo for a minimum of 72 weeks.[32] In study 004, pirfenidone reduced decline in forced vital capacity (FVC) (p=0.001). Mean change in FVC at week 72 was –8.0% (SD 16.5) in the pirfenidone 2403 mg/day group and –12.4% (SD 18.5) in the placebo group, a difference of 4.4% (95% CI 0.7 to 9.1). Thirty-five (20%) of 174 versus 60 (35%) of 174 patients, respectively, had an FVC decline of at least 10%. In study 006, the difference between groups in FVC change at week 72 was not significant (p=0.501). Mean change in FVC at week 72 was –9.0% (SD 19.6) in the pirfenidone group and –9.6% (19.1) in the placebo group. The difference between groups in change in predicted FVC at week 72 was not significant (0.6%, 95% CI –3.5 to 4.7).[32]A recent review by the Cochrane Collaboration concluded that pirfenidone appears to improve progression-free survival and, to a lesser effect, pulmonary function in patients with IPF.[33] Randomised studies comparing non-steroid drugs with placebo or steroids in adult patients with IPF were included. Four placebo-controlled trials of pirfenidone treatment were reviewed, involving a total of 1155 patients. The result of the meta-analysis showed that pirfenidone significantly reduces the risk of disease progression by 30%. In addition, meta-analysis of the two Japanese studies confirmed the beneficial effect of pirfenidone on the change in VC from baseline compared with placebo.[33]
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