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Pirfenidone

Supplier:
Catalogue number:
10-2307-02
Size:
25 mg
Product is available in:
  • USA
  • Canada
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Antifibrotic agent. Pulmonary fibrosis drug; in COVID-19 clinical trials, for suppression of "Cytokine storm". Viveiros Rosa and Santos Rev. Panam. Salud Publica 44:e40, Mar 20, 2020; https://dx.doi.org/10.26633%2FRPSP.2020.40.

  • Datasheet:   view or download
  • Applications:"Cytokine storm" drug (approved, U.S.), in COVID-19 clinical trials
Product Type:

Biochemicals & reagents

CAS Number:

53179-13-8

Range:

1) Kehrer and Margolin (1997), Pirfenidone diminishes cyclophosphamide-induced lung fibrosis in mice; Toxicol.Lett., 90 125 2) Iyet et al. (1999), Effects of pirfenidone on procollagen gene expression at the transcriptional level in bleomycin hamster model of lung fibrosis; J.Pharmacol.Exp.Ther., 289 211 3) Xie et al. (2002), Upregulation of RGS2: a new mechanism for pirfenidone amelioration of pulmonary fibrosis; Respir.Res., 17 103 4) Li et al. (2016), Oral pirfenidone protects against fibrosis by inhibiting fibroblast proliferation and TGF-b signaling in a murine colitis model; Biochem.Pharmacol., 117 57 5) Nakazato et al. (2002), A novel anti-fibrotic agent pirfenidone suppresses tumor necrosis factor-alpha at the translational level, Eur.J.Pharmacol. 446 177 6) Misra and Rabideau (2000), Pirfenidone inhibits NADPH-dependent microsomal lipid peroxidation and scavenges hydroxyl radicals, Mol.Cell Biochem. 204 119 7) Canestaro et al. (2016), Drug Treatment of Idiopathic Pulmonary Fibrosis: Systemic Review and Network Meta-Analysis; Chest, 149 756

Limit of Detection:

185.23

Storage Temperature:

Room Temperature

Additional Information:

Pirfenidone is an antifibrotic agent which prevents lung fibrosis in bleomycin-induced animal models (1). This compound down-regulates bleomycin-induced overexpression of lung procollagen I and III genes (2) and up-regulates RGS2 (Regulator of G-protein Signaling 2) which represents a new mechanism of pirfenidone action (3). It also inhibits fibroblast proliferation (4), suppresses TNF╬▒ production at the translational level (5) and scavenges hydroxyl radicals and inhibits lipid peroxidation in a dose-dependent manner (6). Recently it was approved as a therapeutic agent for idiopathic pulmonary fibrosis (7) and is orally active.