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Idiopathic Pulmonary Fibrosis (IPF) as the name suggests is a progressive disorder with no known aetiology. It is characterised by the thickening of the alveoli due to scarring resulting in cough. It is known to primarily occur in older adults over 60 years of age. The findings of IPF have a known association of Usual Interstitial Pneumonia (UIP) (Raghu et al., 2011; Kawano-Dourado & Kairalla, 2013; Wells, 2013). It has been deemed that the prognosis is generally poor when UIP has been confirmed (King et al., 2001b). The median survival rate of IPF is 50%, typically around two years after diagnosis (Raghu et al., 2011; King et al., 2001b).
Idiopathic Pulmonary Fibrosis (IPF) as the name suggests is a progressive disorder with no known aetiology. It is characterised by the thickening of the alveoli due to scarring resulting in cough. It is known to primarily occur in older adults over 60 years of age. The findings of IPF have a known association of Usual Interstitial Pneumonia (UIP) (Raghu et al., 2011; Kawano-Dourado & Kairalla, 2013; Wells, 2013). It has been deemed that the prognosis is generally poor when UIP has been confirmed (King et al., 2001b). The median survival rate of IPF is 50%, typically around two years after diagnosis (Raghu et al., 2011; King et al., 2001b).
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have not shown any significant decrease in the mortality rates for patients diagnosed with<br />
IPF(Xaubet et al., 2003b; Pinheiro et al., 2008; Taskar & Coultas, 2006; Lee et al., 2011).<br />
Other more novel drugs that have been upcoming in the past few decades such as nintedanib,<br />
etanercept, warfarin, gleevec and bosetan still present conflicting evidence (Luppi et al.,<br />
2012). Of this, Pirfenidone is another novel drug that was given approval by the European<br />
Medicines Agency (EMA) in 2011 for treating IPF (Behr et al., 2009; Taniguchi et al., 2010;<br />
Jiang et al., 2012; Behr & Richeldi, 2013).<br />
There are several researches which attempt to elaborate the mechanisms and the<br />
progress of the disease wherein there is still no definitive mechanism identified for the<br />
disease. It is hence likely to know that there exist several progressing mechanisms through<br />
which the disease progress which further states that no single specific mechanism has been<br />
proved to be effective for the treatment. Therefore, though several clinicians and researchers<br />
have been examining the disease for decades, the clinical outcomes are still unchanged<br />
(Fioret, 2012).<br />
1.1 Background of the Study<br />
The development of two important IPF treatment drugs namely Pirfenidone and NAC<br />
has been elucidated briefly by Myllärniemi and Kaarteenaho, (2015) wherein the previous<br />
researchers has examined the time frame of development of each of the drug. The time frame<br />
elaborated for each of the treatment drug showed variations from their discovery till their<br />
initial use for the treatment of IPF.<br />
1.2 Pirfenidone<br />
Pirfenidone is found to possess anti-oxidant, anti-fibrotic and anti-inflammatory<br />
effects in the experimental models wherein the same potential is also found to be in IPF<br />
human patients. Pirfenidone is Found To Inhibit The Growth Factor-Β (TGF-β) in vitro and<br />
functions as an anti-fibrotic by altering the synthesis, expression and accumulation of<br />
collagen (Iyer et al., 1999b; Misra & Rabideau, 2000; Oku et al., 2008a). Pirfenidone is<br />
found to possess the properties of an anti-oxidant wherein the action involves reactive oxygen<br />
species scavenging (Mitani et al., 2008). Furthermore, prifenidone was found to be better<br />
than placebo towards preservation of Forced Vital Capacity (FVC) and improvisation of<br />
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