a private bio company named FibroGen could have a drug which reverses, not merely minimizes lung scaring caused by lung fibrosis.
your information on the canine study is not accurate but the study did show efficacy. i was present for this study and others, including human use. if you would like to have an offline discussion of some historical details of this drug let me know.
the patent issues are deeper than the time line. hope the management does well for the company and stockholders. at present their burn rate will necessitate fund raising. .
My understanding of the canine data was that it stemmed from a chronic tox study that was aborted due to a mass respiratory infection in the colony, but the pathology was read out anyway and happened to show efficacy.
Dosing seemed to work fine in Japan. And adverse side effects seem to be predictable if nothing else.
Yes, well aware of the long history of this compound and issues with patent life.
In spite of the CAPACITY results, the current management beats the previous one, who really wasted a lot of time and money on the Actimune Phase IIIs, plus the off-label marketing BS that Harkonnen was responsible for. At least these guys are honest, no matter where the chips fell on the science results.
disagree - hamster is much better. certainly not as good as a primate but much better than a mouse.
not advocating 6 month screening tests. simply pointing out that the pulmonary activity for this product was not based upon an acute scar tissue model but a finding that arose out of a safety study.
the canine lungs were demonstrating age related (e.g. chronic idiopathic changes) deterioration and changes. the drug reversed the deterioration without showing toxicity (in a species that very often shows toxicity to these kind of compounds). conclusion: not only was there a histological demonstration of activity, there was an absence of toxicity at the effective doses.
question: why are the clinical studies in USA and Japan showing adverse effects at a dose that does not have clear efficacy? knowing the answer to this question, it is difficult for me to have confidence.
yes there have been a lot of papers published on this product but many are really of no great import. also the plethora of publications may have a negative impact on the politics of drug approval. would it surprise you to know the actual discovery of pharmacologic activity for this product dates back about 50 years?
the price being charged in japan for the product is surprising. market penetration has been slow to materialize. prices bandied about for USA market seem to be commensurate with japan. is it fair to assume any USA approval would be followed by similar slow market penetration?
itmn is too risky for me. many of the posts on this message board appear to be short term speculation and rumor mongering rather than long term investment. on this product, their patent position appears suspect. in general, the company appears to have a history of diluting shareholder equity to continue with flawed research and large overhead. i'm sure people made money on the options with the great volatility.
Hamsters are not really any better than mice or rats for this work - same anatomical issues as other rodents. For the kinds of screening assays used to test for efficacy, there's not a lot to be gained.
If we had to rely on 6 month studies in dogs to provide efficacy data and screen all promising compounds, R & D would be even slower and more expensive. And probably not affordable at the university levels, where much of the pirfenidone work was done.
And what caused the lung scarring in that study?
golden syrian hamster. one needs to create a scarring that is similar to idiopathic scarring - not an acute scar tissue formation that one sees in bleomycin or radiation.
the original study identifying the pulmonary activity of pirfenidone was a 6 month canine safety study. the groups receiving the drug had much clearer lungs than the control/placebo group. not only were the results dose related but canines are very sensitive to this class of compounds. the study showed the efficacy with none of the toxicity. the activity was demonstrated on lung tissue that was not exposed to an acute irritant and the subsequent short term scar tissue formation.
"not quite correct - there are animal models that can mimic human diseases more accurately (even those termed idiopathic). for pulmonary drug efficacy assessment there is a preferred species which will produce a result more consistent than a mouse. "
I agree that rodents are not ideal for the study of airway diseases and injury due to differences in lung structure.
Perhaps there are animal models which give you pathology that looks a lot like the end-stage disease of interest.
But it still ain't the same as IPF - you simply can't "accurately" model something of unknown etiology without making some very large assumptions - like "a-hah, it is all due to IL-13" or TGF or CTGF or IFN-gamma.
In short, this is why development of anti-IPF drugs has been painfully slow. It may work fine in the model(s) (bleomycin or radiation or cyclosporine), but that doesn't mean it will always work in the real world disease. And you just don't know until the phase II or phase III results are in.
Experimental non-clinical work in done in rodents precisely because it is highly reproducible - I'd like to hear, in some detail, about these "preferred species" you refer to.
not quite correct - there are animal models that can mimic human diseases more accurately (even those termed idiopathic). for pulmonary drug efficacy assessment there is a preferred species which will produce a result more consistent than a mouse.
intermune is not using the optimal dosage for this product but so far they have no been able to figure out to how they can use the optimal dosage. it will be interesting to see if they can figure it out before they run out of money and patient investors.
This is an early stage study in animal models of induced fibrosis, not IPF. You are jumping to unfound conclusions. The ITMN and Japanese studies clearly show a decreased in progression and severity of IPF when perfinidone in 2400mg/day doses are used. UP to 72 weeks possible longer. These patients die a horrible death and there is nothing right now to help them. Perfinidone with its low risk profile and shown benefits will be a welcome relief to many of these patients. The FDA knows this (read the FDA advisory panel report; google it). It is only a matter of time before an understanding is worked out. GLTA
Nice factless spin. I don't need to google the FDA Advisory panel report, I was here when it occurred. The members were looking for more data even then. ITMN still did not produce it.
The Japanese and ITMN studies showed very little - thus the letter. You can make stats do whatever you want them to - just like your 72 weeks longer. I can also say perfinidone allowed some to live shorter lives because it killed them.
Of course the animal models had induced fibrosis but they found the scars had healed. This early indication shows a lot more promise than perfinidone (i.e possible cure vs. possible days/weeks of extention of life). By the time InterMune gets their act together and does another phase III, this newcomer might just beat them to market. At a minimum, ITMN doesn't have the market cornered like some pumpers have been trying to suggest.
The FDA and ITMN will come to an understanding after ITMN performs the required phase III on the FDA's term, not their own made up endpoints.
Hey Beav, looks like it's setting up for another down day for you tomorrow. Might be a bigger down day than today. Don't see too many up days on the horizon. You hold tight to those shares though. You're the master. Just another 7-10 trades like your first and we might be even.