Thank you, Spent about 5 mins checking into it. For me the following info is enough for now. Hopefully we will hear more positive info and trials a year or two for HCV SVR with Advanced Fibrosis if applicable.
Phase 1 Study to Evaluate Safety of GR-MD-02 in Subjects With Non-Alcoholic Steatohepatitis (NASH) and Advanced Fibrosis
This study is enrolling participants by invitation only.
Non-Alcoholic Steatohepatitis (NASH)
Drug: GR-MD-02
Drug: Placebo
Phase 1
Exclusion Criteria: #11 of 20
Subject has a history of hepatitis C. Patients found on screening to have hepatitis C antibody, even if PCR negative for HCV RNA, are excluded from this study.
http://clinicaltrials.gov/ct2/show/NCT01899859
Bump..
Big news last week - the release of preliminary results of first HUMAN clinical trial: this Galectin antifibrotic drug DOES work!! This could well mark the beginning of a cure for liver fibrosis and cirrhosis!! Even with its FDA 'fast track' designation, it will take awhile to cycle through the FDA approval process. You can read all about it here:
http://investor.galectintherapeutics.com/releasedetail.cfm?ReleaseID=836644
Thats a good one, thanks. We bought more Gilead today.
Stocks...now were gonna go poof.
Take a look @ $LJPC..ready for take off
Wow, hubby and I were just talking about this. Yes it's going to be very interesting! I'm hoping for the best!
One thing's for certain: SOMETHING is driving this company Galectin Therapeutics' stock, which has more than tripled in value since the Nov 2013 date of the last post in this discussion. I'm keeping my fingers crossed - in anticipation of the first human clinical trial results...to be released in April, only a few weeks away! A possible breakthrough treatment for fibrotic liver diseases!!.
Thank you so much for the link, I'm sending to my friend
rexx, you are correct. and that is exactly the point made in my addendum when I wrote the following:
"...this is assuming that the cause has been removed. if the underlying cause (such as hcv) has not been - or cannot be - removed, then the effectiveness of any antifibrotic would likely be diminished. "
in cirrhosis caused solely by alcohol the cause can always be removed.
in cirrhosis caused by a hepatitis virus the cause can sometimes be removed (...an example is successful treatment of HCV, attaining SVR status).
look forward to results of trials says on clinical trial website results out april 2014
"as we're often reminded, "cirrhosis is cirrhosis - regardless of the cause." and no doubt the same can be said for (its precursor) fibrosis. therefore it's reasonable to expect that an effective antifibrotic would work 'across the board' - regardless of what had actually caused the fibrosis...whether diet, hepatitis, alcohol, whatever".
i dont know iam wrong but i read and heard that an alcohol,or hep-b caused cirrhosis has better chances to improve as an hep-c caused cirrhosis.
altough for me its not logigcal nor understandable,because i thought/think also cirrhosis is cirrhosis no matter what has caused it.
i hope there are some poeple who could explain this,would be interesting to know.
Dee, I'm sending you a PM about this....
addendum to prev post:
"therefore it's reasonable to expect that an effective antifibrotic would work 'across the board' - regardless of what had actually caused the fibrosis...whether diet, hepatitis, alcohol, whatever...."
.
....this is assuming that the cause has been removed. if the underlying cause (such as hcv) has not been - or cannot be - removed, then the effectiveness of any antifibrotic would likely be diminished. .perhaps in such a case the disease progression could at least be slowed down...but these are all things that remain to be seen. meanwhile we can at least hope for progress to be made -
my understanding is that the exclusion of hcv-antibody-positive applicants was done (along with other exclusions) to yield as homogenous-as-possible cohort of subjects for this clinical trial. beyond that, nothing should be read into the exclusion.
as we're often reminded, "cirrhosis is cirrhosis - regardless of the cause." and no doubt the same can be said for (its precursor) fibrosis. therefore it's reasonable to expect that an effective antifibrotic would work 'across the board' - regardless of what had actually caused the fibrosis...whether diet, hepatitis, alcohol, whatever.
If this is http://clinicaltrials.gov/ct2/show/NCT01899859, if you are hcv antibody positive, you are excluded.
This is really great news! Thanks so much for sharing. A friend of mine was asked to joint this trial but as a level 2 she was afraid to try, she has NALFD I think that is it.
I will let her know.
Thanks so much for sharing this.
The only other thing I heard about was the PPC that HepatitisResearcher used to talk about. It is an older post which to my surprise has gotten over 130 responses
http://www.medhelp.org/posts/Hepatitis-C/Research-supported-antifibrotics---do-they-exist/show/346752
I made money on every "liver" stock I have bought. I probably didn't buy enough and I may have sold some too early but they were all winners.
We agree Can-do. I wonder whether it might also help those with autoimmune liver disorders such as PSC or PBC - at least slow down the progression. Time will tell.
I agree, once one is SVR I see no reason why it would not work on us HCV cirrhotics, this is very interesting and being cirrhotic if it pans out I would love to give it a try......... Thanks Mike
I've been burned one too many times with pharma. I will let you have this one. I will stick with my coffee SBUX
I rarely give investment advice but I really like this stock. I think the potential market is huge. They are also suggesting that it can also treat lung fibrosis which is a bigger problem than some people realize. The way I see this stock is that it will either be huge or it will go bust and it depends on the trials. If people start getting sick or if the endpoints are not realized the stock will fall like a stone. If it works without serious side effects then the sky is the limit.
Thanks Mike I have never heard of this company and I follow the pharma's closely. I didn't even know what a galectin protein was. I found this on their website.
Science of Galectin Proteins
Galectins are important therapeutic targets because they are the mediators of fundamental biologic mechanisms in pathological processes. Galectic Science PublicationThere are nearly 3500 scientific publications with “galectin” in the title. Additionally, our company has edited two peer-reviewed books that bring together authoritative articles on the function of galectin proteins in disease.
The latest book includes proceedings from a galectin-focused symposium hosted by Galectin Therapeutics in September 2012, Galectins and Disease Implications for Targeted Therapeutics. The book is edited by Dr. Anatole Klyosov, Chief Scientist at Galectin, and Dr. Peter G. Traber, Chief Executive Officer and Chief Medical Officer of Galectin. These symposium proceedings are currently available here. Print copies of the book are available from Oxford University Press under ISBN: 978-0-8412-2880-1.
There are 15 galectin protein subtypes with the common characteristic of a carbohydrate recognition domain that binds to galactose-containing carbohydrates and glycoproteins. A good review article on the structure and function of galectin proteins is Di Lella 2011. A key factor that differentiates galectin protein subtypes is their oligomerization domains that allow the galectin protein to bind with another protein of the same family, creating a dimer (See the figure below). Secreted galectins have been shown to bind with high affinity to galactose-containing glycoproteins on the cell surface and in the extracellular matrix. Their ability to dimerize creates the opportunity for galectins to link glycoproteins and form a lattice structure on the cellular surface and to promote cell-cell and cell-matrix interactions. The associations between glycoproteins created by galectins can trigger intracellular signaling and potentiate or modulate certain biologic and pathologic effects. Galectin proteins also have intracellular functions, but we are focused on the extracellular functions which are accessible to targeting with our drugs.
Model of Galectins
While galectins are normally expressed in small amounts in many different cell types, they are most highly expressed in macrophages of the immune system. Secreted galectins are markedly increased and have important roles in a wide variety of pathological processes involved in immune regulation, inflammation, fibrogenesis and tumor cell biology. Our drug compounds are designed to bind to and inhibit the function of secreted galectins. With these characteristics, our drugs have the potential to modulate and treat diseases where increased galectins promote or potentiate the pathological situation.