maybe some of you will come around soon and will agree with me that the data from CKD PII trials didn't tell us anything we didn't know already, ok so Zerenex can reduce phosphorus down to 4?? well, PIII trial already showed that, and oral iron can improve Hemoglobin?..that's been known since 1930s..in fact research showed that oral iron can increase hemoglobin by the entire 1 point after 56 days (Zerenex on average increased Hemoglobin by 0.5 over 6 weeks), so, nothing new on iron front either...so, my question is what exactly did we learn from the CKD PII data??? in my opinion the sudden 30% jump in the stock price was not justified, and was just knee-jerk reaction to the words "met all primary and secondary end points"..just my opinion
OK Gas...lets put all the cards on the table. The arguments you made above are the same arguements made by Kolemup. I'm getting the feeling Kolemup is your humorous creation to vent your short leanings while you
hold yourself out as a long. Now you pick at positive phase II data as a non-event.
To start with the normal range of serum phosporus is 3.5 to 5.5 mg/dL
Ron said that phase II data would not be as dramatic as Phase III due to the population at that stage of illness.
In the Phase II study, 149 subjects with stage 3-5 CKD (not on dialysis) with elevated serum phosphorus (≥4.0 mg/dL) and iron deficiency anemia were randomized 1:1 to receive either Zerenex or placebo. The study consisted of a 2-week washout period for subjects on a phosphate binder at screening followed by a 12-weeks of treatment. Intravenous (IV) iron and erythropoiesis-stimulating agents (ESAs) were not permitted in the 8 weeks or 4 weeks before the study, respectively, and oral iron was not permitted during the trial.
Zerenex met both co-primary endpoints, demonstrating highly statistically significant changes in serum phosphorus and transferrin saturation (TSAT) versus placebo (p
Sentiment: Strong Buy
You're an idiot! Just ask a physician. As one, who is NOT a nephrologist, I understand the significance. when speaking to friends who are nephrologists they were looking forward to attending the conference and learning more about Zerenex. In NYC where I like to think some of the greatest physicians are, having an additional way to treat patients, that is much less invasive, is a big deal. They learn with interest and will utilize new tools when they become approved.
YES you must be thrilled that Duschene muscalar distrophy children and adolescents now will
get worse while The FDA requires a P 3 trial. They may even die in the meantime but just as long as a DB like yourself shorted Sarepta it madecyour day. You sedserve a special place in hell you hippocryte. And tgere is no way in hellthat you arent short kerx with your assinine multitude of posts about the P2 trial results as well as the P3 results to date.
YOUR MOTIVES HAVE CLEARLY BEEN EXPOSED NOW SO YOU CAN JUST CRAWL BACK INTO THE BLACKCHOLE YOU CAME FROM YOUR CHARLATAN
Sentiment: Strong Buy
and btw, I went to their board 2 weeks ago and spent a weekend trying to warn SRPT longs that the risk of the FDA not granting AA is pretty high given very few data points SRPT has and inconsistencies between dystrophyn production and 6 minute walk test..nobody listened of course, the only thing I was wrong about is that the stock would drop to $20 on the news, not to $15...
after PIII ESRD data Kerx stock tripled in few sessions, and now after CKD PII data we are sitting at $12-$13 per share. heck, we almost touched $12 even before PII data, and pumpers still don't believe me and want to say the CKD data are blockbuster... I tell you want blockbuster means: phosphorus level at 3.5 and Hb increase of at least 1point or higher, now that would be blockbuster, but what Zerenex showed is marginal on all counts and thus market reaction is mute, $12-$13 per share can be justified just by ESRD, really good CKD data would move this stock to $20+ overnight as CKD is 4x bigger market than ESRD..so I am not sure why this is still a debate when markets have spoken loud and clear _"we are ok with the CKD data but not impressed"
Once again--you are wrong. When you start to use the stock price and the 'market' as your justification you have run out of ammunition. When the P3 ESRD data came out and the stock shot from $3 to $10 and then settled back in the $6's, according to your rationalization, the 'market' would have indicated that it was not impressed with the results, but we all know that is not the case, as the data has become more compelling, the target prices have continually been raised and are now averaging about $21/share, and the stock did reach a recent high of $14.60. Gasbag, you know how the market works--buyers/sellers....investors/sellers/shorts. It is a very complex dynamic and gives no true indication of a stock's longer-term price. Shame on you and you should be embarrassed for even resorting to such uneducated reasoning. The stock price increases as the company reaches each milestone and establishes a higher base at each level. From the $3's to the $6's to the $8's and now to the $12's.........Japanese approval takes the stock to another level, FDA approval takes it to the next level and finally CKD takes it up all the way into the mid $20's or higher---without any buyout prior to that, which becomes more likely every day. Your numbers are wrong, you are not a nephrologist and have minimal or no advanced knowledge of blood chemistry and resorting to using the 'market' to justify your position is rediculous.
Sentiment: Strong Buy
If the CKD data given for phase ll were so unimpressive, why did 100% of the analysts covering the stock raise their price targets by 50% on average right after the news ? Do these analysts have no idea of the unimpressive results of phase ll for CKD patients that you know is true. By the way, what is your backround in general medicine ? I think maybe hschlauch is a big more knowledgable- no ?
A few key points I ask myself after reading the abstract: 1) What were the baseline Hgb levels in the study? 2) How long were those Hgb levels sustained? 3) How many patients were enrolled in the study? 4) How long were the washout periods, if any? Virtually nothing is known about the parameters and methods, at least within the abstract.
Additional points related to safety and efficacy: 4) What were their ferritin levels like at the culmination of the study? 5) What were the GI issues? 6) Why is there non-compliance with the oral preparations? These are very important questions, because the answers are what differentiates Z from existing oral iron supplements.
Keryx reported AVERAGE (i.e., mean) hemoglobin change, which does not reflect a percentage (of patients) change greater than or = to 1 g/dL. The patients enrolled in the ND-CKD study may not have had significantly low hemoglobin levels to begin with - again stats are mean levels at baseline and end of treatment. It's much easier to achieve a 1 g/dL change when hemoglobin levels are below 11 g/dL or lower. The key is whether or not that oral iron is absorbed appropriately by the intestines. Zerenex is easily absorbed by the intestines and, when the body no longer needs the iron, it slows down intake of Zerenex. That is why patients reach a plateau with Zerenex. Give a patient with hemoglobin levels under 10 g/dL Zerenex, and that patient will reach appropriate and sustainable levels, therefore exceeding 1 g/dL. Give a patient with hemoglobin levels at 11.5 g/dL Zerenex , and that patient's body does not need to absorb a lot of iron, therefore it would require probably less than 1 g/dL. Can we say that a traditional oral iron supplement is capable of reaching and maintaining appropriate levels of hemoglobin? No, not even close.
There are plenty of reasons why Zerenex is a much better choice for ND-CKD IDA than traditional oral iron supplements aside from it's overwhelming efficacy.
Sorry, I cannot agree with you on your main points. There is quite a bit we didn't know about the non-dialysis population - Zerenex's endpoints had never before been clinically evaluated in the US. I had my doubts prior to the preliminary data release, specifically in regards to hemoglobin benefits. I no longer question Z's efficacy on that endpoint.
Curious, what oral iron supplements have clinically demonstrated improved hemoglobin by "1 point" in CKD non-dialysis patients? Dr. Lewis presented evidence at the ASN meeting that clinical trials using common oral iron supplements 'are not sufficient for maintaining ferritin levels and do little or nothing to raise hemoglobin vs. placebo'. Does the oral iron supplement you refer to have the benefit of maintaining ferritin? Also, what are its side effects?
I have no issue with near-term price volatility. That 30% jump may look like chump change next year at this time. The significance of those words - "met all primary and secondary endpoints" - will likely resonate with nephrologists, so it probably isn't a small matter and deserves some reaction.
I attached below part of the abstract for paper I came across this weekend, just to back up the claim regarding Hb increase by 1 point or greater in 30% of patients on oral iron, if you google "oral iron for CKD patients" there is a sea of literature out there, I can't copy and paste it all...good luck
Iron supplementation in the non-dialysis chronic kidney disease (ND-CKD) patient: oral or intravenous?
Department of Renal Medicine, King's College Hospital, Bessemer Road, London SE5 9RS, UK. email@example.com
The management of iron-deficiency anaemia in patients with non-dialysis chronic kidney disease (ND-CKD) remains controversial, particularly regarding the use of oral versus intravenous iron supplementation.
A PubMed search from 1970 to February 2009 was conducted to identify relevant research articles.
Iron supplementation is advisable for all iron-deficient CKD patients receiving erythropoiesis stimulating agents (ESAs), and intravenous iron may be preferable to oral iron. However, there is also a growing body of data indicating that iron supplementation may avoid or delay the need for ESA therapy in some ND-CKD patients. In each of four randomised trials that included ND-CKD patients without ESA, the haemoglobin response was greater with i.v. versus oral iron. Moreover, some ND-CKD patients who remain anaemic on oral iron may subsequently respond to i.v. iron. Newer preparations (ferric carboxymaltose and ferumoxytol) permit rapid, high-dose administration. In a randomised study, a single 15-minute injection of ferric carboxymaltose, with up to two additional doses as required, resulted in 53.2% of ND-CKD patients achieving or =1 g/dL increase in haemoglobin by day 56 without ESA, compared to 29.9% of patients given oral iron supplements. Two large, randomised, ongoing trials will address the important question of whether i.v. or oral iron supplementation affects the progression of renal dysfunction. While i.v. iron is more costly than oral iron, the cost differential over time may be lower than widely believed, and i.v. therapy avoids the poor absorption, gastrointestinal intolerance and non-compliance... associated with oral preparations.