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Re: TRBN
Sorry I didnt see your response, bladrerunner. TRU-O15 is only one part of the Trubion story but to answer your question, yes the numbers are impressive. Both TRU-015 and SBI-087 were designed to target CD20 but also have reduced complement activation (ie better safety profile). The other part of the story is the technology platform (the SMIP and Scorpion technologies) and their cancer programs.
I could easily see this company being taken out at a significant multiple just for their technology platform alone. Ab engineering / novel scaffolds are red hot. A lot of companies are interested in multi-specific Ab approaches (Genentech and Abbott have published recent articles on their internal work). Trubion's Scorpion technology fits that bill.
(sidenote: Its also not a bad thing to have Mikael Dolsten, President of BioTherapeutics at Wyzer,present your clinical data at ACR to every important rheumatologist in the country.)
Full Disclosure: I'm now long this stock.
BTW, I found this one guy's summary of ACR pretty useful and I like his other summaries as well, so I thought I would share it with the board. His name is Alex To:
https://crosscurrentllc.com/uploads/10-21-09_Happenings_at_ACR.pdf
Hope that helps answer your questions, good luck.
PC
Re: TRBN
I have to agree with Wedbush's comments. Trubion is definitely a company under the radar right now, very little volume on this name.
- 60 million in cash with a 77 million dollar market cap
- Strong Partnership with Wyeth / Pfizer (CD-20)
- Strong Partnership with Facet (CD-37)
- Very Interesting novel Ab scaffold tech platform play (SMIP and Scorpion)
- Strong mgmt team
Jan '10 investor presentation (on website) was impressive.
so who bought another big slug of shares?
NEA?
Hmmm, the opinion of Dr. Stephen Howell or RPRX message board user, "Hptaxis".
http://www.businesswire.com/portal/site/google/?ndmViewId=news_view&newsId=20090417005150&newsLang=en
Real tough call there. (Rolls eyes).
Just to throw in my two cents in here re: this Idzi fellow. A small cap biotech that has solid data on two late state products with a declared desire to sell itself to the highest bidder (and could in fact be sold at a nice multiple to any pipeline starved Big Pharma at any time) may not be a good bet to short. Unless you dont mind losing your house. There are hundreds of other better short bets out there. All my humble opinion of course.
That Bill is excellent PR for RPRX. Thx for posting.
Modern Finance: How 600 billion in subprime led to a multitrillion dollar mess:
From:
http://www.thedeal.com/newsweekly/features/chain-of-fools.php
Akasidney,
This is my last post on the matter, b/c I want the RPRX board to stay on message (and I do appreciate your continued advocacy of the Company).
Please refer to the article below, which discusses how an ACORN-like organization, the Greenlining Institute, got away with shaking down banks for upwards of 2.4 Trillion (yes that's Trillion) dollars worth of poor loans.
http://www.theamericanprowler.com/dsp_article.asp?art_id=13948
Financial Affirmative Action
By Matthew Vadum
Published 9/29/2008 12:08:01 AM
When the history of the Great Economic Meltdown of 2008 is written, in-your-face shakedown groups like the Greenlining Institute will be held to account.
Greenlining, headquartered in Berkeley, California (where else?), is a left-wing pressure group that threatens nasty public relations campaigns against lenders that refuse to kneel before its radical economic agenda. Its principal goal is to push politicians and the business community to facilitate "community reinvestment" in low-income and minority neighborhoods.
The Greenlining name is a play on the unlawful practice of "redlining." That's when financial institutions designate areas, typically those with a high concentration of racial minorities, as bad risks for home and commercial loans. The Institute wants banks to give a green light to loans in these areas instead.
Recently profiled by John Gizzi, Greenlining uses carrot-and-stick tactics to blackmail public agencies, banks, and philanthropists to achieve its objectives. The Institute brags it has threatened banks into making more than $2.4 trillion in loans in low-income communities.
Was this a good idea?
Not according to University of Texas economist Stanley Liebowitz. He wrote that the current mortgage market debacle is "a direct result of an intentional loosening of underwriting standards -- done in the name of ending discrimination, despite warnings that it could lead to wide-scale defaults."
Liebowitz isn't alone is pointing out that U.S. financial markets are now being asphyxiated by a terrible credit crunch that might have been avoided if lenders had refrained from doling out loans they ought to have known were doomed to default.
Activist groups were encouraged to agitate by the Carter-era Community Reinvestment Act, which enshrined in law a kind of lending protection racket. Banking regulators were given the power to make trouble for banks that failed to lend enough money to so-called underserved communities. Banks that paid enough -- whatever that means -- got left alone, but banks that didn't, got their legs broken.
How much money is enough to satisfy the law? Even the Federal Reserve Board can't say for sure. From the Fed's online summary of the Act:
The CRA requires that each depository institution's record in helping meet the credit needs of its entire community be evaluated periodically. That record is taken into account in considering an institution's application for deposit facilities.
Neither the CRA nor its implementing regulation gives specific criteria for rating the performance of depository institutions. Rather, the law indicates that the evaluation process should accommodate an institution's individual circumstances.
One can almost imagine a CRA commissar saying, "It'd be a real shame if something happened to that nice bank of yours." When in doubt about potential CRA liability, don't risk committing a crime against diversity: make the loan. Or else.
After CRA came into effect, Saul Alinsky-inspired "community organizer" groups such as Greenlining, ACORN, and National Council of La Raza got into the shakedown business. They preach the hateful class-warfare rhetoric of their fellow community organizers Jeremiah Wright, Jesse Jackson, Al Sharpton, and Michael Pfleger.
They rage against capitalism and demand crushing taxes and aggressive wealth-redistribution programs. They demand more government spending on social programs, a higher minimum wage, and gun control. Depending which way the economic wind is blowing, they demand more subprime lending, or curbs on subprime lending, which through the magic of dysphemism, is linguistically transformed into "predatory lending."
La Raza ("The Race," in Spanish), which has lobbied to strengthen CRA, performed an amazing sleight of hand last year. After decades of demanding more loans for racial minorities, the group performed a dramatic about-face, suddenly warning that lenders, realtors, and investors who bought up subprime loans could be sued under a federal law that forbids housing discrimination.
It was the lenders' responsibility to "match families to the sustainable loans that they should have gotten in the first place," said Janet Murguia, La Raza's president. Pointing to 2005 data that show subprime loans with high interest rates comprised more than 50% of all mortgages taken by African-Americans and 40% of Latino borrowers, compared to 19% of white borrowers, she raised the specter of racism. Murguia failed to mention that without a subprime market many members of racial minority groups would have remained renters, unable to buy a home.
And the Greenlining Institute played rough with Rabobank, an international Netherlands-based "megabank" (assets: $740 billion) that was expanding its U.S. operations.
Even though Rabobank had received an "Outstanding" rating in its most recent CRA performance evaluation by the Federal Reserve Bank of San Francisco, that wasn't enough for Greenlining.
The group targeted Rabobank, demanding that it shell out $7.5 billion for loan programs to help farmworkers buy their own farms. When the bank balked, Greenlining launched a campaign last year against its proposed acquisition of another bank.
Activists noisily picketed Rabobank until it caved.
"Congratulations to everyone," "Rabobank is totally afraid of you," Greenlining's top legal dude Robert Gnaizda yelled in offering congratulations to at demonstrators through a bullhorn. "Rabobank is totally afraid of you." Earlier this year, Greenlining proudly unveiled what it called a "unique agreement" with Rabobank "to turn San Joaquin farmworkers into farmowners."
This is the kind of political activism that drove banks to make irresponsible decisions, and that now threatens to put taxpayers on the hook for bank bailout packages costing potentially trillions of dollars.
Even though the left's pathological preoccupation with economic egalitarianism never takes a vacation, the left isn't entirely to blame for Wall Street's current troubles.
The Federal Reserve Board encouraged bad behavior by keeping interest rates artificially low for far too long after the 9/11 attacks. Since money was cheap, bankers went overboard with exotic mortgage products, and investors kept inflating the housing bubble, sending home prices into the stratosphere.
But no one can deny the fateful role that these liberal financial activist groups played in making a bad situation much worse.
Matthew Vadum is a senior editor at Capital Research Center, a Washington, D.C. think tank that studies the politics of philanthropy.
Akasidney,
This mess is a complicated matter, but please don't disregard the role of Fanny/Feddy and the Dems in this catastrophe.
From today's NYT:
http://www.nytimes.com/2008/10/05/business/05fannie.html?pagewanted=2&_r=1&hp
Quote from today's NYT:
"Capitol Hill bore down on Mr. Mudd as well. The same year he took the top position, regulators sharply increased Fannie’s affordable-housing goals. Democratic lawmakers demanded that the company buy more loans that had been made to low-income and minority homebuyers.
“When homes are doubling in price in every six years and incomes are increasing by a mere one percent per year, Fannie’s mission is of paramount importance,” Senator Jack Reed, a Rhode Island Democrat, lectured Mr. Mudd at a Congressional hearing in 2006. “In fact, Fannie and Freddie can do more, a lot more.”
But Fannie’s computer systems could not fully analyze many of the risky loans that customers, investors and lawmakers wanted Mr. Mudd to buy."
Community Redevelopment Act
Akasid,
Read this and go into it with an open mind:
http://www.city-journal.org/html/10_1_the_trillion_dollar.html
That article is from 2000!
Paulson, Bernanke, etc., are specifically not placing blame on anyone right now b/c they need the bailout (as do all of us).
Best,
PC
Dude.
I call it as I see it. I fully blame Bush for getting us into Iraq. However, this financial mess fully goes to the Dems and their desire to reduce lending standards to put more low income individuals in homes. Fannie Mae and Fredie Mac acted in concert with Congress, the Clinton Administration, and community activists (hello Obama) to eliminate "discriminatory" lending and force banks to issue higher risk loans. Ever hear of the Community Reinvestment Act? Do some research, bud!
BTW, Go Repros!
Doc, Ive always been ashamed of Pelosi. However, today Ive never been more ashamed that she's my Rep.
Off Topic: Pelosi
My friends, today I've never been more ashamed of my Congresswoman, Nancy Pelosi.
What on Earth prompted her to give a hyper-partisan speech right before such a critical vote?
Sigh.
Excellent Deal for Repros
1. Repros gets the cash they need until 2010 at a solid valuation (especially in today's market).
2. Repros gets a nice, fresh, timely dose of credibility as existing investor Efficacy Capital effectively "doubles down" after signing a confidentiality agreement, performing necessary due diligence and reviewing all recent data.
3. The Company gains significantly more exposure, additional credibility, and extensive connections (ie fat rolodex) with the addition of a BSD like Dr. John Reed to the Board. Seriously, the guy has a 114 page resume:
http://www.burnham.org/downloads/Reed_CV_2005.pdf
http://www.burnham.org/default.asp?contentID=215
All in all, a very good day for Repros.
Further, if you happen to know that management has been unable to garner any significant partnership interest and is not currently in any meaningful discussions then the short was/is a sure bet.
If you happen to know that, then you happen to know inside information, and that happens to be illegal.
Risk of shorting RPRX
There are hundreds of stocks that should be shorted ahead of RPRX.
Why? This is a company that has long stated that their goal is to be acquired. Why would you short a company that at any moment could be taken out by a pipeline-starved big pharma at a significant multiple?
Makes no sense at all.
Endo/Neurocrine article in this week's BioCentury:
Product Development
The elagolix fix
By Aaron Bouchie
Senior Writer
All marketed endometriosis drugs have problematic side
effects, especially when taken long term. Doctors would like
to have a drug that can be taken safely over a long period of
time, and Neurocrine Biosciences Inc. thinks its elagolix
will fill the bill. The company recently released top-line Phase
II data that it believes showed that once-daily oral elagolix
can reach target estradiol levels without the side effects of
marketed drugs, which include bone loss, weight gain and
bleeding.
“There is a huge need in treating
endometriosis pain. The goal is to have
a long-term drug that wouldn’t cause
bad side effects like bone loss or weight
gain,” said Robert Schenken, chair of
the department of obstetrics and gynecology
at the University of Texas
Health Science Center at San Antonio
and former president of the
American Society for Reproductive
Medicine (ASRM).
David Adamson, director of Advanced
Reproductive Care Inc. and
president of ASRM, agreed. “No data
exist so far to demonstrate that any
class of drug is superior to another for pain relief [in
endometriosis]. Side effects matter. The choice of what drug
to take is based on cost and side effects,” he said.
Neither has been involved in clinical trials for endometriosis,
a condition in which tissue similar to endometrium in the
uterus is found elsewhere, primarily in pelvic areas.
Although the cause of endometriosis is unknown, the
main pharmaceutical strategy is to treat pain caused by the
disease by lowering estrogens, particularly estradiol, which
promote growth of endometrial tissue.
Drugs used to treat the condition include GnRH/LHRH
receptor agonists like Lupron Depot from Abbott Laboratories
and Synarel naferelin from Pfizer Inc.; progestins
like Pfizer’s depo-subQ provera 104 (DMPA); off-label oral
contraceptives consisting of progestins and estrogens; and
danazol, a generic synthetic androgen.
While progestins and oral contraceptives are inexpensive,
they can have severe side effects including irregular
vaginal bleeding, depression, acne, weight gain and bloating.
Danazol can cause weight gain, acne, body hair growth and
irreversible voice lowering.
Laparoscopic surgery and hysterectomy generally are
seen as last resorts, especially in women of childbearing age.
GnRH/LHRH receptor agonists work by overstimulating
the receptors, initially causing an increase in symptoms.
After about two weeks, the cells become exhausted and stop
releasing gonadotropins, resulting in a lowering of estradiol
and relieving symptoms.
The major problem with Lupron Depot is that it lowers
estradiol from an average monthly level of about 125 pg/mL
to below 15 pg/mL, according to Adamson. Such low levels
induce menopausal symptoms, such as hot flashes and loss in
bone mineral density (BMD), he said.
Because of the risk of bone loss, Lupron Depot’s label
recommends the drug be used for only six months. If
symptoms recur, another six-month course of Lupron Depot
is recommended, plus an “add-back medication” of a lowdose
estrogen or progestin. A third treatment is not recommended.
Adamson noted that Synarel lowers estradiol to about 30
pg/mL, but the inconvenience of a daily nasal spray makes it
less popular than the long-acting injections of Lupron Depot.
Adamson said the idea of lowering
estradiol to levels that are efficacious
but not so low that they cause bone loss
has been around since the early 1990s,
but no one has been able to do that in
a way that is convenient.
“If you can titrate the dose where
you can predictively and uniformly get
the estradiol level within that range,
then that would be progress,” he said.
According to Neurocrine CMO Chris
O’Brien, lowering estradiol starts to
show beneficial effects when it reaches
about 60 pg/mL, while the potential for
bone loss becomes worrying at levels in
the 10-15 pg/mL range, although that varies from patient to
patient.
“If you can keep estradiol levels around 10-60 pg/mL,
then the drug is probably safe and efficacious,” he said.
According to O’Brien, Neurocrine thinks it will be able to
do this with elagolix because it is a GnRH/LHRH receptor
antagonist that shows a dose response.
Top-line data from the double-blind, U.S. Phase II PETAL
study in 252 patients showed that 150 mg once-daily and 75
mg twice-daily elagolix resulted in median estradiol levels of
45 pg/mL and 30 pg/mL, respectively, at six months.
Both doses met the primary safety endpoint of change in
mean BMD from baseline for both the spine and femur. The
specific endpoint agreed with FDA was for the lower bound
of the 95% confidence interval (CI) at six months to not
exceed a -2.2% change from baseline.
The -0.11% change in mean BMD for the spine at six
months for the once-daily dose was not significantly different
from baseline (95% CI: -0.7%, 0.48%). The once-daily dose
showed a mean change of -0.47% from baseline for the femur
(95% CI: -0.96%, 0.02%).
The twice-daily dose showed mean change of -1.3% (95%
CI: -1.86%, -0.75%) for the spine and -0.99% (95% CI: -1.46%,
-0.53%) for the femur.
The trial used DMPA as a positive control in order to
show that the bone scans provided reliable data. DMPA is a
progestin that results in 1-2% bone loss at six months. In
PETAL, DMPA resulted in a -0.99% mean change in BMD
from baseline for the spine (95% CI: -1.61, -0.37) and -1.29%
for the femur (95% CI: -1.8, -0.77).
“The bone loss with DMPA was exactly what we expected,”
O’Brien said, noting that long-term use of DMPA
can result in 4-6% bone loss.
O’Brien said Lupron Depot results in 4-10% bone loss at
six months. “Women wouldn’t enroll in the trial if we were
going to use Lupron as the positive control because of the
bone-loss side effects,” he added.
The trial also met the secondary efficacy endpoints of
reduction in endometriosis pain from baseline using four
different measurements, including total composite pelvic sign
and symptoms score (CPSSS) and visual analog scale (VAS)
(p<0.0001 for all). The results were comparable to the
DMPA arm.
At baseline, patients had a mean CPSSS of 9.1; patients on
the once- and twice-daily doses of elagolix reported declines
of 5.5 and 5.2 points, respectively, compared with a 5.3-
point decline for DMPA.
VAS scores declined from a baseline of 78.7 by 31.8 and
33.4 points for patients on the once- and twice-daily doses,
respectively, and by 35.5 points with DMPA.
Responder rates were similar (74-86%) across all three
arms.
On quality of life measures, 24% of patients said pain from
endometriosis “never or rarely” interfered with their ability
to walk at baseline. At six months, that measure improved to
82% and 78% for the once- and twice-daily doses, respectively,
compared with 73% for DMPA.
Elagolix was well tolerated, with headache being the most
common adverse event. Discontinuation due to adverse
events was more common in the DMPA arm (16%) than the
once-daily (5%) or twice-daily (7%) dosages of elagolix.
Patients are being followed for another six months.
O’Brien said he is not worried about bone loss from longterm
use. He said earlier studies showed elagolix did not
change plasma levels of n-telopeptide, a biomarker of bone
resorption, at three months.
“Because the estradiol level is constant and n-telopeptide
does not change, we can figure that bone loss won’t increase
over the long term,” said O’Brien. He noted that Phase III
trials will provide one-year safety data.
The compound is in two six-month Phase IIb trials (NBI-
56418-0702 and NBI-56418-0703), both evaluating 150 mg
and 250 mg once-daily doses. O’Brien said the twice-daily
dose has been dropped because it showed “a hint that there
might be more bone loss without improving efficacy.”
The company added the 250 mg dose because it hasn’t yet
hit maximum tolerated dose (MTD), and O’Brien wants to
reach that before meeting with FDA to plan Phase III trials.
“We want to explore a dose that might be slightly too much
for a small proportion of women so that we will have good
evidence for Phase III dosing.”
The U.S. ’702 trial is fully enrolled with 150 patients, who will
receive elagolix or placebo for three months followed by three
months of elagolix. Top-line data are expected in 1Q09.
The ’703 trial has begun enrolling 180 patients in Central
and Eastern Europe. In this trial, subjects will receive elagolix
or Lupron Depot for three months followed by elagolix for
three months. Top-line data are expected in 2Q09.
The company hopes to have an end-of-Phase II meeting
with FDA in 2H09 and start Phase III testing shortly thereafter.
According to O’Brien, 750-800 patients will have been
treated with elagolix by that time.
Gorman told BioCentury he hopes to find a partner to codevelop
the compound for multiple indications, including
endometriosis, uterine fibroids, polycystic ovaries, precocious
puberty, benign prostatic hyperplasia (BPH) and in vitro
fertilization.
“We are not going to partner on an indication-byindication
basis. Ideally, we would have a single partner,” he
said.
“We are ready for Phase II in fibroids now,” Gorman
added. Only one more Phase I trial is needed before entering
Phase II in BPH.
Aeterna Zentaris Inc.’s cetrorelix is a GnRH/LHRH
receptor antagonist that has completed three Phase II trials
in endometriosis and is in Phase III testing for BPH. In one
double-blind, placebo-controlled Phase II trial in 50 patients,
cetrorelix significantly decreased pain at 24 weeks (p<0.001).
The company also said that cetrorelix was well tolerated and
associated with “only a slight and transient suppression of
serum estrogen levels.”
Aeterna has not disclosed plans for cetrorelix in the
endometriosis indication.
The drug is marketed as Cetrotide for in vitro fertilization
procedures by Merck KGaA’s Merck Serono S.A. division in
the U.S. and Europe and by Shionogi & Co. Ltd. in Japan.
COMPANIES AND INSTITUTIONS MENTIONED
Abbott Laboratories (NYSE:ABT), Abbott Park, Ill.
Advanced Reproductive Care Inc., Palo Alto, Calif.
Aeterna Zentaris Inc. (TSX:AEZ; NASDAQ:AEZS), Quebec City,
Quebec
American Society for Reproductive Medicine, Birmingham, Ala.
Merck KGaA (Xetra:MRK), Darmstadt, Germany
Neurocrine Biosciences Inc. (NASDAQ:NBIX), San Diego, Calif.
Pfizer Inc. (NYSE:PFE), New York, N.Y.
Shionogi & Co. Ltd., Osaka, Japan
University of Texas Health Science Center at San Antonio,
San Antonio, Texas
HPtaxis, your long meandering posts, containing dozens of "scare quotes" and frequent use of boldface do not hide the fact that you are a poseur in every sense of the word. From what Ive seen you're no expert.
But I must admit that you are good for a laugh.
It's hysterical that you have "uncovered" that RPRX has licensed the composition of matter from the NIH. Wow, man you're some investigator.
It's also equally funny that you presume to define to us dummies that a "provisional" patent is well um... provisional. Wow man, great insight.
I look forward to your further rigorous analysis.
Oh and by the way, HAVE A GREAT DAY!
Thoughts on slide 12?
Folks what are your thoughts on the Fibroid Reduction Volume at 3-month ultrasound slide. For the 12.5 mg dose the reduction was about 65% with a p-value of 0.017, whereas for the 25 mg dose, the reduction was less, and not stat stig. Thoughts? Any reason why they have to do a 3D graph for 2D data?
Thanks in advance.
Pre_Clinical
No offense, but Im not sure why one would bother to compare RPRX with GTCB. The biggest difference betwen Proellex and Atryn is that the first is a small molecule and that the latter is a highly complex biological molecule made in goat's milk. To me the risk with GTCB has never been about efficacy of Atryn, which I knew would perform as well as the plamsa derived material, but that the darn thing is manufactured literally by a herd of goats. It's a chemisty, manufacturing, and control nightmare. And I'm saying that as an owner of both stocks (however Im much much more deep in RPRX than GTCB.
Thanks Bio_Pete, iHub must be bombarding the site b/c I cant seem to connect!
Nerf,
To your point, the mgmt team is not A+ when compared to the like of other small biotechs. Also, there's the Zonagen history and the fact that the company is based in Woodlands, TX.
This company absolutely needs to publish their clinical data in a high quality peer reviewed journal, get some really top shelf clinicians on board, and have THEM pump the benefit of the drugs for you in articles and at meetings- really increase the exposure.
JMHO of course.
"Somewhere there's a serious problem with this company and I just cannot find it. "
------------------------------------------
There's not a serious issue with this company. The simple answer is that there has been a mass exodus of money from Biotech. How do you explain a ZGEN down 44% over the past year AFTER getting FDA approval for recothrom? Or Javelin, down around 70% over the past year after getting British approval for Dyloject. Heck, even a company like Seattle Genetics (SGEN) is only up around 6% despite having a hell of a year. As someone else said, IDIX was trading at cash despite having an approved drug. As I posted on the JAV board, just hang tight, it will cycle back.
Recent Timeline Slide from BIO CEO Conference. I love how he has the end of 08 anemia NDA submission in boldface.
I found this presentation to be the most effective one yet for Joe. He delivered a spot on speech. My only concern is that the while the data is top-notch, some of the graphs need to be more clearly displayed. While I understood it as a scientist, I could easlily see how the data could fly right over the head of banker types. I continue to have no idea why any savvy biotech investor would pass on investing in this stock.
Hang in there folks. All the biotechs are getting hammered.
There have been rumors that Amgen is going to acquire AMAG. I do think that ferumoxytol will be approved and I in fact owned AMAG for about half a year. However I got out b/c it looks like approval is already baked into their share price and I think there are far more undervalued stocks out there with better upside for the savvy investor.
JMHO of course.
PC
Re: Article
Weird. Of all the biotech stocks to pick he talks about RPRX, ZGEN, and GTCB. Now there's a guy that must have been reading ihub. JMHO.
In my humble opinion, if you agree 100% that Proellex "works", then you should be buying. Actual efficacy (not the Hedge fund but actual "efficacy") is the biggest risk in biotech. If you think this drug works, then the risk/reward, (ie upside) is way way bigger than the downside. It was pretty well articulated in the seeking alpha article, which I agreed with for the most part.
Bio_Pete,
You can download the JP Morgan power point presentation here:
http://www.reprosrx.com/presentations.htm
PC
I would also add peer reviewed publications to that list, corpstat. Its shocking how many docs dont know about this drug.
Bio_Pete,
Im not concerned about near term vs. long term catalysts for this issue. There are two questions I ask here, do the drugs work and what is the exit? IMO, yes the drugs work. So then what is the exit? Given that this is a company that openly has stated they want to be taken out, frankly a buyout can happen at any time. Given the market sizes at play here, I cant possibly believe that big pharma isn't sniffing around RPRX big time. And at $111MM market cap, bp could take this company out with the change at the bottom of their couches at a very nice multiple for all of us.
At least that's how Im playing it. Thoughts?
PC
I just bought another slug at 8.86 but it took about an hour to fill the order.
Interesting Paper, the discussion section is snipped below with a couple interesting parts underlined:
----------------------------------------------------
QUOTE:
"To our knowledge, this is the first prospective population-based study to show that low serum testosterone is associated with increased risk of death in older community-dwelling men. Men with total testosterone levels below the 25th percentile for this population (241 ng/dl) had 40% higher risk of death over the following 20 yr, compared with men with higher endogenous testosterone, independent of age, obesity, and lifestyle choices. These results were similar for the bioavailable fraction of testosterone and were not explained by overall health status.
Testicular function is suppressed in many acute and chronic illnesses, resulting in reduced serum testosterone (12). Low testosterone has been reported in type 2 diabetes, chronic obstructive pulmonary disease, alcoholic liver disease, and chronic renal disease (12). In addition, several cohort studies (22), including this one, have observed lower testosterone in men with the metabolic syndrome, and as many as one in four men with coronary heart disease has testosterone levels in the hypogonadal range (23). Low testosterone could be a marker of preexisting disease and not an independent risk factor for death. However, exclusion of men with diabetes, the metabolic syndrome, or cardiovascular disease had negligible effect on the association of low testosterone with all-cause mortality in this study. Furthermore, the risk estimates for total testosterone were stronger for cardiovascular and respiratory deaths when deaths that occurred during the first 5 yr of follow-up were excluded, suggesting that the testosterone-mortality association is not explained by concurrent disease, whether known or hidden.
Research suggests a role for metabolic effects of androgen deficiency in the link between low testosterone and mortality. We, and others, have shown that low testosterone precedes the development of central obesity (24, 25), the metabolic syndrome (26, 27), and diabetes (6, 27, 28) over the following 10–15 yr in nonobese men without these conditions at baseline. In this study, lower total testosterone levels were associated with central obesity and established CVD risk factors including insulin and insulin resistance, glycemia, lipid profile, and blood pressure as well as emerging risk factors such as leptin, adiponectin, IL-6, and CRP. In intervention studies, testosterone therapy improves, and testosterone ablation worsens, central obesity and many of these biomarkers (29), evidence for a causal association. Adjustment for most of these factors had minimal effect on the association of low testosterone with increased mortality. Although a subset analysis suggested some mediation by inflammatory processes, low testosterone was not associated with mortality in men with elevated levels of CRP. Nonetheless, the strong association of androgen deficiency with central obesity and obesity-related factors remains a plausible pathway through which testosterone influences the development of disease and subsequent mortality.
These results differ from those in other prospective studies of testosterone and mortality in relatively healthy community-dwelling men. Testosterone levels were not associated with all-cause mortality in either the Caerphilly Study (13) of 2512 men or the Massachusetts Male Aging Study (MMAS) (14) of 1686 men. The mean duration of follow-up in those studies (16.5 and 15.3 yr, respectively) was somewhat longer than ours (12.4 yr), but the proportion dying was much lower (19 and 31%, respectively, vs. 68% for Rancho Bernardo men), reflecting the almost 20 yr older average age of men in the Rancho Bernardo Study. The absent association in the earlier studies may reflect other population differences or hormone assay differences, or the importance of low testosterone for survival may become increasingly important as men age.
The observed low testosterone-mortality association was not specific to a single etiology. After excluding the first 5 yr of follow-up (to minimize reverse causality by comorbidity), testosterone was strongly associated with deaths due to cardiovascular and respiratory disease. An association of low testosterone with respiratory disease mortality was also reported by the MMAS (14). Unlike the present study, the association in MMAS was observed only with calculated free testosterone and not with total testosterone. In Rancho Bernardo, measured bioavailable testosterone, which includes both the albumin-bound and free testosterone fractions, was significantly associated with respiratory disease death as well as with all-cause mortality; free testosterone was not assayed.
The prevalence of hypogonadism in male populations is not known with certainty, in part due to a lack of consensus on the threshold that should be used to define testosterone insufficiency. Some investigators recommend a total testosterone less than 300 ng/dl; others advocate cut points of 250 or even 200 ng/dl (29). The median testosterone level for the present study (300 ng/dl) was lower than that reported for two population-based cohorts of men of similar age: the Osteoporotic Fractures in Men study of men 65 yr old and older reported a mean total testosterone level of 423 ng/dl (30), and the Health in Men study of men aged 70 yr and older reported a mean of 444 ng/dl (31). Lower testosterone levels in our study are likely due to differences in assay methods: both the Osteoporotic Fractures in Men and Health in Men studies measured testosterone using direct assays, whereas the RIA used in this study was preceded by two purification steps (organic solvent extraction and celite column chromatography), minimizing cross-reactivity with interfering substances (32).
Based on the lower overall mean testosterone, it could be argued that our cut point of 241 ng/dl was too high and overestimates the prevalence of low testosterone. Nonetheless, the 25% of men with values below this threshold were at a 40% increased risk of death over the following 20 yr, suggesting that a sizable proportion of older community-dwelling men may have clinically significant testosterone insufficiency. In a sensitivity analysis, lowering the threshold to 200 ng/dl reduced the proportion of men with low testosterone to 12% and increased the excess mortality risk to 45% (P = 0.007). It should be noted that use of these thresholds is arbitrary. There is no current consensus on what constitutes a testosterone insufficient state in older men, or indeed, if one even exists.
There is ongoing debate over the risk-benefit potential of testosterone therapy for men who are not clearly hypogonadal (33, 34). Results of the present study suggest that raising circulating testosterone levels above 300 ng/dl (the median for this population) offers no additional benefit, at least in terms of survival. This, plus the limited availability of information on safety of testosterone replacement, argues against a recommendation for testosterone supplementation to offset effects of male aging in men without documented androgen deficiency.
The present study has some limitations. Results were based on an almost entirely Caucasian middle- to upper-middle-class community and may not apply to other ethnic and socioeconomic groups. Repeat sampling of men with an initially low testosterone level is recommended to confirm androgen deficiency (35), but this and other epidemiological studies were based on a single measurement of testosterone. However, misclassification of men with low testosterone would be expected to underestimate, not cause, associations. In addition, blood for testosterone samples was obtained in the morning from fasting men, minimizing any diurnal variation still present in this age group, and sampling at a single time point fairly reliably reflects mean annual testosterone levels for older men (36). Although it is possible that testosterone exerts its benefit by conversion to estradiol, the addition of estradiol to these analyses did not materially change the results, and estradiol was less strongly associated with CVD risk factors than testosterone (data not shown).
In summary, in this cohort, older men with low levels of circulating total testosterone had a 40% increased risk of death over the following 20 yr, compared with men with normal testosterone, independent of age, adiposity, and lifestyle. This association was not explained by preexisting disease and was not specific to a single cause of death. Testosterone levels above the median for this population did not confer any additional survival benefit, offering no support for widespread testosterone therapy for aging men. Randomized, placebo-controlled trials are necessary to determine whether physiological testosterone replacement can safely extend the quality and duration of life for older men with well-documented testosterone insufficiency.
OT: io_io, Full disclosure: Right now I own, BMRN, RPRX, ZGEN, SGEN, JAV, and GTCB.
As for ZGEN, I ultimately think that recothrom sales are going to be ~500 MM/year, and that is conservative.
I get to this conclusion by assuming that (a) recothrom will dominate the current 250 MM/year market and (b) the total market is going to double. I was shocked to hear B.Carter say that current cattle-derived plasma thrombin is used in only 12% of surgical procedures with diffuse bleeding. Even a modest improvement of that number to 24% gets you to a $500 MM /year revenue. If you take a 6 times sale multiple, you are looking at a 3B market cap, which gets us to 4X the current market cap. Not too shabby.
And yes I'm not including the 20% owed to Bayer over the next two year, but Im also not including the rest of the pipeline, which looks pretty interesting when you closely examine Atacicept, IL-21, and Peg IL-29. On top of that you've got an A++ team in mgmt, with Bruce Carter the CEO and CSO Doug Williams. (Williams of Enbrel fame).
Take Care,
PC
io_io
At eleven bucks a share, Zymo is a complete steal.
I dont know how high she goes today, it may depend on scripts to move this stock. I found it is very interesting that current thrombin purified from source material is used in only 12% of surgical procedures with diffuse bleading. If zymo can expand that, and given that current standalone thrombin is around 250 MM in sales, we are talking potential blockbuster here. Plus the terms of the Bayer partnership are extremely favorable to Zymo. And then there's Atacicept, IL-21, and Peg IL-29. This one should be in every value investor's portfolio.
Congrats fellow longs, Aschoff's credibilty is now zero.
ZGEN
Zymogenetics initiated with a Sell at Brean Murray- tgt $7 (12.52 )
Brean Murray initiates ZGEN with a Sell and a $7 tgt based on the co's lead development program, Recothrom, a recombinant form of human thrombin. The firm questions the product's outright approvability based on the clinical safety data generated to date, ZymoGenetics' manufacturing capabilities, and the co's claims to superior safety in regards to live-sourced thrombin. They believe the next significant, near-term catalyst for the stock is January 17, 2008, which is the PDUFA action date for Recothrom. They believe the FDA will issue ZymoGenetics a Complete Response Letter. In 3Q08, they expect top-line results will be announced from Recothrom's Phase 3b trial, and believe the FDA will await these results before approving Recothrom in an already well-served market.
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Interesting. StreetInsider puts it this way:
Brean Murray Starts ZymoGenetics (ZGEN) at Sell
More News related to ZGEN
Brean Murray initiates coverage on ZymoGenetics (Nasdaq: ZGEN) with a Sell rating and a $7 price target.
The firm said ZymoGenetics will have a difficult time receiving FDA approval for its lead clinical development candidate, Recothrom, as the product has returned seemingly weak clinical data so far in its trials.
Tomorrow, Jan. 17, the FDA will provide ZymoGenetics with a Complete Response Letter, which could provide investors with a near-term catalyst. Brean Murray said the FDA will likely wait until the third quarter to announce Recothrom approval, as clinical data from the product's Phase 3b trial will be ready by then. Notably, the firm said Recothrom, if approved, will be entering "an already well-served market."
So from both news releases we have:
"questionable safety data"
"questionable manufacturing capacity"
"non-superior safety compared to plasma thrombin"
"Weak clinical data"
"Wait for more data from the phase 3b"
"already well served market (if approved)"
"will provide with a Complete Response Letter"
Seems like an awfully excessive amount of negatives in there to me. Thoughts?
I bought in at 20 and am currently holding for the long term (up around 75%). Rather than sell and take the short term cap gain, I plan on holding through to 2009 to see how the phenylase program does. By the way the stock should still go up as I believe the Aldurazyme and Naglazyme will continue to grow.
Bottom line is that this stock is a gem.
Good thing I waited until more news to buy in. Stock takes a 50% haircut on Genentech abandoning plans to develop crystallized GH.