Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
Was speaking of Punk, ThinkE, et al including any new ones.
why do you have the idea that they haven't been banging the table all week
they have
Panacos Announces First Cohort Results of Phase 2b Study
Tuesday December 19, 4:02 pm ET
Company to Hold a Conference Call at 5:00 p.m. EST Today
whoop mom, wrong formulation
WATERTOWN, Mass.--(BUSINESS WIRE)--Panacos Pharmaceuticals, Inc. (Nasdaq:PANC - News), a biotechnology company dedicated to developing the next generation of antiviral therapeutic products, today announced preliminary results from the first cohort of a Phase 2b study of bevirimat (PA-457) in patients failing HIV therapy due to drug resistance. The data confirm the clinical antiviral activity of bevirimat shown in previous studies; however, the bevirimat plasma concentrations were lower than anticipated, suggesting that the tablet formulation used for this study did not deliver the drug as expected.
ADVERTISEMENT
After 14 days of dosing with 400 mg of bevirimat tablets administered on top of patients' failing background regimens, an antiviral effect was seen in the bevirimat treatment group. Two out of twelve patients with multiple-drug-resistant HIV who received bevirimat achieved an undetectable level of virus. These two patients and one other individual had a viral load reduction of greater than 1 log10. However, the overall antiviral response in this first cohort was less than expected, in line with the patients' lower than anticipated bevirimat plasma concentrations. A previous bioavailability study had predicted that the plasma concentrations, and therefore the antiviral response, of the 400 mg tablet dose would be comparable to the highest (200 mg) dose of the oral solution used in the Phase 2a study. Instead, both the plasma concentrations and the antiviral response observed in the 400 mg tablet cohort were similar to the 100 mg Phase 2a oral solution dose. The data suggest that the lower plasma concentrations of drug resulted from the properties of the 50 mg tablet, a prototype designed specifically for use in the Phase 2b trial. Panacos has been working for some time on new tablet formulations for late-stage development and commercialization. Preliminary analysis of the safety profile of bevirimat in the first cohort indicated that bevirimat was generally safe and well tolerated.
Graham Allaway, Panacos' President and COO said, "While this first cohort did not produce the bevirimat levels we had hoped for, we were encouraged that some patients exhibited a very good antiviral response. Overall, the data are consistent with the relationship between plasma concentrations and response that we have seen previously, and we believe the results support going to higher doses, potentially with alternative formulations, with the aim of generating greater responses. We are submitting a proposal to the FDA designed to continue bevirimat dose escalation in Phase 2b as soon as possible while we continue to develop an optimized formulation of bevirimat for commercialization."
First Cohort Results
The initial Phase 2b bevirimat tablet dose of 400 mg was chosen based on an earlier clinical bioavailability study indicating that the tablet had approximately 60% of the oral bioavailability of an oral solution formulation. As a result, this 400 mg tablet dose was expected to be comparable to a 200 mg oral solution dose, which in a 10 day bevirimat Phase 2a monotherapy study had generated a median 1 log10 viral load reduction. However, analysis of bevirimat plasma levels in this Phase 2b study found that these levels were about half what was expected and closer to levels that were seen in patients using 100 mg of oral solution in the earlier Phase 2a study.
Consistent with these lower drug plasma concentrations, the antiviral responses seen in the 400 mg tablet cohort of the Phase 2b study were also lower than expected. At day 15, the mean viral load reduction was 0.36 log10 in bevirimat-treated patients compared to 0.02 log10 reduction in placebo-treated patients. A total of three patients on bevirimat had greater than 1 log10 reduction in viral load and continued on to the extended dosing portion of the study, including two who achieved an undetectable level of virus (less than 400 viral copies/ml). One additional patient who had a viral load change of just under 1 log10 on day 15 was continued on therapy by special investigator request.
During the initial 15 day dosing period, there were no reports of drug-related serious adverse events or withdrawals due to adverse events. One patient on bevirimat withdrew after 12 days for reasons not related to the drug. A day 15 viral load sample was obtained from that patient and the patient was not replaced. These data continue to confirm the good safety and tolerability profile of bevirimat found in previous studies.
Given the similar bevirimat plasma concentrations seen in the Phase 2b 400 mg tablet cohort and the 100 mg oral solution cohort in the Phase 2a study, the viral load changes in the two studies were compared. The mean viral load changes on day 11, the appropriate comparator time point, were -0.39 log10 and -0.37 log10 in the current study and the Phase 2a 100mg cohort respectively. In the current study, four of the twelve patients (33%) had a greater than 0.5 log10 reduction in viral load on day 11, and three of these had a greater than a 1 log10 reduction. In the 100 mg liquid dose cohort of the prior Phase 2a study, three of six (50%) had greater than a 0.5 log10 viral load reduction, and no patients had greater than a 1 log10 reduction.
About the Phase 2b Bevirimat Study
only because I am nice
Susquehanna International Group, LLP (SIG)
And Biotechnology Analyst Jason Kolbert
Invite you to a Conference Call at 10:00am (ET) Today!
Please join us for a review of this morning’s release of VX-950 PROVE-1 data with
S. Chris Pappas, MD, JD
Access Number: 866-306-3230
Access Code: 458744
Please join us for a review of the VX-950 PROVE-1 data with
Dr. S. Chris Pappas, Visiting Professor of Medicine, University of Texas Medical School, Houston, and Clinical Research Regulatory Compliance Officer at the University of Texas Health Sciences Center. From 1998 to 2002, Dr. Pappas was the International Medical Director for Pegasys at Hoffmann-La Roche and oversaw the medical launch of Pegasys for hepatitis C.
Here’s the NUVO terse PR for archival purposes.
I feel bad for NUVO’s CEO, Ted Love, who seems
like a nice guy. He was close to crying on the CC
don't feel so bad, he wasn't crying because of the patients that won't get the benefit. he was crying because he saw his option values evaporate
desmoteplase is vs. placebo
I don't think they give TPA often passed the 3 hour time window, it causes hemorrhages
Bioenvision Announces Latest Data on Evoltra(R) in Pediatric and Adult Leukemias
Sunday December 10, 1:44 pm ET
Data Presented at the 48th Annual Meeting of the American Society of Hematology
ORLANDO, Fla.--(BUSINESS WIRE)--Bioenvision, Inc. (NasdaqGM:BIVN) announced the latest results from clinical studies of clofarabine (Evoltra®) were presented in seven posters today at the 48th Annual Meeting of the American Society of Hematology (ASH) in Orlando, Florida. The posters featured data on the efficacy and safety of clofarabine in Acute Lymphoblastic Leukemia (ALL), Acute Myeloid Leukemia (AML) and Myelodysplastic Syndrome (MDS). Of the data presented, Bioenvision's data included:
A pooled analysis of three studies, BIOV-121, UWCM-0001 and AML-14, showed a 46% complete response rate (CR/CRi) in elderly AML patients with adverse cytogenetics who were unsuitable for standard intensive treatment. The current standard of care low dose Ara-C (LDAC) had a 0% complete response rate. The one-year survival rate for Evoltra was 21%, compared with 0% for LDAC. (Abstract 1985; Poster 163)
A dose-ranging study assessing the combination of Evoltra® and daunorubicin showed an overall response rate of 65%. In the 20mg cohort the response rate was 100%. The overall survival at 1 year for the full cohort of 37 patients was 62%. The combination of clofarabine 20mg/m2 plus daunorubacin 50mg/m2 was well tolerated with acceptable toxicity. This combination has been chosen for the NCRI Phase III AML-16 Intensive Study which is now enrolling patients. (Abstract 1950; Poster 128)
The latest update from study BIOV-111 showed a complete response rate (CR + CRp) of 31% in heavily pre-treated pediatric patients with relapsed/refractory ALL. These data confirm the results of the pivotal US CLO-212* study and further establish Evoltra® as the standard of care for pediatric patients with relapsed/refractory ALL . (Abstract 1859; Poster 37)
"We are very encouraged about the potential these new data show for Evoltra® to be used alone or in combination with other therapies to treat acute leukemia in children and adults," said Professor Christopher Wood, M.D., Chief Executive Officer and Chairman, Bioenvision. "Based on these results, we are moving ahead with new clinical studies of Evoltra® in other disease areas, such as MDS, chronic leukemias and solid tumors."
"Evoltra® provides elderly patients with AML who are unsuitable for intensive chemotherapy a much higher response rate and a real survival advantage, especially in those patients with additional poor prognostic factors," said Hugh Griffith, Chief Operating Officer, Bioenvision. "These data, along with data to be presented tomorrow, will form the basis for our marketing authorization application to the European Medicines Agency (EMeA) for a label extension of Evoltra® for adults with AML who are unsuitable for intensive chemotherapy."
On Monday at 2:30 p.m., data from Bioenvision's pivotal Phase II trial of Evoltra® in adult AML will be featured in an oral presentation entitled "A Phase II Study (BIOV-121) of Clofarabine Monotherapy First Line in Patients Aged 65 Years or Older with Acute Myeloid Leukemia for Whom Standard Intensive Chemotherapy Is Not Considered Suitable." Alan Burnett, M.D., Chairman of the UK National Cancer Research Institute (NCRI) Hematological Oncology Study Group, will present these data in Hall F5.
Investor Conference Call and Meeting at ASH
In conjunction with the release of the data at ASH, Bioenvision will host an investor meeting, conference call and webcast on Monday, December 11, 2006 at 7:15 p.m. ET.
Conference Call Information:
Date: 12/11/06
Time: 7:15 p.m. ET
Toll free: 866-585-6398
International: 416-849-9626
Web cast: www.bioenvision.com
A replay of the call and web cast will be available for 14 days.
Replay number toll free: 866-245-6755
Replay number international: 416-915-1035
Replay passcode: 780114
Web cast replay: www.bioenvision.com
About Evoltra® (clofarabine)
have you looked at conjuchem's recent data?
it has 230 million share outstanding and has another 100 million warrants with a strike priceo of a dollar.
so if you look at it as 330 million share outstanding with currently 70 million in the bank and 100 million to come in with the warrants their once a week injection appears to be at least as good as the amlyn lar.
I would say about 2 billion of amlyn's market cap is because of the lar.
conjuchem's delivery process can also be used to extend other biologics
paion's trial is in stroke patients passed the 3 hour window.
the other drugs would cause bleeding so I don't understand your question
How do you go about enrolling stroke patients when you have to give the drug 3 hours after they have had a stroke?
You have them take the bar exam. If they can pass that they are able to take the drug. That is part of the Democratic party agenda to make sure the pharma companies aren't taking advantage of sick people
ChemGenex Investigators Report Activity of Ceflatonin(R) and Gleevec(R) Combination Therapy in CML Patients Resistant to Gleevec(R) Alone
Sunday December 10, 8:30 am ET
Positive Phase 2 Data Presented at American Society of Hematology Meeting
I think this is pretty good data considering that the patients enrolled in the trial had failed gleevec, sprycell and
novartis's follow on drug Tasigna
MELBOURNE, Australia, & MENLO PARK, Calif.--(BUSINESS WIRE)--ChemGenex Pharmaceuticals (ASX: CXS, NASDAQ: CXSP) announced today the presentation of new phase 2 clinical data supporting the use of Ceflatonin® (homoharringtonine or HHT) in combination with imatinib mesylate (Gleevec®) to treat chronic myeloid leukemia (CML) patients who have developed resistance to Gleevec® and other tyrosine kinase inhibitors.
ADVERTISEMENT
The study was undertaken by Dr Jorge Cortes, Dr Hagop Kantarjian and colleagues from the M.D. Anderson Cancer Center in Houston, Texas and data were presented in a poster at the American Society of Hematology (ASH) Annual Meeting held over the weekend at Orlando, Florida. The presentation described the effects of the Ceflatonin® and Gleevec® combination therapy on CML patients who were either refractory or resistant to prior Gleevec® therapy. Twelve patients were treated: two in chronic phase, four in accelerated phase and six in blast phase. Following treatment with the drug combination, five (42%) patients achieved a hematologic response (reduction of leukemic cells in the blood), consisting of three complete hematologic responses (CHR) and two hematologic improvements. Two of the three patients showing a CHR also achieved complete cytogenic responses (no Ph+ leukemic cells in the blood).
The patients treated in this study had failed a median of three prior therapies, including the tyrosine kinase inhibitors Gleevec® (nine patients), dasatinib (Sprycel®) (five patients) and nilotinib (Tasigna®) (three patients). Mutations in the Bcr-Abl kinase domain were identified in four (33%) patients, including one patient with the T315I mutation known to be associated with resistance to tyrosine kinase inhibitors. The most common grade 3 or 4 side effects were neutropenia (10 patients, 82%), anemia (10 patients, 82%) and thrombocytopenia (9 patients, 75%). Seven of the 12 patients, including the three patients in CHR, remain on the combination therapy.
The authors concluded that the combination therapy of Ceflatonin® and Gleevec® "is well tolerated and has clinical activity in patients in CML in all phases, including in some who have failed prior therapy with imatinib mesylate and other tyrosine kinase inhibitors".
"These results are a strong confirmation of the potential role for Ceflatonin® to improve the outlook for the increasing number of CML patients who develop resistance to tyrosine kinase inhibitor therapies," said Greg Collier, Ph.D., ChemGenex's Managing Director and Chief Executive Officer. "Realizing the potential opportunities for long-term combination therapy is complementary to our first priority - seeking approval for Ceflatonin® as a single agent therapeutic for CML patients who have the T315I Bcr-Abl point mutation."
Dr. Collier noted that ChemGenex is currently treating patients in a registration-directed phase 2/3 clinical trial of Ceflatonin® as a single agent, with the goal of completing enrollment in that trial by H2 2007. ChemGenex is also working with Dr Cortes and Dr Kantarjian to complete the ongoing phase 2 Ceflatonin® and Gleevec® combination therapy trial.
Ceflatonin® is a registered trade-mark of ChemGenex Pharmaceuticals Limited.
Gleevec® is a registered trade-mark of Novartis AG.
Sprycel® is a registered trade-mark of the Bristol-Myers Squibb Company.
Tasigna® is a registered trade-mark of Novartis AG.
About Ceflatonin®
Ceflatonin® (homoharringtonine or HHT) is a potent inducer of apoptosis (programmed cell death) in myeloid cells and inhibits angiogenesis (blood vessel formation). In phase 2 studies, Ceflatonin® demonstrated clinical activity in patients with CML, both as a single agent and in combination with other chemotherapeutic drugs. ChemGenex is developing Ceflatonin® for the treatment of CML, myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML).
Ceflatonin has a different mechanism of action than tyrosine kinase inhibitors (TKIs), which are widely used in the treatment of CML. A registration-directed, international phase 2/3 clinical study is currently in progress, investigating the effectiveness of Ceflatonin® in the treatment of CML patients who have developed resistance to TKI therapy due to the T315I Bcr-Abl point mutation. Ceflatonin® was recently granted Fast Track status by the U.S. Food and Drug Administration (FDA) for this clinical indication. Additional studies will assess the activity of Ceflatonin® in CML patients who are refractory to, or intolerant of treatment with TKIs and investigate if combination therapy with Ceflatonin®, TKIs and other agents increases the cytogenetic and molecular response rates in CML patients.
Ceflatonin® is not approved by the FDA as a treatment in any indication and is being evaluated in clinical trials for efficacy and safety for future regulatory applications.
About ChemGenex Pharmaceuticals Limited (www.chemgenex.com)
ChemGenex Pharmaceuticals is a pharmaceutical development company dedicated to improving the lives of patients by developing therapeutics in the areas of oncology, diabetes, obesity, and depression. ChemGenex harnesses the power of genomics for target discovery and validation, and in clinical trials to develop more individualized therapeutic outcomes. ChemGenex's lead compound, Ceflatonin®, is currently in phase 2/3 clinical trials for chronic myeloid leukemia and Quinamed® is in phase 2 clinical development for prostate, breast and ovarian cancers. The company has a significant portfolio of anti-cancer, diabetes, obesity and depression programs, several of which have been partnered with international pharmaceutical companies. ChemGenex currently trades on the Australian Stock Exchange under the symbol "CXS" and on NASDAQ under the symbol "CXSP".
PAION announces last patient randomized in Phase III ischemic strokestudy (DIAS-2) with Desmoteplase
If it didn't have the clinical hold for 2 days the stock would now be double what it is trading for.
As people get comfortable that the trial is fully enrolled and the data should be out in 4 to 5 months for a stroke drug that could increase the window of therapy from 3 to 9 hours or more interest should get generated
Dendreon is up 13 out of the last 26 weeks with a net increase of 4%. The biotech index ^BTK is up 14 out of the last 26 weeks with a net increase of 18%.
I am not a fan of DNDN and I have no clue whether the drug will get approved but the comment you made above is an axample of a situation where you can alway use statistics to prove a point.
The BTK has outperformed the Nasdaq Biotech Index which would be a better comp to dendreon. In that case the dendreon performance is probably similar to the NBIO.
Although the point is moot. If the drug gets approved the stock will go up, if it doesn't it will go down.
Acorda was trading at 2 and heading down before they released the MS data and MDV was at about 4 dollars before they release the Russian Alzheimer data. Anyone looking at the stock price wouldn't have been close to getting trial success right.
US based and i take an interest in bios wherever they are.
i wouldn't touch china, but those have done well
The letter to shareholder speaks about infectious disease and collaborations Bill Radvak as also mentioned alliances in his webcasts.
since they were already dealing with 3m on staph it didn't take much of a leap
why Response didn't go up more.
A fund that has been getting redemptions needed cash and sold this morning as it was going up, but there was a block for 3 million shares. They must have cleaned him out.
There is more good news comming the stock will be fine. You can't always get a double in a day/.
response bio
I believe it has more to do with the 3m collaboration, although NT bnp will be in the news also.
Response has the best bnp test but it will take a while for the market to recognize it. Nanogen is making noise in their p/r's but the test doesn't compare
Sciences and Medicine A Catastrophe For Pfizer
Matthew Herper 12.02.06, 9:55 PM ET
why would you want to own pfizer when in three years or so they lose over 10 billion in sales and aquisitions they make to make up for the lose in sales will probably be dilutive.
Funny how they had the dsmb meet two days after an analyst day. Strange or deliberate timing, you pick.
New York - Pfizer (nyse: PFE - news - people ) has shelved its most promising experimental drug because the medicine increased the risk of death in a giant clinical trial, a disaster for the world's largest drug company.
The medicine, torcetrapib, was designed to prevent heart attacks and strokes by raising the so-called "good cholesterol," HDL. Just last week, chief executive Jeffrey Kindler said the drug might be "one of the most important developments in our generation."
Pfizer had poured $800 million into studies to test torcetrapib, more than has been spent on tests for any other drug. Its hope: that the drug could repeat the success of Lipitor, the drug giant's crown jewel and the best-selling pill in the world, with annual sales of $12 billion. If torcetrapib had worked, Pfizer executives had said it could be as big as Lipitor.
But Pfizer said in a press release Saturday night that it had to stop a 15,000-patient study meant to show that torcetrapib saves lives and prevents heart attacks three years early. An independent committee monitoring the study found patients who received the drug were more likely to die or have a cardiovascular event than those who did not. That dashes any hopes that the medicine will make it to market.
In a prepared statement, Kindler said that the news is "both surprising and disappointing," but that Pfizer's focus was on the best interests of patients, so it is ceasing development of the drug. "With regard to our business," Kindler added, "we understand the challenge that this represents, and we will respond quickly and aggressively to it. It is important to put this information in the context of both our commitment to transform Pfizer and our overall product and financial strength."
For Pfizer, the news is bleak, as no other experimental drug is likely to replace torcetrapib's sales potential on its own. Torcetrapib's failure is also a huge disappointment for doctors who hoped the pill would reduce the 900,000 heart attacks and strokes that are caused every year by clogged arteries. Existing cholesterol-lowering pills like Lipitor and AstraZeneca's (nyse: AZN - news - people ) Crestor reduce the risk of heart attack by at least a third. Blood pressure pills also have a big effect, but heart disease remains the leading cause of death.
"It's sad news," says Steven Nissen, chairman of cardiology at the Cleveland Clinic and one of the researchers who has been studying the drug. "I had great hopes for this for patients." He says that Pfizer deserves credit for putting so much money into an untried method of preventing heart attacks.
The news is likely to lead to rough times at Pfizer. Lipitor could see its sales almost entirely eroded by cheap generic knockoffs when a key patent expires four years from now. Torcetrapib was Pfizer's best chance of dulling that blow. Already, Pfizer's sales are flat because of generic competition for products like antibiotic Zithromax and nerve-pain drug Neurontin. The company expects to grow earning by reducing costs. Last week, Pfizer raised earnings forecasts slightly but also announced it would lay off more than 2,000 salespeople, a fifth of its marketing force.
Pfizer, which has an annual research budget of $7 billion, has many other irons in the fire. At a research meeting last week, it outlined 30 research programs, of which torcetrapib was only one. The company is developing promising drugs against obesity, cancer, HIV and Alzheimer's. Pfizer may prosper because of these medicines, but the loss of torcetrapib is still going to sting.
Torcetrapib's failure may also lead to doubts about similar medicines being developed by Pfizer's rivals. Roche is a few years behind Pfizer with a torcetrapib-like pill, and Merck (nyse: MRK - news - people ) is thought to be developing one as well. Pfizer has several other similar drugs in the early stages of human tests.
It is not clear why torcetrapib didn't work. Doubts have swirled around the medicine because the drug raises blood pressure, a side effect that can itself cause heart attacks. Scientists have also speculated that the kind of HDL "good cholesterol" made by a drug like torcetrapib might be dysfunctional. Roche and Merck's entrants are not thought to raise blood pressure, but they raise HDL in exactly the same way as torcetrapib.
Even if all those drugs fail, other methods of raising HDL might prove effective. Merck is working on a drug that counteracts a major side effect of Niacin, an HDL-raiser that is already on the market. Kos Pharmaceuticals sells a prescription version of Niacin. Pfizer, Novartis (nyse: NVS - news - people ) and others are working on synthetic HDL that can be injected or even swallowed. Pfizer was out ahead of all of these potential treatments. Now it has fallen far behind.
"There was always concern with the increase in blood pressure and not knowing what type of HDL was made," says Prediman K. Shah, a cholesterol expert at Cedars Sinai Medical Center. "There was always a cloud hanging over torcetrapib."
Targeted Genetics. Anyone know why the price spiked and more unexpectedly with no news, the price held
Chemotherapy Can Be More Toxic To Brain Cells Than To Cancer Cells And May Cause Brain Damage
It has always been known that the chemo agents cause neurotoxicity but I don't think it is any where as huge as the article states, mainly because of the blood brain barrier. The chemo agents aren't getting passed the BBB whereas in the study they were bombarding the neural cells in a dish.
link to Medicure analyst date
http://phx.corporate-ir.net/phoenix.zhtml?c=108925&p=irol-EventDetails&EventId=1411105
Found this on stockhouse conjuchem board regarding Byetta LAR
-----------------------------------------------------
I dont know if I read this correctly, but Amylin may be striving with a needle issue, though they say there are various ways to deal with the problem. When asked whether changing the formula would require more PK data, which means delays, the COO practically says "yes but I dont want to talk about it". At least for the patients this should be an interesting story to follow... Remember that Amylin LAR works by using human made micro sphere of various sizes that determine the release of the product after injection, quite a complex technology imo:
May 2006 conference:
UNIDENTIFIED SPEAKER: Are there any milestones that you can offer us to help us understand where you are on that manufacture scale process or are we going to need to wait till second half 2008 when you say either hey guys we made it or we didn't?
DAN BRADBURY: I think we will probably give guidance along the way as we achieve scale up. One of the things that we're looking at here is with the clinical study that we've just started to use material that has been scaled up in the extension of that study so that we can generate clinical data using material that's been done at a higher scale. I guess if we go forward with the extension you'll know that we're doing it at a higher scale.
UNIDENTIFIED SPEAKER: And that goes to the next question, do you think you'll need to do bridging studies to show comparable pharmacokinetics or is that extension study going to be adequate?
DAN BRADBURY: So, one of the things that we do need to do is agree with the FDA exactly what is the CMC, chemistry manufacturing control strategy, going forward. And that will include the agreement on the exact details as to what would be required with regards to demonstrating comparability. Comparability can be demonstrated both using in vitro testing as well as in vivo. I think we will have to do some clinical work, although I think the vast majority of it would be in vitro testing. That's all to do with development and specification around the product.
UNIDENTIFIED AUDIENCE PARTICIPANT: A follow-up to that last question. On your conference call, the Eli Lilly earnings call, the gentlemen who was speaking on behalf of LAR made the statement that they would have to do a study, the clinical work with LAR being done, was in small batches. That once this validation batches were produced and up to scale, they would have to do another study. I ask him--.
DAN BRADBURY: Yes --.
UNIDENTIFIED AUDIENCE PARTICIPANT: Hold on let me finish. I asked him, I said, "This is basically a bridging study?" He said, "No, we don't call it a bridging study." I said, "What do you want to call it?" He said, "He said, "Ask Amylin." What exactly is he referring to, and the second question I asked him was, "When will you do this study? When the validation batches are finished or when? When the plant has been put up, when you start manufacturing? When will that study be done? In 2008? [Let me] ask Amylin."
DAN BRADBURY: Yes. Okay. [You can say, "ask Amylin." Just to say that it all comes down to agreeing with the agency exactly what the requirements would be. I think it's pretty clear, firstly some confuse validation batches here with what we need to do for comparability. You do the comparability work way before you do validation.
Validation batches, validation is really just being able to show that you can manufacture consistently at the scale that you intend to sell the product. That's a different thing altogether. Comparability is part of the development program, so that would be done in parallel with the work that we'd be doing to scale up the commercial process. And what we're talking about there is really a PK study.
UNIDENTIFIED SPEAKER: Okay. One of the questions that people bring up a lot is with the [bead] technology from Alkermes, what type of ingestion sites reactions should we assume will occur with this drug and how big will the needle need to be?
DAN BRADBURY: To answer that question exactly in terms of injection site reactions, that actually hasn't been a major concern in the clinical studies to date. Obviously you have some level because any injection you have some level at injection sites --.
UNIDENTIFIED SPEAKER: Is it worse than BYETTA?
DAN BRADBURY: At this point it's certainly not clear to us that there is any major challenge with regards to injection site reactions. In fact, remember, one of the key aspects of this product is that you only give it once a week, so it's very different from BYETTA which you're giving twice a day. So 14 versus one injection a week is very different context to look at.
With regards to the needle size, certainly we're continuing to refine that. We haven't given out details of the final product specification because we've continued to work on that and at this point I can't comment on what size the final product will be.
UNIDENTIFIED SPEAKER: But theoretically I doubt it can get a down an insulin needle. Theoretically, how small do you think you can get the needle?
DAN BRADBURY: I'd prefer to leave that at this point because there are things that we're looking at that can change how that needle looks and just to say that there's a lot of work continuing to go on there.
...
UNIDENTIFIED AUDIENCE PARTICIPANT: In order to change the needle size to make it as small as possible do you have to change the product at all for LAR?
DAN BRADBURY: So, clearly, part of the determination of the needle size is the size of the [micro sphere] and because that's what we're injecting through. But also, it's the volume of injection, how diluted the product is. So those things are being looked at and actually whether or not you need to change any aspects of the product, I really don't think I can comment at this point in time.
UNIDENTIFIED AUDIENCE PARTICIPANT: But wouldn't you know if you just take the proxy up now and just try to put -- isn't it just kind of physics? Could you just put it through a smaller needle and see if it works or does it not work that way?
DAN BRADBURY: Yes, you can do that and there are other things you can do, as well. I'd just say that there are other things that we're looking at, as well, that we'll perhaps potentially change what the profile of the product looks like.
UNIDENTIFIED SPEAKER: And if you did change the market share what portions of your clinical development plan would you need to redo?
DAN BRADBURY: You'd have to show comparability in terms of the PK question that the gentlemen asked earlier.
...
So I would say that the market is extremely large. The opportunity for improving outcomes for patients is significant. And the good news about having other companies, major companies coming in, and talking in the marketplace about a product is that it helps drive physician awareness of the need to drive to goal and that in most cases, in fact in almost all pharmaceutical markets, you look at it, it actually increases market opportunity.
-----
NewsBlast Sign-Up
StockHouse NewsBlast: Receive company sponsored news and information via email.
Cancer Clues from Pet Dogs
http://www.sciam.com/print_version.cfm?articleID=C9F7F979-E7F2-99DF-3D97694D2A702FED
Studies of pet dogs with cancer can offer unique help in the fight against human malignancies while also improving care for man's best friend
By David J. Waters and Kathleen Wildasin
Imagine a 60-year-old man recuperating at home after prostate cancer surgery, drawing comfort from the aged golden retriever beside him. This man might know that a few years ago the director of the National Cancer Institute issued a challenge to cancer researchers, urging them to find ways to "eliminate the suffering and death caused by cancer by 2015." What he probably does not realize, though, is that the pet at his side could be an important player in that effort.
Reaching the ambitious Cancer 2015 goal will require the application of everything in investigators' tool kits, including an openness to new ideas. Despite an unprecedented surge in researchers' understanding of what cancer cells can do, the translation of this knowledge into saving lives has been unacceptably slow. Investigators have discovered many drugs that cure artificially induced cancers in rodents, but when the substances move into human trials, they usually have rough sledding. The rodent models called on to mimic human cancers are just not measuring up. If we are going to beat cancer, we need a new path to progress.
Now consider these facts. More than a third of American households include dogs, and scientists estimate that some four million of these animals will be diagnosed with cancer this year. Pet dogs and humans are the only two species that naturally develop lethal prostate cancers. The type of breast cancer that affects pet dogs spreads preferentially to bones--just as it does in women. And the most frequent bone cancer of pet dogs, osteosarcoma, is the same cancer that strikes teenagers.
Researchers in the emerging field of comparative oncology believe such similarities offer a novel approach for combating the cancer problem. These investigators compare naturally occurring cancers in animals and people--exploring their striking resemblances as well as their notable differences.
Right now comparative oncologists are enlisting pet dogs to tackle the very obstacles that stand in the way of achieving the Cancer 2015 goal. Among the issues on their minds are finding better treatments, deciding which doses of medicines will work best, identifying environmental factors that trigger cancer development, understanding why some individuals are resistant to malignancies and figuring out how to prevent cancer. As the Cancer 2015 clock keeps ticking, comparative oncologists ask, Why not transform the cancer toll in pet dogs from something that is only a sorrow today into a national resource, both for helping other pets and for aiding people?
Why Rover?
For decades, scientists have tested the toxicity of new cancer agents on laboratory beagles before studying the compounds in humans. Comparative oncologists have good reason to think that pet dogs with naturally occurring cancers can likewise become good models for testing the antitumor punch delivered by promising treatments.
One reason has to do with the way human trials are conducted. Because of the need to ensure that the potential benefits of an experimental therapy outweigh the risks, researchers end up evaluating drugs with the deck stacked against success; they attempt to thrash bulky, advanced cancers that have failed previous treatment with other agents. In contrast, comparative oncologists can test new treatment ideas against early-stage cancers--delivering the drugs just as they would ultimately be used in people. When experimental drugs prove helpful in pets, researchers gain a leg up on knowing which therapies are most likely to aid human patients. So comparative oncologists are optimistic that their findings in dogs will be more predictive than rodent studies have been and will help expeditiously identify those agents that should (and should not) be tested in large-scale human trials.
--------------------------------------------------------------------------------
If we are going to beat cancer, we need a new path to progress.
--------------------------------------------------------------------------------
Pet dogs can reveal much about human cancers in part because of the animals' tendency to become afflicted with the same types of malignancies that affect people. Examples abound. The most frequently diagnosed form of lymphoma affecting dogs mimics the medium- and high-grade B cell non-Hodgkin's lymphomas in people. Osteosarcoma, the most common bone cancer of large- and giant-breed dogs, closely resembles the osteosarcoma in teenagers in its skeletal location and aggressiveness. Under a microscope, cancer cells from a teenager with osteosarcoma are indistinguishable from a golden retriever's bone cancer cells. Bladder cancer, melanoma and mouth cancer are other examples plaguing both dog and master. In a different kind of similarity, female dogs spayed before puberty are less prone to breast cancer than are their nonspayed counterparts, much as women who have their ovaries removed, who begin to menstruate late or who go into menopause early have a reduced risk for breast cancer.
ADVERTISEMENT
Canine cancers also mimic those of humans in another attribute--metastasis, the often life-threatening spread of cancer cells to distant sites throughout the body. Solving the mystery of how tumor cells metastasize to particular organs is a top research priority. When certain types of cancers spread to distant organs, they tend to go preferentially to some tissues over others, for reasons that are not entirely clear. Because metastasis is what accounts for most deaths from cancer, researchers would very much like to gain a better understanding of its controls. Studies in pet dogs with prostate or breast cancer might prove particularly useful in this effort, because such tumors frequently spread in dogs as they do in humans--to the skeleton. Indeed, research in pet dogs is already attempting to work out the interactions between tumor cells and bone that make the skeleton such a favorite site for colonization.
Scientists also have deeper theoretical grounds for thinking that pet dogs are reasonable models for human cancer. Evolutionary biologists note that dogs and humans are built like Indy race cars, with successful reproduction as the finish line. We are designed to win the race, but afterward it does not matter how rapidly we fall apart. This design makes us ill equipped to resist or repair the genetic damage that accumulates in our bodies. Eventually this damage can derange cells enough to result in cancer. In the distant past, our human ancestors did not routinely live long enough to become afflicted with age-related cancers. But modern sanitation and medicine have rendered both longevity and cancer in old age common. Much the same is true for our pets. Pet dogs, whom we carefully protect from predation and disease, live longer than their wild ancestors did and so become prone to cancer in their later years. Thus, when it comes to a high lifetime risk for cancer, pets and people are very much in the same boat.
Aside from acquiring cancers that resemble those in people, pet dogs are valuable informants for other reasons. Compared with humans, they have compressed life spans, so scientists can more quickly determine whether a new prevention strategy or therapy has a good chance of improving human survival rates. Finally, although veterinarians today are far better equipped to treat cancer than they used to be, the standard treatments for many canine tumors remain ineffective. Because most pet cancer diagnoses end in death, dog owners are often eager to enroll their animals in clinical trials that could save their pet's life--and possibly provide the necessary evidence to move a promising therapy to human clinical trials.
Advancing Cancer Therapy
Various cancer treatment studies featuring pet dogs have now been carried out or begun. Some of the earliest work focused on saving the limbs of teenagers with bone cancer. Twenty-five years ago a diagnosis of osteosarcoma in a youngster meant amputation of the affected limb, ineffective or no chemotherapy (drugs administered into the bloodstream to attack tumors anywhere in the body), and almost certain death. Today limb amputation can be avoided by chiseling out the diseased bone tissue and replacing it with a bone graft and metal implant--a process partially perfected in pet dogs by Stephen Withrow and his colleagues at Colorado State University. Withrow's team pioneered technical advances that reduced the likelihood of complications, such as placing bone cement in the marrow space of the bone graft. The researchers also showed that preoperative chemotherapy delivered directly into an artery could convert an inoperable tumor into an operable one. The group's work is credited with significantly increasing the percentage of teenagers who today can be cured of osteosarcoma.
Although a tumor's local effects are often controllable using surgery or radiation, metastasis is much harder to combat. For that, drug therapy is required. New compounds under development aim to disrupt key cellular events that regulate the survival and proliferation of metastatic tumor deposits as well as their sensitivity to cancer-fighting drugs. One experimental agent, ATN-161, which inhibits the formation of new blood vessels that foster tumor growth and metastasis, is currently being evaluated in large-breed dogs with bone cancers that have spread to the lungs. The ability of ATN-161 to enhance the effects of conventional chemotherapies is also under study. If these trials succeed, they could smooth the way toward clinical trials in humans.
Cancer researchers are also turning their attention to more familiar kinds of pharmaceuticals, including nonsteroidal anti-inflammatory drugs (NSAIDs), the class of compounds that includes ibuprofen. Certain NSAIDs have exhibited significant antitumor activity against a variety of canine tumors. In studies of pet dogs with bladder cancer, for example, the NSAID piroxicam showed such impressive antitumor activity that the drug is now in human clinical trials to see if this treatment can derail the progression of precancerous bladder lesions to life-threatening cancer.
Developing new cancer therapies is not just about finding novel drugs. It is about optimizing drug delivery to the patient. In your vein or up your nose? That is the kind of information scientists testing new agents against lung cancer need to know. If the right amount of drug does not make it to the tumor, then even substances with impressive credentials for killing tumor cells in a petri dish will not stand a chance of working in human patients. Moreover, delivering pharmaceuticals directly to the target--so-called regional therapy--has the added benefit of avoiding the toxicity associated with systemic therapy.
Investigators have used pet dogs to study the intranasal delivery of a cytokine, a small immune system molecule, called interleukin-2 (IL-2) to treat naturally occurring lung cancers. Positive results from these experiments led to feasibility trials of inhaled IL-2 in human patients with lung metastases, further leading to trials with another cytokine, granulocyte colony stimulating factor. Pet dogs can also aid researchers in optimizing the dosing and delivery protocols for drugs that have already made their way into human trials.
Another challenge that pet dogs are helping to overcome is determining the extent of tumor spread, called clinical staging. Accurate staging is critical for devising therapeutic game plans that will maximally benefit the patient while minimizing exposure to harsh treatments that are unlikely to help at a given disease stage. For example, the odds that a teenager will survive osteosarcoma are increased by accurate identification (and subsequent surgical removal) of lung metastases.
Doctors typically determine the presence and extent of such metastases with noninvasive imaging techniques, such as computed tomography (CT). To assess how accurate such scanning is, one of us (Waters), along with investigators from Indiana University School of Medicine, collected CT images of the lungs from pet dogs with metastatic bone cancer and then examined the tissue at autopsy to verify that what was interpreted as a "tumor" on the scan really was a tumor and not a mistake. Results showed that state-of-the-art imaging with CT--the same type used in clinical staging of bone cancer in teenagers--significantly underestimates the number of cancer deposits within the lung. By revealing the limited accuracy of existing and experimental techniques, pet dogs are helping optimize the next generation of technologies for improved cancer detection.
Taking Aim at Cancer Prevention
But cancer researchers are shooting for more than improved detection and better treatment; they also want to prevent the disease. Surprisingly, prevention is a relatively new concept within the cancer research community. What cardiologists have known for a long time--that millions of lives can be saved through the prevention of heart disease--is just now gaining traction in the cancer field. The term "chemoprevention" was coined 30 years ago to refer to the administration of compounds to prevent cancer, but scientists did not gather nationally to debate cutting-edge knowledge of cancer prevention until October 2002.
--------------------------------------------------------------------------------
Comparative oncologists ask, Why not transform the enrmous amount of cancer in pet dogs into a national resource, both for helping other pets and aiding people?
--------------------------------------------------------------------------------
Today the pace is quickening as investigators are examining a diverse armamentarium of potential cancer-protective agents. But finding the proper dose of promising agents has always been challenging. Indeed, failure to do so proved disastrous for some early human trials of preventives. For example, in two large lung cancer prevention trials, people receiving high doses of the antioxidant nutrient beta-carotene had an unexpected increase in lung cancer incidence compared with placebo-treated control subjects.
Can dogs accelerate progress in cancer prevention? Recently canine studies have helped define the dose of an antioxidant--the trace mineral selenium--that minimizes cancer-causing genetic damage within the aging prostate. The message from the dogs: when it comes to taking dietary supplements such as selenium to reduce your cancer risk, more of a good thing is not necessarily better. Elderly dogs given moderate doses ended up with less DNA damage in their prostates than dogs given lower or higher amounts. Comparative oncologists hold that dog studies conducted before large-scale human prevention trials are initiated can streamline the process of finding the most effective dose of cancer preventives and can enable oncologists to lob a well-aimed grenade at the cancer foe.
Pet dogs can assist in preventing human cancers in another way. For years, dogs in the research laboratory have advanced understanding of the acute and long-term effects of high doses of cancer-causing chemicals. But pet dogs, just by going about their daily lives, could serve as sentinels--watchdogs, if you will--to identify substances in our homes and in our backyards that are carcinogenic at lower doses. If something can cause cancer, the disease will show up in pets, with their compressed life spans, well before it will in people.
Take asbestos. Most human cases of mesothelioma (a malignancy of tissues lining the chest and abdomen) stem from asbestos exposure. Symptoms can appear up to 30 years after the incriminating exposure. Investigators have now documented that mesothelioma in pet dogs is also largely related to encountering asbestos, most likely through being near a master who came into contact with it through a hobby or work. But in dogs, the time between exposure and diagnosis is comparatively brief--less than eight years. So the appearance of the cancer in a dog can alert people to look for and remediate any remaining sources of asbestos. Also, closer monitoring of exposed individuals might lead to earlier diagnosis of mesothelioma and render these cancers curable.
Pet dogs could assist in discovering other environmental hazards. Some well-documented geographic "hot spots" show an unusually high incidence of certain cancers. For example, women living in Marin County, California, have the country's highest breast cancer rate. Scientists typically try to identify the factors contributing to cancer in hot spots by comparing the genetics and behavior of people who become afflicted and those who do not. To advance the effort, comparative oncologists are now establishing cancer registries for pet dogs in those areas. If both pets and people living in a particular community experience higher-than-normal cancer rates, the finding would strengthen suspicions that these malignancies are being triggered by something in the environment.
Analyzing tissues of dogs could even potentially speed identification of the specific hazard. Many toxic chemicals, such as pesticides, concentrate themselves in body fat. So it might make sense to collect tissues from dogs during common elective surgical procedures (for example, spaying) or at autopsy. Later, if an unusually high number of people in an area acquire a certain form of cancer, investigators could analyze levels of different chemicals in the samples to see if any are particularly prominent and worth exploring as a contributing factor.
Why Uncle Bill Avoided Cancer
Because cancer in pet dogs is so commonplace, the animals might be able to assist in solving an age-old mystery. Almost everyone has an Uncle Bill who smoked two packs a day and never got lung cancer. So what factors determine cancer resistance? One way to tease out the answer is to find populations resistant to cancer and study them closely--their genetics, their diet and their lifestyle.
Such a population has been found--human centenarians. It turns out that most folks who live to be 100 die of disorders other than cancer. But it is nearly impossible to collect reliable information from a 102-year-old woman on her dietary habits and physical activity when she was a teenager or in her mid-40s. So one of us (Waters) asked a simple question: Is this phenomenon of cancer resistance in the oldest old operational in pet dogs? The answer is yes. Now by interviewing owners of very old pet dogs, comparative oncologists can construct accurate lifetime histories of "centenarian" dogs. Combine this prospect with the ability to collect biological samples (such as blood for genetic analysis and for tests of organ function) from very old dogs as well as from several generations of their offspring, and you have a unique field laboratory for probing the genetic and environmental determinants of cancer resistance.
The puzzle of cancer resistance can also be addressed in another way--by examining differences in cancer susceptibility between dogs and humans. In people, obesity and diets rich in animal fat are known to increase risk for colon cancer. In contrast, colorectal cancer in dogs is uncommon, even though many pet dogs are obese and consume a high-fat diet. Scientists are now contemplating the use of dogs as a "negative model" of colon cancer in the hope of identifying factors able to confer cancer resistance to people whose style of living strongly favors colon cancer development. Knowledge of resistance factors could suggest new interventions for nonresistant individuals.
A Growing Effort
Historically, comparative oncology research has been conducted in university-based hospitals and laboratories where veterinary oncologists are trained. But other organizations have begun to recognize the potential for this kind of research to translate into better care for people, and these institutions are now actively engaged in comparative oncology research.
--------------------------------------------------------------------------------
Pet dogs could serve as sentinels--watchdogs, if you will--to identify substances in our homes and backyards that are carcinogenic.
--------------------------------------------------------------------------------
The Gerald P. Murphy Cancer Foundation began in 2001 to accelerate the discovery of improved methods for preventing and treating prostate and bone cancers affecting both people and pets. The Animal Cancer Foundation in New York City has funded comparative oncology studies and has recently established a repository of biological specimens of diseased and healthy animals as a resource for researchers chasing biological indicators of cancer risk. And in 2003 the National Cancer Institute developed the Comparative Oncology Program, which designs trials involving dogs with naturally occurring cancers and also provides researchers with high-quality, canine-specific reagents needed for in-depth studies of the molecular biology, protein chemistry and genetics of dog tumors.
Moreover, the sequencing of the canine genome is now complete. Discovery that a particular gene is involved in some form of cancer in dogs will enable investigators to determine whether--and how--the same gene operates in human cancers. Scottish terriers with bladder cancer, rottweilers with bone cancer and golden retrievers with lymphoma--each breed can help elucidate the calamitous combinations of genes and environment that lead to cancer.
Of course, there are limitations inherent in the use of animals to mimic human cancer--whether you are talking about rodents, dogs or other species. No single, ideal animal model for cancer exists. The best science is done by asking good questions and then using the research tools most likely to yield meaningful answers. At times, following that rule in cancer research will mean turning to dogs to track down that hard-to-win knowledge.
The intriguing similarities between the cancers of people and pets--once a mere curiosity--are now being systematically applied to transform cancer from killer to survivable nuisance. Comparative oncologists are not inducing cancer in animals but are compassionately treating pet dogs suffering from the same kinds of lethal cancers that develop naturally in both man and man's best friend. They are putting our canine companions on the trail of a killer in ways that can save both pets and people.
© 1996-2006 Scientific American, Inc. All rights reserved.
Reproduction in whole or in part without permission is prohibited.
I sold part of it on the day it went up on pre clinical data but still own a lot
I can't believe it is down here on no bad data. This is what they do to stocks that need money.
somehow arena can keep raising a 100 million at a time with drugs that are very early.
if you have something in phase 3 no one wants the risk.
Things are the opposite of what they should be righ now.
avnr
at this point it probably pays to stay away.
The neurodex trials only have safety data on 460 people or so and the analysts have been blowing up projections that the drug would be used on over a half million people.
do you see the fda approving a drug for a half million people that has only been tested on 450
You seem compare of MC-1's failure with the peak CK-MB greater than or equal to 50ng/ml measure to pexelizumab's failure with the 100ng/ml measure.
MC-1 was very successful with the 100ng/ml.
As you will see in my next post the normal endpoint marker is 100, they made the endpoint in the phase 2 50 thinking that the trial was to small to get significance in the normal endpoint. they were wrong. the drug worked better then they thought it would and the 50ng is not a good endpoint.
The 250 mg dose of MC-1 had a 14.0% reduction in the primary endpoint composite of death, non-fatal myocardial infarction (peak CK-MB greater than or equal to 50ng/ml), and non-fatal stroke versus placebo (p equals 0.312).
Since you follow the space and are aware of the alxn results you also know that the peak ck-mb of 100ng/ml is the most appropriate endpoint and medicure's data shows that it reduces the risk of MI and death when that marker is used.
The phase 2 only had 900 patients and they thought by lowering the endpoint to 50ng/ml they would see more events but it created noise.
but then again I am sure you knew that
Pinchas Cohen
when a doctor with his stature makes presentations on behalf of a company with a crappy product they reduce their prestige in my eyes.
His presentations on behalf of Tercica only masks the significant advantages of iplex over increlex and give crediblilty to Increlex as a product. If he is a Doctor he should know better
Pinchas Cohen
it is amazing that he can be such a proponent of igfbp3 and accept grants from tercica so that he becomes one of their proponents when he makes presentations supporting them. I would consider it dirty money after all Tercica and Genentech never put in any money to develop bp3 and they are trying to kill Insmed's attempts to develop it. I don't get it.
Tercica, Inc. (TRCA) Announces Two Presentations At Pediatric Academic Societies 2005 Annual Meeting
SOUTH SAN FRANCISCO, Calif., May 13 /PRNewswire-FirstCall/ -- Tercica, Inc. announced today that two poster presentations related to the frequency of primary insulin-like growth factor-1 (IGF-1) deficiency (Primary IGFD) and safety of recombinant human IGF-1 (rhIGF-1) therapy in children with short stature will be presented at the Pediatric Academic Societies (PAS) 2005 Annual Meeting. The meeting is being held May 14-17 in Washington, D.C.
Presentations include:
IGF-1 Deficiency with Short Stature, a New Diagnostic Sub-set Separate from ISS? Presented by Dr. Pinchas Cohen, director of pediatric endocrinology at Mattel Children's Hospital at UCLA
Data presented highlight the frequency of IGF-1 deficiency (IGFD) among patients currently classified as idiopathic short stature (ISS) or short stature due to unknown causes, in an observational study of U.S. children referred for growth failure. The presentation will take place as part of PAS on Sunday, May 15 at 8:00 a.m. in room 151.
Absence of Hypoglycemia in Response to Varying Doses of Recombinant Human Insulin-Like Growth Factor-I (rhIGF-I) in Children and Adolescents with Low Serum Concentrations of IGF-I, Presented by Dr. Arlan Rosenbloom of the University of Florida
These preliminary findings will examine the correlation between children with low concentrations of IGF-I and insulin-like growth factor-binding protein 3 (IGFBP3) and their risk for hypoglycemia in response to rhIGF-I administration. The presentation will take place as part of PAS on Sunday, May 15 at 8:00 a.m. in room 151.
"These presentations underscore the important rationale for diagnosis and treatment of Primary IGFD in a significant number of short children with a previously unrecognized disorder," said George Bright, M.D., Vice President and Medical Director of Endocrinology at Tercica.
About IGF-1 and Primary IGFD
IGF-1 is the principal hormone necessary for statural growth. IGF-1 is released in response to stimulation by growth hormone. Primary IGFD, a cause of short stature that is 1.5 times more common than growth hormone deficiency, may be diagnosed in children who have normal or elevated secretion of endogenous growth hormone and whose height and serum IGF-1 levels are more than two standard deviations below normal. A sub-set of these children, whose height and serum IGF-1 levels are more than three standard deviations below normal, may be diagnosed with Severe Primary IGFD.
Primary IGFD can be caused by abnormalities of either the growth hormone receptor or growth hormone signaling pathway. If untreated, Primary IGFD may lead, in children and adults, to a range of other metabolic disorders including lipid abnormalities, decreased bone density, obesity and insulin resistance.
Primary IGFD afflicts an estimated 30,000 children evaluated for short stature in the United States. Approximately 6,000 children suffer from Severe Primary IGFD and could become eligible for Increlex(TM) therapy if approved by the FDA.
About Increlex(TM)
Tercica, Inc., acquired exclusive rights to develop, commercialize and manufacture Increlex from Genentech, Inc. Tercica currently is conducting a broad-scale Phase IIIb clinical study to evaluate the safety and efficacy of Increlex in children with Primary IGFD. These patients will have less severe disease than the patients in Tercica's Phase III studies included in the company's NDA.
medicure analyst day
Why doesn't mc-1 seem like an undervalued asset, in your opinion. The first 30 days after cabg surgery has about a 15 percent risk of heart attack or death.
The phase two trial reduced that risk but 40 percent. There is no approved drug for that indication. It would be at least a 500 million dollar opportunity in the US and about equal that size in Europe. The nearest competitiors are in phase 1 trials.
They only have to get aggrastat to about 30 million by taking share from integrilin and reopro. With a sales force concentrating on docs that haven't been seen for several years that shouldn't be impossible.
Medicure to Host Analyst & Investor Day
Tuesday November 7, 7:00 am ET
http://biz.yahoo.com/iw/061107/0181187.html
If you want a cheap stock that is very undervalued, my opinion anyway, listen to the analyst day webcast.
WINNIPEG, MANITOBA--(MARKET WIRE)--Nov 7, 2006 -- Medicure Inc. (TSX:MPH.TO - News)(AMEX:MCU - News), a cardiovascular focused biopharmaceutical company, today announced it will host an Analyst & Investor Day at 12:00 PM Eastern on Friday, November 17, 2006 in the Metropolitan Suite of the Four Seasons Hotel in New York City. The aim of the presentations is to provide institutional investors and analysts with a clinical and therapeutic update on Medicure's acute cardiovascular products, MC-1 and AGGRASTAT(r). Presentations will be made by the Company's senior management and cardiovascular opinion leaders, including:
- Dr. Paul W. Armstrong, MD ,FRCP©,FACC, Professor of Medicine, Division of Cardiology, Director Canadian VIGOUR Centre, University of Alberta, Chair, Medicure's Scientific Advisory Board
- Christopher B. Granger, MD, Associate Professor of Medicine, Director, Cardiac Care Unit, Co-Director, Cardiovascular Clinical Trials, Duke University Medical Center, Duke Clinical Research Institute
- Harvey D. White, MB, ChB, DSc, Professor of Medicine, University of Auckland, New Zealand, Director, Coronary Care and Cardiovascular Research, Green Lane Hospital & Auckland City Hospital
To register to attend, please contact Hogan Mullally of Medicure at hmullally@medicure.com or Lee Stern of the Trout Group at lstern@troutgroup.com. The presentation will be made available by webcast and can be accessed on the Investor Relations page of the Medicure website at www.medicure.com.
ADVERTISEMENT
About Medicure Inc.
Medicure is a biopharmaceutical company focused on the research, development and commercialization of novel compounds to treat cardiovascular disorders. The Company's solid position in this field is highlighted by the following:
- Two drugs, MC-1 & MC-4232, in late stage clinical development
- Four positive Phase II trials completed with MC-1
- FDA Fast Track designation for MC-1
- U.S. rights to AGGRASTAT® Injection (tirofiban hydrochloride)
- Dual action antithrombotic, MC-45308, with positive preclinical results
Medicure also has a medicinal chemistry based Drug Discovery program focused on discovery and advancement of novel small molecule anti-ischemics and antithrombotics towards human clinical studies.
you are right
vnda
the drug was going to be a blockbuster, it was partnered with novartis and novartis dropped the drug because of qt interval elongations. This was the first time I had ever heard of the problem
That is why it will be a niche drug
I sent this as an answer to randy
Aggrastat is in a class in the twilight stages
Integrilin is doing 400 million a year in sales and Merck is selling 90 million worth of Aggrastat in europe
Medicure paid 17 million for it and if they can get the sales to 30 million by grabbing some share from integrilin and reopro it is a home run for them
Shering-plough is has paid plenty to buy the rights back lately
July 26, 2005 - Investor Frequently Asked Questions (FAQ’s)From time to time, Investor Relations will provide FAQs on various topics of interest to investors. The following is a compilation of FAQ related to the restructured agreement with Millennium Pharmaceuticals whereby Schering-Plough will acquire exclusive U.S. development and commercialization rights for INTEGRILIN. Schering-Plough and Millennium have been co-promoting INTEGRILIN in the U.S. and sharing profits since 2002.QWhy did Schering-Plough enter into a strategic alliance with Millennium? What are the general terms of the deal?AAcquiring exclusive U.S. rights to INTEGRILIN will give Schering-Plough:• A stronger foundation on which to build and expand Schering-Plough’s cardiovascular portfolio, and to increase the company’s long-term importance to customers in this large sector;• More direct control over the management of the U.S. INTEGRILIN franchise, allowing for quicker decision-making and greater efficiencies;• Increased flexibility to optimize sales force effectiveness for INTEGRILIN and other cardiovascular products, and to gain additional product promotion; and• The potential for improved INTEGRILIN profitability over time, with the product under the management of one company rather than two.QWhat are the financial terms of the agreement? AUnder the terms of the agreement, Schering-Plough will pay to Millennium an upfront payment of $35.5 million and royalties over the U.S. lifespan of INTEGRILIN. In 2006 and 2007, minimum royalty payments for each year are set at $85 million, with some extraordinary conditions that could reduce these minimums.In addition, Schering-Plough will buy approximately $45-50 million of existing INTEGRILIN inventories from Millennium. Schering-Plough plans to integrate into its sales force a significant number of Millennium’s 180 member US INTEGRILIN sales personnel.QAre there any upfront payments associated with this collaboration?AUnder the terms of the agreement, Schering-Plough will pay to Millennium an upfront payment of $35.5 million.QWhere will the $35.5 million payment be reflected in Schering-Plough’s financial statements?AThe $35.5 million payment will be recorded as an intangible asset on the balance sheet.
--------------------------------------------------------------------------------
Page 2
Page 2QWhat is the financial impact on Schering-Plough?AIn the near term Schering-Plough expects the overall impact of the new agreement on the Company’s earnings to be relatively neutral, but to offer the potential for improved profitability of INTEGRILIN over time, with the product under one management rather than two.QWhat are the sales of INTEGRILIN?ASchering-Plough reported the following INTEGRILIN sales: 2004: U.S. sales were $301 millionInternational sales were $24 million2005: (YTD June 2005)U.S. sales were $150 millionInternational sales were $8 millionSchering-Plough will continue to record the sales for INTEGRILIN in its territories(which exclude Europe).QHow will this agreement affect Schering-Plough’s operating expenses?ATransferring from profit-sharing in the U.S. to a royalty structure will have substantially offsetting effects – generally, reduced SG&A expenses will be offset by increased COGs expenses. In particular, • Selling, General & Administrative expenses will decrease due to the elimination of profit sharing payments that had been reflected in SG&A. This benefit will be partly reduced by expenses associated with integrating a significant number of employees from Millennium’s 180 member INTEGRILIN U.S. sales force into Schering-Plough.• Cost of goods will increase as a result of the royalty payments to Millennium. In the near term we expect the overall impact of the new agreement on its earnings is expected to be relatively neutral.QWhat is the impact on Schering-Plough’s gross margin?ASchering-Plough’s gross margin will be unfavorably affected by the restructured agreement. Royalty rates are not being disclosed; however, minimum royalty payments in 2006 and 2007 are set at $85 million per year, with some extraordinary conditions that could reduce these minimums.It is expected that these increased royalty payments will be substantially offset bya decreased SG&A expense due to the elimination of profit sharing payments that had been reflected in SG&A.
--------------------------------------------------------------------------------
Page 3
Page 3The information in this FAQ contains certain “forward-looking” statements, including statements relating to the potential strategic benefit and potential financial impact of the agreement and the market potential for INTEGRILIN. Forward-looking statements relate to expectations or forecasts of future events. Many factors could cause actual results to differ materially from Schering- Plough’s forward-looking statements. The extent that the product listed above will be prescribed will be determined by market forces and the market viability of any particular product is subject to substantial risks and uncertainties. In addition, the forward-looking statements may also be affected by general market and economic factors, product availability, current and future branded, generic or over-the-counter competition, federal and state regulations and legislation, the regulatory process, manufacturing issues, trade buying patterns, patent positions and the outcome of litigation and investigations. Schering-Plough does not assume the obligation to update any forward-looking statement. For further details and a discussion of other risks and uncertainties that may affect forward-looking statements, see the company’s Securities and Exchange Commission filings, including the company’s first quarter 2005 10-Q.
Aggrastat is in a class in the twilight stages
Integrilin is doing 400 million a year in sales and Merck is selling 90 million worth of Aggrastat in europe
Medicure paid 17 million for it and if they can get the sales to 30 million by grabbing some share from integrilin and reopro it is a home run for them
Shering-plough is has paid plenty to buy the rights back lately
July 26, 2005 - Investor Frequently Asked Questions (FAQ’s)From time to time, Investor Relations will provide FAQs on various topics of interest to investors. The following is a compilation of FAQ related to the restructured agreement with Millennium Pharmaceuticals whereby Schering-Plough will acquire exclusive U.S. development and commercialization rights for INTEGRILIN. Schering-Plough and Millennium have been co-promoting INTEGRILIN in the U.S. and sharing profits since 2002.QWhy did Schering-Plough enter into a strategic alliance with Millennium? What are the general terms of the deal?AAcquiring exclusive U.S. rights to INTEGRILIN will give Schering-Plough:• A stronger foundation on which to build and expand Schering-Plough’s cardiovascular portfolio, and to increase the company’s long-term importance to customers in this large sector;• More direct control over the management of the U.S. INTEGRILIN franchise, allowing for quicker decision-making and greater efficiencies;• Increased flexibility to optimize sales force effectiveness for INTEGRILIN and other cardiovascular products, and to gain additional product promotion; and• The potential for improved INTEGRILIN profitability over time, with the product under the management of one company rather than two.QWhat are the financial terms of the agreement? AUnder the terms of the agreement, Schering-Plough will pay to Millennium an upfront payment of $35.5 million and royalties over the U.S. lifespan of INTEGRILIN. In 2006 and 2007, minimum royalty payments for each year are set at $85 million, with some extraordinary conditions that could reduce these minimums.In addition, Schering-Plough will buy approximately $45-50 million of existing INTEGRILIN inventories from Millennium. Schering-Plough plans to integrate into its sales force a significant number of Millennium’s 180 member US INTEGRILIN sales personnel.QAre there any upfront payments associated with this collaboration?AUnder the terms of the agreement, Schering-Plough will pay to Millennium an upfront payment of $35.5 million.QWhere will the $35.5 million payment be reflected in Schering-Plough’s financial statements?AThe $35.5 million payment will be recorded as an intangible asset on the balance sheet.
--------------------------------------------------------------------------------
Page 2
Page 2QWhat is the financial impact on Schering-Plough?AIn the near term Schering-Plough expects the overall impact of the new agreement on the Company’s earnings to be relatively neutral, but to offer the potential for improved profitability of INTEGRILIN over time, with the product under one management rather than two.QWhat are the sales of INTEGRILIN?ASchering-Plough reported the following INTEGRILIN sales: 2004: U.S. sales were $301 millionInternational sales were $24 million2005: (YTD June 2005)U.S. sales were $150 millionInternational sales were $8 millionSchering-Plough will continue to record the sales for INTEGRILIN in its territories(which exclude Europe).QHow will this agreement affect Schering-Plough’s operating expenses?ATransferring from profit-sharing in the U.S. to a royalty structure will have substantially offsetting effects – generally, reduced SG&A expenses will be offset by increased COGs expenses. In particular, • Selling, General & Administrative expenses will decrease due to the elimination of profit sharing payments that had been reflected in SG&A. This benefit will be partly reduced by expenses associated with integrating a significant number of employees from Millennium’s 180 member INTEGRILIN U.S. sales force into Schering-Plough.• Cost of goods will increase as a result of the royalty payments to Millennium. In the near term we expect the overall impact of the new agreement on its earnings is expected to be relatively neutral.QWhat is the impact on Schering-Plough’s gross margin?ASchering-Plough’s gross margin will be unfavorably affected by the restructured agreement. Royalty rates are not being disclosed; however, minimum royalty payments in 2006 and 2007 are set at $85 million per year, with some extraordinary conditions that could reduce these minimums.It is expected that these increased royalty payments will be substantially offset bya decreased SG&A expense due to the elimination of profit sharing payments that had been reflected in SG&A.
--------------------------------------------------------------------------------
Page 3
Page 3The information in this FAQ contains certain “forward-looking” statements, including statements relating to the potential strategic benefit and potential financial impact of the agreement and the market potential for INTEGRILIN. Forward-looking statements relate to expectations or forecasts of future events. Many factors could cause actual results to differ materially from Schering- Plough’s forward-looking statements. The extent that the product listed above will be prescribed will be determined by market forces and the market viability of any particular product is subject to substantial risks and uncertainties. In addition, the forward-looking statements may also be affected by general market and economic factors, product availability, current and future branded, generic or over-the-counter competition, federal and state regulations and legislation, the regulatory process, manufacturing issues, trade buying patterns, patent positions and the outcome of litigation and investigations. Schering-Plough does not assume the obligation to update any forward-looking statement. For further details and a discussion of other risks and uncertainties that may affect forward-looking statements, see the company’s Securities and Exchange Commission filings, including the company’s first quarter 2005 10-Q.
You came up with Leerink Swann's analysis of the CEO change at CAMH. Might you know if they wrote anything after CAMH's third quarter earnings? If they did, and you have access to it, I would be most appreciative if you would post it.
Best regards,
Geoff
I knew that you were concerned about the ceo leaving so I wanted to alleviate your concern in that regard, but I can't spend too much time getting snippets about every company mentioned on this site.
I hope you understand
Think equity hcv notes
PANELISTS
Dr. Francis Chisari, M.D. is a Professor in the Department of Molecular and Experimental Medicine and Head of the Division of Experimental Virology at Scripps Research Institute La Jolla, California
Dr. John McHutchison, M.D. is a Professor of Medicine at Duke University and Director of GI/Hepatology Research at the Duke Clinical Research Institute
Dr. Stefan Zeuzem, M.D. is Professor of Internal Medicine and Director of the Department of Internal Medicine, Gastroenterology at Saarland University Hospital, Homburg/Saar, Germany
Initial Comments:
There is a new in vitro system in last year (Toray) that will allow for experimentation and observation of the entire virus life cycle; this will lead to many newer drug candidates.
Both polymerase and protease inhibitors will be key, but entry inhibitors l also be used in cocktail approach.
Although we know the virus lives primarily in hepatocytes, there is a possibility there are residual cells elsewhere in the body and new drugs may systemically target that in an immune stimulatory way (away from INFs)
Lowering viral load early makes sense.
SGP: 007 will have data in 07. They added another arm which caused a delay, and why there was no data at AASLD.
Cocktail approach including immune stimulation (INF or vaccine) will suppress virus efficiently which will reduce stress on autoimmune system. But nothing close to clinic in this area. TLR may be a good substitute for IFN as immune stimulant
PIII design for protease inhibitor:
Dr. McHutchinson: 2 ways to look at patients, naive or pretreated. Strategies vary and depend on potency and safety. Need to compare to standard of care with adequate control arm and show better efficacy if same length of treatment or look at shorter treatment.
Dr Zeuzem: Efficacy drives treatment; What regulators will ask for is unknown. If PII shows much better and shorter, don't know if will have to compare to standard of care are i.e. 48 wks, +24 wks….
Dr. McHutchinson: Accelerated approval system may evolve if you can really change outcomes. Data will drive FDA. Recent FDA hearing on trial designs was schizophrenic with few answers, but its early days…Question from audience: Define 'much better'
Dr. Zeuzem: 10% increase in svr would do it
Dr McHutchinson: as this evolves, expecting multiple arms to be needed
Sub group inclusion in trials?
Difficult to treat groups may be PIV commitments. Drug/drug interaction studies are going to be required in many areas. Need data in advanced liver disease too. Worst and largest group are non-responders, as well as most vocal and well informed group. Do you give monotherapy?
In non responders, where do you begin?
Depends where non-response is coming from. Is virus blocking INF effect? Using a PI or polymerase may re-sensitize to INF. All theory though. Cocktail therapy in this case will work, but patient populations are heterogeneous.
Albuferon
Rapid onset cud be an extra feature in combo with antivirals
Size and uptake of 950
Assuming 90% efficacy will be immediate and get many pts on the bubble of getting treated too. Would be .little reason not to use. More and more pts are elderly and can't tolerate INF and defer treatment.
Will you use all new drugs up front or sequentially.
Substitution of Ribavirin would be great. Using PI and polymerase with INF is right way to go, not keeping one drug in reserve
Paion Research and Development Day
http://www.paion.de/
Friday, November 10, 2006 12:00 p.m. ET
Webcast Presentation Help
Click here to listen with Windows Media
Click here to listen with Real Media
Event Details
Title Paion Research and Development Day
Date and Time Friday, November 10, 2006 12:00 p.m. ET
Duration 4 Hours
Location W NY
Lexington and 49th
New York, NY
Supporting Materials Paion Research and Development Day
Dr. Mariola Söhngen
Dr. Max Wintermark
Dr. Wolfgang Söhngen
Professor Karl-Uwe Petersen, MD
Werner Hacke, BSc, MD, PhD.
Anthony J Furlan MD.
Dr. Howard A. Rowley
response biomedical Unterberg webcast link
http://www.wsw.com/webcast/ceut5/register.aspx?conf=ceut5&page=index&url=http%3A//www.wsw.co...
I don't think there are more than 500 people with the disease
There were 35 patients enrolled in each oral insulin arm of the trial, and 36 in placebo. Results showed that the total number of patients achieving a hemoglobin A1c (HbA1c) decrease of more than 1.1% among the 35 patients dosed at the 10 mg QID dose of oral insulin was statistically significantly higher than in the 36 placebo patients (p=0.0368).
i read this wrong