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Institutional and Mutual Funds now own 63% of CYTK!! You won`t find many .76 cent stocks with that kind of holders. Not to mention 90+ million in cash and NO debt!! http://data.cnbc.com/quotes/CYTK/tab/8
Needham & Company Analysts Begin Coverage on Cytokinetics (CYTK)
Posted by Jeff Wilder on Jul 2nd, 2012 // Read 0 Times // No Comment
Needham & Company started coverage on shares of Cytokinetics (NASDAQ: CYTK) in a research note issued on Monday. The firm set a “buy” rating and a $2.50 price target on the stock.
Separately, analysts at MLV Capital initiated coverage on shares of Cytokinetics in a research note to investors on Thursday, April 12th. They set a “buy” rating and a $4.00 price target on the stock.
Cytokinetics opened at 0.64 on Monday. Cytokinetics has a 52-week low of $0.57 and a 52-week high of $1.45. The company’s market cap is $49.6 million.
Cytokinetics, Incorporated (Cytokinetics) is a biopharmaceutical company focused on the discovery and development of small molecule therapeutics that modulate muscle function for the potential treatment of serious diseases and medical conditions.
http://www.dailypolitical.com/finance/stock-market/needham-company-analysts-begin-coverage-on-cytokinetics-cytk.htm
Yup,I`m in the same bag! They have alot going for them. I will hold! If we get a Positive update on this Study to Evaluate the Safety and Efficacy of IV Infusion Treatment With Omecamtiv Mecarbil in Subjects With Left Ventricular Systolic Dysfunction Hospitalized for Acute Heart Failure. (BIG BANG)!!
Estimated Enrollment: 600
Study Start Date: April 2011
Estimated Study Completion Date: April 2013
Estimated Primary Completion Date: January 2013
Locations
United States, Alabama
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Moblie, Alabama, United States, 36608
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Inglewood, California, United States, 90301
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La Jolla, California, United States, 92037
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http://clinicaltrials.gov/ct2/show/study/NCT01300013?term=Omecamtiv+mecarbil&rank=2&show_locs=Y#locn
Poster Presentation at the American Academy of Neurology 64th Annual Meeting
A poster titled "A Study to Evaluate Safety and Tolerability of CK-2017357 in Patients with Amyotrophic Lateral Sclerosis Using a Twice-Daily, Dose-Titration Regimen" was also presented by Dr. Shefner. The poster summarized data from a Phase II clinical trial evaluating CK-2017357 in patients with ALS (CY 4025). The authors concluded that the twice-daily dose-titration regimen evaluated in the trial was generally safe and well-tolerated, that the majority of patients could be titrated successfully to a CK-2017357 dose level of 250 mg twice daily, and that encouraging trends toward functional improvements were observed on CK-2017357 versus placebo.
Design and Results
This Phase II clinical trial was a randomized, double-blind, placebo-controlled study in which CK-2017357 was administered for 21 days using a twice-daily, dose titration regimen to patients with ALS taking riluzole at the reduced dose of 50 mg per day. Patients were randomized 3:1 to receive twice daily oral doses of CK-2017357 or placebo. After seven days of treatment with CK-2017357 at the starting dose of 125 mg twice daily, the dose was escalated to 125 mg in the morning and 250 mg in the evening, and after seven days at this dose, to 250 mg twice daily for the final seven days of dosing. Patients who did not tolerate a dose escalation returned to the previous tolerated dose level and remained at that dose level to complete the study. Placebo patients underwent a similar dummy dose titration to maintain the blind. The primary objective of CY 4025 was to assess the safety and tolerability of CK-2017357 when administered using this twice-daily dose titration regimen to patients with ALS and to determine if the total daily dose of CK-2017357 could be increased from the 375 mg once daily dose (that had been evaluated in earlier trials of CK-2017357 in patients with ALS) to a target of 250 mg dosed twice daily in patients enrolled in this trial.
Twenty-seven patients were treated in CY 4025. All six patients randomized to placebo completed three weeks of dosing. Of the 21 patients randomized to treatment with CK-2017357, 14 were escalated to the highest dose of 250 mg twice daily and completed three weeks of dosing; two others terminated the study prematurely while receiving 250 mg twice daily due to adverse events that required hospitalization. One of these patients was admitted for ataxia and confusion believed to be related to treatment with CK-2017357; the other was hospitalized for treatment of cellulitis believed to be unrelated to treatment with CK-2017357. Three other patients also withdrew from the study prematurely. One patient was hospitalized for an upper respiratory infection believed to be unrelated to treatment with CK-2017357 after receiving a week of treatment with CK-2017357 125 mg in the morning and 250 mg in the evening. Two patients withdrew from study for non-serious adverse events while receiving 125 mg of CK-2017357 twice daily, one for dysarthria and another for complaints of unsteadiness, decreased appetite, fatigue, dizziness, and nausea. Finally, two patients completed the study after a downward dose titration. As was observed in CY 4024, dizziness was the most frequently reported adverse event in CY 4025. None of the six patients who received placebo in CY 4025 reported dizziness, while 12 of 21 patients experienced dizziness during dose titration with CK-2017357. In 10 of these patients, dizziness was mild; the other two patients experienced moderate dizziness.
CY 4025 was not designed or powered to evaluate statistically the effects of CK-2017357 on the various outcome measures that were assessed during the study; nevertheless, increases in the ALSFRS-R and MVV were observed on CK-2017357 relative to placebo that were similar in direction and magnitude to those observed in CY 4024. For example, on Day 22, within 2 hours after the final dose of double-blind study drug, the mean change from baseline in the ALSFRS-R was -1.9 points in the six patients who had received placebo, while the mean difference from placebo was +0.3 points in the 16 patients who had competed three weeks of dosing with CK-2017357 (14 on 250 mg dosed twice daily, one on 125 mg dosed twice daily, and one on 125 mg dosed once daily. Similarly, the mean change from baseline to Day 22 in the MVV was -0.4 L/min on placebo, while the mean difference from placebo was +3.6 L/min on CK-2017357.
Additional Poster Presentation at the American Academy of Neurology 64th Annual Meeting
Cytokinetics' scientists presented a poster titled "The Fast Skeletal Troponin Activator, CK-2017357, Increases Muscle Function and Survival in SOD1 (G93A) Mice; a Model of ALS". The objective of this preclinical study was to examine the effects of CK-2017357 in SOD1G93A mutant transgenic mice, a model of ALS in humans. The authors concluded that mice treated with CK-2017357 maintained hindlimb grip strength during disease progression and that CK-2017357 increased muscle strength of a nerve-muscle pair in situ. In addition, there appeared to be a delay in the time to a pre-specified humane endpoint in the CK-2017357-treated mice compared to the age-matched control SOD1 mice. Overall, the authors concluded that the current preclinical findings support the hypothesis that CK-2017357 may benefit patients with ALS by increasing force generation in fast skeletal muscle fibers.
Cytokinetics Announces Encouraging Results From Two Phase II Clinical Trials Evaluating CK-2017357 in Patients With Amyotrophic Lateral Sclerosis
Safety and Tolerability of CK-2017357 in These Two Trials Support Progression to Registration Stage Program
SOUTH SAN FRANCISCO, CA--(Marketwire -04/25/12)- Cytokinetics, Incorporated (CYTK - News) announced today encouraging results from two Phase II clinical trials evaluating CK-2017357 in patients with amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's Disease. In these studies, CK-2017357 was determined to be safe and well-tolerated when dosed with riluzole, the only approved treatment for ALS. The clinical trials results were reported in an oral presentation and a poster at the American Academy of Neurology 64th Annual Meeting in New Orleans, Louisiana.
"The results of these two Phase II clinical trials which evaluated the multi-week safety and tolerability of different doses and dosing schedules of CK-2017357, with and without riluzole, are encouraging," stated Jeremy M. Shefner, MD, PhD, Professor and Chair of the Department of Neurology at the Upstate Medical University at the State University of New York. "I believe the novel mechanism of CK-2017357 may afford meaningful clinical benefit to ALS patients and I look forward to larger and longer studies with the goal of more conclusively demonstrating sustained functional improvements in patients with ALS."
"We are encouraged that the trends to increased function that were observed in the patients receiving CK-2017357 in these studies are consistent with results observed in prior clinical trials of CK-2017357 in patients with ALS," said Andrew A. Wolff, MD, Senior Vice President and Chief Medical Officer at Cytokinetics. "In these two clinical trials, the dizziness reported by patients receiving CK-2017357 was mostly mild and generally abated with continued dosing over the two and three week treatment periods we evaluated. Together with the results of our earlier studies of CK-2017357 in patients with ALS, these new data inform our registration strategy and support the progression of CK-2017357 into later-stage clinical development for the potential treatment of ALS."
In addition, company scientists presented encouraging results with CK-2017357 in a preclinical model of ALS in another poster presentation, also at the same meeting today.
Oral Presentation at the American Academy of Neurology 64th Annual Meeting
An oral presentation by Dr. Shefner titled "A Study to Evaluate Safety and Tolerability of Repeated Doses of CK-2017357 (CK-357) in Patients with Amyotrophic Lateral Sclerosis" included data from Part B of a two-part, randomized, double-blind, placebo-controlled, multiple dose, safety, tolerability, pharmacokinetic and pharmacodynamic clinical trial of CK-2017357 in patients with ALS (CY 4024). Results from Part A of this clinical trial were presented at the 22nd International Symposium on ALS and Motor Neurone Diseases in Sydney, Australia, in November 2011.
Dr. Shefner concluded that CK-2017357 appeared to be safe and well-tolerated dosed daily at 125 mg, 250 mg, and 375 for two weeks, and that encouraging trends were observed in the ALSFRS-R and MVV. As expected, plasma concentrations of CK-2017357 were unaffected by co-administration with riluzole, while riluzole levels increased during co-administration with CK-2017357. Adverse events and clinical assessments during treatment with CK-2017357 appeared similar, with or without co-administration of riluzole at the reduced dose of 50 mg daily. Dizziness, the most commonly reported adverse event, was mostly mild and generally began and resolved early after initiating treatment.
Design and Results
This clinical trial was designed to evaluate the safety and tolerability of two weeks of dosing with CK-2017357 in patients with ALS. In Part A, 24 ALS patients not taking riluzole were randomized to receive daily oral doses of placebo or 125 mg, 250 mg, or 375 mg of CK-2017357, respectively, for two weeks. Part B was identical in design to Part A of the study, except that all patients in Part B received riluzole at a reduced dose of 50 mg daily throughout the 14 days of treatment with CK-2017357 or matching placebo. In the complete study (i.e., both Parts A and B combined), a total of 49 patients were randomized to treatment with placebo (n = 13) or CK-2017357 at daily doses of 125 mg (n = 12), 250 mg (n = 12), or 500 mg (n = 12).
In Part B of this trial, CK-2017357 appeared to be as well-tolerated by those patients receiving riluzole as by those not receiving riluzole in Part A. As was observed in Part A of this study, dizziness was the most frequently reported adverse event. None of the 13 patients who received placebo reported dizziness, compared with 3 of 12 patients who received 125 mg of CK-2017357 daily (1 in Part A and 2 in Part B), 5 of 12 who received 250 mg daily (3 in Part A and 2 in Part B) and 6 of 12 who received 375 mg daily (4 in Part A and 2 in Part B). Again, as was observed in Part A of the study, dizziness was mostly mild, began early after the initiation of treatment, and resolved with continued dosing, usually within the first few days of continued treatment. No patients in Part B reported severe dizziness, and only one, on 250 mg of CK-2017357 dosed daily, reported moderate dizziness.
No patients in Part B discontinued the study prematurely; however, one patient in Part B experienced a change in mental status after receiving 375 mg of CK-2017357 dosed daily for 4 days that resulted in a hospital admission for observation and diagnostic testing, thereby defining her mental status change as a serious adverse event. Her symptoms responded to the administration of supplemental oxygen over a period during which study drug was withheld for one day. Because the patient tolerated the re-initiation of treatment with CK-2017357 while receiving oxygen without a recurrence of her mental status changes, and she completed the study, her symptoms were believed to be due to hypoxemia (which is not uncommon in patients with ALS) and not to treatment with CK-2017357.
While the trial was not designed or powered to evaluate statistically the effects of CK-2017357 on the various outcome measures that were assessed during the study, a combined analysis of patients from Parts A and B suggests encouraging trends that appear dose-related and potentially clinically meaningful in magnitude. Trends were observed in the ALS Functional Rating Scale in its revised form (ALSFRS-R) and in Maximum Voluntary Ventilation (MVV). There were no statistically significant differences in these outcomes measures between patients in Part A and those in Part B.
The ALSFRS-R is a clinically validated instrument designed to measure disease progression and changes in functional status in ALS patients; the average change in the ALSFRS-R score for patients with ALS is approximately -0.9 points per month. In this trial, the ALSFRS-R was evaluated twice, on Days 8 and 15. On Day 8, approximately 24 hours after the previous dose of double-blind study drug and before administration of the Day 8 dose, the mean change from baseline in the ALSFRS-R was -0.4 points in patients receiving placebo, while the mean differences from placebo were -0.1, +0.4, and +0.9 points in patients receiving CK-2017357 at 125 mg, 250 mg, and 375 mg daily, respectively. On Day 15, approximately 24 hours after the final dose of double-blind study drug, the mean change from baseline in the ALSFRS-R was -0.4 points in patients who had received placebo, while the mean differences from placebo were -0.6, +0.4, and +0.4 points in patients who had received CK-2017357 at 125 mg, 250 mg, and 375 mg daily, respectively. In a post-hoc analysis, combining data from both Days 8 and 15, the mean change from baseline in the ALSFRS-R was -0.5 points on placebo and the mean differences from placebo were -0.3, +0.4, and +0.6 points on CK-2017357 at dose levels of 125 mg, 250 mg, and 375 mg daily, respectively; the p-value for this dose-response relationship was 0.10.
MVV is a clinical assessment of pulmonary function and endurance that measures the maximum volume of air that patients can inhale and exhale, expressed in units of L/min. In this trial, MVV was evaluated on Days 8 and 15. Four hours after dosing with double-blind study drug on Day 8, the mean change from baseline in MVV was +5.4 L/min in patients receiving placebo, while the mean differences from placebo were -2.8, +1.3, and +1.5 L/min in patients receiving doses of CK-2017357 at 125 mg, 250 mg, and 375 mg daily, respectively. On Day 15, approximately 24 hours after the final dose of double-blind study drug, the mean change from baseline was +1.6 L/min in patients who had received placebo, while the mean differences from placebo were -0.9, +4.7, and +4.5 L/min in patients who had received doses of CK-2017357 at 125 mg, 250 mg, and 375 mg daily, respectively.
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YES!!! Cytokinetics Announces Clinical Trial Data Relating to CK-2017357 to Be Presented at the 64th Annual Meeting of the American Academy of Neurology
Additional Preclinical Trial Data to Be Presented at the 2012 Experimental Biology Conference
SOUTH SAN FRANCISCO, CA--(Marketwire -04/18/12)- Cytokinetics, Incorporated (NASDAQ: CYTK - News) announced today that one oral presentation and two poster presentations are scheduled to be presented at the 64th Annual Meeting of the American Academy of Neurology, to be held April 21-28, 2012 in New Orleans, LA. In addition, a poster presentation containing preclinical data relating to CK-2017357 is scheduled to be presented at the 2012 Experimental Biology Conference being held April 21-25, 2012 in San Diego, CA.
CK-2017357 is the lead drug candidate that has emerged from the company's skeletal muscle contractility program. CK-2017357 selectively activates the fast skeletal muscle troponin complex by increasing its sensitivity to calcium, which increases skeletal muscle force in response to neuronal input and delays the onset and reduces the degree of muscle fatigue.
Oral Presentation at the 64th Annual Meeting of the American Academy of Neurology
Date: Wednesday, April 25, 2012
Presentation Time: 2:00 PM - 3:45 PM Central Daylight Time
Presentation #: S25.005
Session: S25: Anterior Horn
Title: A Study to Evaluate Safety, and Tolerability of Repeated Doses of CK-2017357 (CK-357) in Patients with Amyotrophic Lateral Sclerosis
Presenter: Jeremy M. Shefner, MD, PhD, Professor and Chair, Department of Neurology at the Upstate Medical University, State University of New York
Poster Presentation at the 64th Annual Meeting of the American Academy of Neurology
Date: Wednesday, April 25, 2012
Presentation Time: 7:30 AM - 9:00 AM Central Daylight Time (poster displayed 7:30 AM - 12:00 PM)
Poster #: P04.155
Session: P04: Anterior Horn: Therapeutics
Title: A Study to Evaluate Safety and Tolerability of CK-2017357 (CK-357) in Patients with Amyotrophic Lateral Sclerosis Using a Twice-Daily, Dose-Titration Regimen
Presenter: Jeremy M. Shefner, MD, PhD, Professor and Chair, Department of Neurology at the Upstate Medical University, State University of New York
Date: Wednesday, April 25, 2012
Presentation Time: 5:30 PM - 7:00 PM Central Daylight Time (poster displayed 2:00 PM - 7:00 PM)
Poster #: P05.169
Session: P05: Anterior Horn: Basic Science
Title: The Fast Skeletal Troponin Activator, CK-2017357, Increases Muscle Function and Survival in SOD1 (G93A) Mice; a Model of ALS
Presenter: Fady I. Malik, MD, PhD, FACC, Cytokinetics, South San Francisco, CA
Poster Presentation at 2012 Experimental Biology Conference:
Date: Wednesday, April 25, 2012
Presentation Time: 12:30 PM - 2:45 PM Pacific Daylight Time (poster displayed 7:30 AM - 5:30 PM)
Abstract #: S85 1121.7
Title: The Fast Skeletal Troponin Activator, CK-2017357, Improves Resistance to Fatigue in Healthy, Conscious Rats
Presenter: Adam R. Kennedy, PhD, Cytokinetics, South San Francisco, CA
http://finance.yahoo.com/news/cytokinetics-announces-clinical-trial-data-200000907.html
March 24-27, 2012
61st Annual Scientific Session & Exp
Chicago, IL
Host: American College of Cardiology
Braunwald's Heart Disease.Diagnosis and Management of Acute Heart Failure Syndromes
Description: ... 133a Preliminary data from studies of the CMA, omecamtiv mecarbil (CK-1827452), given http://search.cardiosource.org/vivisimo/cgi-bin/query-meta.exe?v:sources=acc-bundle&v:project=acc&query=Omecamtiv%20mecarbil&author=0
Stock Price Targets
High: $6.00
Median: $4.00
Low: $3.00
http://quotes.barrons.com/CYTK/research-ratings Study Locations
United States,Australia,Belgium,Canada,Czech Republic,Finland,France,Germany,Greece,Hungary,Italy,
Lithuania,Norway,Poland,7 Russian Federations,and Slovakia !!! http://clinicaltrials.gov/ct2/show/study...
Amgen Among Biotechs That May Become Acquirers in 2012 to Pursue Growth
QBy Meg Tirrell, Ryan Flinn and Jeffrey McCracken - Jan 6, 2012 2:11 PM MT Amgen Inc. (AMGN) and Celgene Corp. (CELG) may dive into deal-making this year as the biggest biotechnology companies seek to return to the industry’s high-growth roots.
Amgen and Celgene are trying to boost investor returns that have lagged behind peers and may have to compete with traditional acquirers from the pharmaceutical industry, such as New York-based Pfizer Inc. (PFE) and Bristol-Myers Squibb Co (BMY), to do it. In the past five years, the Nasdaq Biotechnology Index has risen 36 percent while Amgen, the world’s largest biotechnology company, fell 6 percent and Celgene gained 18 percent.
The biotechs have historically been less active than their pharmaceutical industry counterparts. Bristol-Myers has completed 17 acquisitions (BMY) since 2007, a period in which Amgen had nine and Celgene three.
“We expect the large biotechs to be active acquirers in 2012,” said Henry Gosebruch, managing director of health-care mergers and acquisitions at JPMorgan Chase & Co. (JPM) “Investors have rewarded strategic acquisitions that enhance long-term growth and companies that continue their history of developing innovative therapies, as opposed to turning into dividend- paying, share-repurchase type low-growth stocks.”
Amgen, based in Thousand Oaks, California, will see a smorgasbord of potential targets next week at the 30th annual J.P. Morgan Healthcare Conference in San Francisco.
The meeting will draw 8,000 participants and 395 presenting companies, according to its host. Bristol-Myers and Pfizer, the world’s largest drugmaker, will join Amgen, Celgene, based in Summit, New Jersey, and Biogen Idec Inc. (BIIB), of Weston, Massachusetts, in scouting trips that often pack 200 meetings into the week.
Biotech’s ‘Lollapalooza’
“It’s certainly a good time to meet not just with investors, but other companies that may become partners,” said Patrick Mahaffy, chief executive officer of Boulder, Colorado- based Clovis Oncology Inc. (CLVS), which will present at the conference for the first time.
The meeting, which Mahaffy described as the health-care industry’s “Lollapalooza,” is a chance for smaller companies to impress the crowd, he said.
Companies looking to buy assets or forge partnerships attend the start-of-the-year conference with new budgets and fresh investment track records, JPMorgan’s Gosebruch said. Biotech and medical-device companies use presentations to set expectations for the year, and investor reaction can be a barometer of their ability to stay independent.
Temperature Check
“It’s always a bit of a temperature check on how people feel about the year,” Gosebruch said. “People pay pretty careful attention to what those companies will say at the conference about their objectives and milestones.”
Amgen gained less than 1 percent to $64.76 at the close in New York, while Gilead (GILD) Sciences Inc. rose less than 1 percent to $42.78. Celgene declined 1.9 percent to $67.22, and Biogen increased less than 1 percent to $115.50.
Gilead’s $10.8 billion purchase of Princeton, New Jersey- based Pharmasset Inc. (VRUS), announced Nov. 21, was the highest valuation on record for drug-industry acquisitions greater than $500 million, according to data compiled by Bloomberg. Gilead agreed to pay 70 times the net assets of Pharmasset, a maker of hepatitis C drugs, 94 percent higher than the company’s 20-day trading average.
‘Enormous Premiums’
“That’s what we’re starting to see now,” said Raghuram Selvaraju, an analyst with Morgan Joseph TriArtisan Group in New York. “There’s much more willingness for big companies to pay enormous premiums to get control of high-value assets.”
Michael Yee, an analyst with RBC Capital Markets, suggested Amgen should be shopping. The biotech had $17.7 billion in cash (AMGN) and short-term investments as of Sept. 30, compared with $8.2 billion held by Bristol-Myers, according to data compiled by Bloomberg.
Amgen, with a market value of $56.5 billion, declared its first quarterly dividend last year, and announced a $10 billion buyback program, promising to return more value to stockholders. It’s not enough for investors, RBC’s Yee suggested.
“This company has not had a successful history of business development,” Yee said in an interview after Amgen announced Dec. 15 that CEO Kevin Sharer would be replaced in May by Chief Operating Officer Robert Bradway.
“Amgen needs to go on an aggressive business development spree to in-license and partner high-impact new drugs in Phase 2 so they can have Phase 3 read-outs over the next three to five years,” Yee said.
Amgen’s Largest Deal
Amgen’s largest deal in the past five years was its $425 million purchase of BioVex Group Inc. in 2010 for its experimental cancer drugs. One of the BioVex drugs, Oncovex for skin cancer, is in late-stage testing along with trebananib, for ovarian cancer, and ganitumab, a therapy for pancreatic cancer, according to data collected by Bloomberg.
Mary Klem, an Amgen company spokeswoman, said, future acquisitions by the company “will be borne out of our growth strategy, including our desire to expand our global footprint.”
Companies with market values of $3 billion to $10 billion may be the most likely targets for larger biotechs, JPMorgan’s Gosebruch said. That’s a shift from 2010, when French drugmaker Sanofi pursued Genzyme Corp., the largest maker of medicines for rare diseases, in a deal worth $20.1 billion that closed last April.
Celgene’s largest buy was its $2.8 billion purchase of Pharmion Corp. in 2007. The company, with a market value of $30.4 billion, also has completed seven other equity or partnership deals, according to data compiled by Bloomberg.
Celgene’s Medicines
“We’re constantly out there canvassing what’s going on in hematology and oncology to make sure we’re on top of technology and compounds that are in development,” said Chief Financial Officer Jacqualyn Fouse, in an August interview. “If the right thing comes along, we can and will do it.”
Celgene has two experimental drugs, including the cancer treatment pomalidomide, in Phase 3 testing, the last of three stages usually required for U.S. regulatory approval. Four existing products are in late testing for additional uses, said Brian Gill, a Celgene spokesman.
“Celgene has been very active on the business development front and will continue to work in partnerships with companies,” he said yesterday in a telephone interview.
While biotechnology stocks outperformed the broader market last year, newly public drugmakers and companies trying to sell new products found conditions more difficult, ripening their takeover prospects.
The Nasdaq Biotechnology Index (NBI) gained 12 percent in 2011, compared with little change in the Standard & Poor’s 500; however, Dendreon Corp. (DNDN) and Human Genome Sciences Inc. (HGSI) brought their first drugs to the market with disappointing early sales, and dropped 78 percent and 69 percent, respectively.
Share Sales
Some newly public biotechs are in a similar position. Eleven of 20 drugmakers to have initial public offerings since 2010 have declined, with six falling 60 percent or more, according to data compiled by Bloomberg.
“There are a lot of biotech companies that have become public over the years that really were either not prepared, or the kind of companies that weren’t well-positioned to be public entities,” Robert Moore, general partner at Frazier Healthcare Ventures, said in an interview. “They were going public because it was their least costly form of capital they could raise.”
To contact the reporters on this story: Meg Tirrell in New York at mtirrell@bloomberg.net; Ryan Flinn in San Francisco at rflinn@bloomberg.net; Jeffrey McCracken in New York at jmccracken3@bloomberg.net
To contact the editor responsible for this story: Reg Gale at rgale5@bloomberg.net
Want to save this for later? Add it to your Queue!
http://www.bloomberg.com/news/2012-01-06/amgen-may-join-gilead-as-biotechs-seek-acquisitions-to-grow.html
(old article,just better written)!! Amgen, Cytokinetics heart failure class shows promise in Phase II
The first in a new class of drugs to treat heart failure called cardiac myosin activators has shown encouraging activity in a small Phase II trial published in The Lancet (August 20).
The new drug, called omecamtiv mercabil, was developed by US drugmaker Cytokinetics and is licensed to Amgen. It targets the motor proteins that cause muscle contraction and prolongs the action of the left ventricle of the heart, which pumps blood around the body.
Rather than make the heart beat more often like current medicines, omecamtiv mercabil makes the heart muscles contract for longer, which increases the volume of blood the heart pumps with each stroke without increasing the amount of energy used. That means it should not exhaust the heart, which can occur with currently-used inotropic agents and contribute to cardiac ischaemia.
The Phase II trial compared the intravenously-administered drug to placebo in 45 heart failure patients with impaired function of the left ventricle, who were also taking background therapy with ACE inhibitors and beta blockers. Omecamtiv mercabil increased left ventricular ejection time and stroke volume compared to control, alongside a small reduction in heart rate, suggesting that the hearts were working more effectively and efficiently.
Heart failure affects around 10 million people in the EU alone, according to Professor John Cleland of the University of Hull in the UK, who led the trial. While two-year survival rates among heart failure patients have advanced dramatically over the last 20-30 years, at least for those who receive advanced treatment, it still has a high mortality rate despite existing treatments.
"This is a totally new concept," said Prof Cleland. "We need to see whether the improvements in cardiac function translate into real benefits for patients, in terms of their symptoms and quality of life, and whether it can impact on mortality and morbidity."
Another Phase IIb trial should start next year, and if successful the drug could be on the market within the next three to four years, said Prof. Cleland. Cytokinetics is also developing oral formulation of omecamtiv mercabil, but this is unlikely to be ready to submit for approval for five years or more.
Links
www.thelancet.com
http://www.pharmatimes.com/article/11-08-19/Amgen_Cytokinetics_heart_failure_class_shows_promise_in_Phase_II.aspx
Cytokinetics Announces First Publication on Smooth Muscle Myosin Inhibitors in The Journal of Pharmacology and Experimental Therapeutics
Findings Demonstrate the Potential Therapeutic Application of Inhibitors of Smooth Muscle Myosin for the Treatment of Hypertension
Press Release Source: Cytokinetics, Inc. On Tuesday September 27, 2011, 7:30 am EDT
SOUTH SAN FRANCISCO, CA--(Marketwire -09/27/11)- Cytokinetics, Incorporated (NASDAQ: CYTK - News) announced the publication of preclinical research relating to its program directed to the inhibition of smooth muscle myosin as a novel therapeutic approach for the potential treatment of hypertension in the October 2011 issue of The Journal of Pharmacology and Experimental Therapeutics. This publication reveals, for the first time in a peer-reviewed journal, the role of inhibitors of smooth muscle myosin in preclinical models of hypertension.
"We are excited to have Cytokinetics' novel scientific research relating to inhibitors of smooth muscle myosin published in this prestigious journal," stated Fady I. Malik, MD, PhD, FACC, Cytokinetics' Vice President of Biology and Therapeutics. "This publication summarizes pioneering work performed by our research team to leverage our expertise in the biology of muscle function and establishes this novel mechanism as a potential approach to treating patients with hypertension."
The publication titled "Inhibition of Smooth Muscle Myosin as a Novel Therapeutic Target for Hypertension" discusses the potential application for therapies that directly inhibit smooth muscle myosin based on work in preclinical models of hypertension. In this publication, the authors compared the efficacy in conscious dogs with renal-induced hypertension of CK-2018488, a small molecule direct inhibitor of smooth muscle myosin, to that of a calcium channel blocker, amlodipine. Dogs were instrumented chronically for the measurement of arterial pressure, cardiac output and regional blood flow and hypertension induced. In the hypertensive state, mean arterial pressure increased from 101±3.8 to 142±1.9 mmHg. At the doses selected, CK-2018448 and amlodipine similarly increased cardiac output (30±11% vs. 33±6.4%) and similarly reduced mean arterial pressure (-22±3.6% vs. -16±3.4%) and total peripheral resistance (-36±5.9% vs. -37±5.8%). However, CK-2018448 had the greatest vasodilator effect in the renal bed, where renal blood flow increased by 46±9.0%, versus 11±3.4% for amlodipine (p < 0.01). CK-2018488 produced significantly less vasodilation in the limb, where iliac blood flow did not change; in contrast, it rose by 48±12% with amlodipine (p < 0.01). The authors noted that the minimal effects of CK-2018488 on limb blood flow could limit the development of peripheral edema, an adverse side effect of calcium channel blockers. Additionally, in a rodent model of hypertension, oral administration of this smooth muscle myosin inhibitor resulted in a sustained antihypertensive effect. Thus, the authors concluded that the preferential effect of smooth muscle myosin inhibition on renal blood flow may make this drug mechanism particularly appealing, since many patients with hypertension have renal insufficiency, and patients with heart failure could benefit from afterload reduction coupled with enhanced renal blood flow.
Background on Cytokinetics' Smooth Muscle Contractility Program
Cytokinetics' smooth muscle contractility research program is directed to smooth muscle myosin, the motor protein responsible for the contraction of the smooth muscle cells that surround airways in the lungs and the blood vessels that control blood pressure. By inhibiting the function of the myosin motor central to the contraction of smooth muscle, potent small molecules arising from this program may directly contribute to the relaxation of contracted smooth muscle. Cytokinetics' smooth muscle myosin inhibitors have demonstrated encouraging pharmacological activity in preclinical models that may relate to uses for the potential treatment of diseases such as asthma, chronic obstructive pulmonary disease (COPD) and systemic hypertension. Cytokinetics continues to conduct research and non-clinical development of its smooth muscle myosin inhibitors.
Yes,a bloated Pig$$$$$$$!!
Oh my! POOR LITTLE PIG$$$$$$$$$$$$
Thursday June 2, 2011, 4:00 pm EDT
Cytokinetics Announces Successful Completion of Phase IIA "Evidence of Effect" Clinical Trial of CK-2017357, in Patients With Claudication Associated With Peripheral Artery Disease
Clinical Trial Demonstrates Translation of Mechanism of Action of Novel Drug Candidate in 2nd Disease Population
SOUTH SAN FRANCISCO, CA--(Marketwire - 06/02/11) - Cytokinetics, Incorporated (NASDAQ:CYTK - News) announced the successful completion of its Phase IIa "Evidence of Effect" clinical trial of CK-2017357, a fast skeletal muscle activator, in patients with claudication associated with peripheral artery disease in connection with a poster presentation today at the 22nd Annual Sessions of the Society for Vascular Medicine being held June 2-4 in Boston, MA. In addition, a second poster presentation today highlighted the potential role of a novel functional endpoint, bilateral heel raise testing, in clinical trials in patients with claudication associated with peripheral artery disease. CK-2017357 is the lead drug candidate from the company's skeletal muscle contractility program.
Phase IIa Evidence of Effect Clinical Trial Presentation
A poster titled "A Phase II, Double-Blind, Randomized, Placebo-Controlled, Three-Way Crossover Pharmacokinetic and Pharmacodynamic Study of CK-2017357, a Fast Skeletal Muscle Troponin Activator, in Patients with Claudication" was presented by Alan Hirsch, MD, Cardiovascular Division and Lillehei Heart Institute, University of Minnesota, on June 2, 2011.
This poster summarized the results of a recently completed Phase IIa Evidence of Effect clinical trial in patients with calf muscle claudication associated with peripheral artery disease. The authors concluded that CK-2017357 increased calf muscle performance in these patients as evidenced by an increase in work achieved during bilateral heel raise testing, a performance measure in this patient population developed for this trial and presented by Dr. Hirsch in a second poster described below. The authors also concluded that increases in calf muscle performance and adverse events appear related to both increasing dose and to the plasma concentration of CK-2017357.
"This clinical trial successfully translated the mechanism of fast skeletal muscle activation with CK-2017357 to an improvement in human skeletal muscle function, as evidenced by the ability of these patients with claudication due to peripheral artery disease to do more calf muscle work before intolerable claudication or limiting fatigue," stated William R. Hiatt, MD, Principal Investigator of this clinical trial, President, CPC Clinical Research and Professor of Cardiovascular Research, University of Colorado School of Medicine. "The increases in calf muscle performance, evidenced during bilateral heel raise testing, were observed after only a single dose of CK-2017357. Further studies are warranted to refine the choice of dose and duration of treatment to minimize systemic adverse effects while still retaining the potential clinical benefit."
"We designed this clinical trial to develop hypotheses that could inform the further development of our fast skeletal muscle troponin activators and therefore we are pleased that it produced pharmacodynamic results that are encouraging and consistent with data generated in our preclinical and Phase I studies," stated Andrew A. Wolff, MD, FACC, Cytokinetics' Senior Vice President of Clinical Research and Development and Chief Medical Officer. "We now have clinically relevant hypotheses regarding CK-2017357 for the possible treatment of claudication associated with peripheral artery disease that we believe warrant further exploration, much as was the case with our previously announced clinical trial of this same drug candidate in patients with amyotrophic lateral sclerosis."
Phase IIa Clinical Trial Design
This Phase IIa Evidence of Effect clinical trial was a double-blind, randomized, placebo-controlled, three-way crossover, pharmacokinetic and pharmacodynamic study of CK-2017357 in male and female patients with symptoms of claudication associated with peripheral artery disease. The primary objective of this trial was to demonstrate an effect of single doses of CK-2017357 on measures of skeletal muscle function and fatigability in patients with peripheral artery disease and claudication. The secondary objectives of this clinical trial were to evaluate and characterize the relationship, if any, between the doses and plasma concentrations of CK-2017357 and its pharmacodynamic effects, and to evaluate the safety and tolerability of CK-2017357 administered as single doses to these patients. Accordingly, in this hypothesis-generating trial, multiple pharmacodynamic assessments were made without specifying a single primary pharmacodynamic endpoint.
A total of 61 patients were enrolled in this three-period crossover trial; in random order and with a 6 to 10 day wash-out period between each of the three treatments, 56 patients received a single dose of CK-2017357 at 375 mg, 33 received a single dose of CK-2017357 at 750 mg, and 57 received a single dose of matching placebo. As was previously announced, the protocol was amended after 33 patients were dosed so that the patients enrolled subsequently received a maximum dose of 500 mg (n = 27). Maximum plasma concentrations of CK-2017357 were generally achieved between 3 and 6 hours after dosing, which is when most assessments were made.
Bilateral heel raise testing was performed before each dose of study drug, and 3 hours and 6 hours after each dose. Six measurements were made during bilateral heel raise testing: time, number of repetitions, and work performed to claudication onset, as well as time, number of repetitions, and total work performed to intolerable claudication or calf muscle fatigue, when the test was ended. Work performed during each repetition was calculated by multiplying the maximal heel elevation achieved during that repetition (measured by an instrument attached to the patient's ankle called an electrogoniometer) by the patient's weight; work to the end of testing was the sum of work performed during all repetitions performed during the test. In addition, a six-minute walk test was conducted at 4 hours after dosing, in which the distance walked by the patient during a six minute period was measured.
Phase IIa Clinical Trial Results
The authors concluded that there was an overall trend for CK-2017357 to increase the parameters of calf muscle function as assessed by bilateral heel raise testing. In general, these increases were most evident after the 750 mg dose and at the highest plasma concentrations achieved during the trial. In addition, they were more prominent at 6 hours than at 3 hours, on measurements taken at the end of testing than at the onset of claudication, and on work performed than on time or number of repetitions. For example, at 6 hours after dosing, the change from baseline in work performed to the end of testing increased by a median value of 5.7 kg-m on placebo, 14.2 kg-m on 375 mg of CK-2017357, 20.2 kg-m on 500 mg of CK-2017357, and 34.1 kg-m on 750 mg of CK-2017357 (p = 0.097, 0.181, and 0.002 for 375, 500, and 750 mg of CK-2017357 versus placebo, respectively). In addition, the overall relationship between CK-2017357 dose and work performed to the end of testing achieved conventional statistical significance (p = 0.007).
Increases in work performed to the end of testing were related not only to dose but also to the plasma concentration of CK-2017357 measured at the time of the test. At the highest concentrations observed in the trial ( > 14 mg/mL, n = 37 observations), the change from baseline in work performed to the end of testing increased by an average of 24.4 kg-m versus placebo (p = 0.007). In the concentration ranges from 0 to 7 ng/mL (n = 50 observations), > 7 to 10 ng/mL (n = 72 observations), and > 10 to 14 ng/mL (n = 45 observations), the average increases versus placebo were 9.5 kg-m (p = 0.247), 5.4 kg-m (p = 0.440), and 16.6 kg-m (p = 0.047), respectively. In addition, the relationship between total work performed to the end of testing and the plasma concentration of CK-2017357 also achieved conventional statistical significance (p = 0.005).
In contrast to the increases in calf muscle performance observed during bilateral heel raise testing, there were dose- and plasma concentration-related decreases in the six-minute walking distances. From a mean baseline six-minute walk distance of 1079 feet, after CK-2017357 doses of 375 mg , 500 mg, and 750 mg, the average six-minute walk distances declined versus placebo by 23.8 feet (p = 0.147), 34.1 feet (p = 0.120), and 106.6 feet (p < 0.001), respectively, and the relationship of these declines in six-minute walk distance to dose was also statistically significant (p < 0.001). Similar decreases in the six-minute walk distance were also observed in relation to increasing plasma concentrations of CK-2017357 (p < 0.001).
The authors also concluded that the single doses of CK-2017357 administered in this study appeared safe and generally well-tolerated by the patients in this trial. A substantial majority of the adverse events reported in the study were deemed mild or moderate and were consistent with those observed in prior studies with CK-2017357; however, the percentage of patients reporting severe adverse events during the trial increased with the dose of CK-2017357. The most commonly reported adverse event was dizziness, which was observed in 80% of the patients in the trial and was dose-related. Severe dizziness was reported by more patients than was any other severe adverse event; all four patients who reported severe dizziness did so after receiving the 750 mg dose. The authors speculated that dizziness and other dose-related adverse events may have negatively impacted walking distance but not heel raise testing because walking is a more complex functional task, requiring integration of numerous abilities in addition to calf muscle performance (vision, balance, and coordination, for example). As previously reported, two patients experienced serious adverse events after treatment with CK-2017357 at 750 mg, which were judged to have been related to treatment with the study drug. Both patients required hospitalization but recovered fully without specific therapy. A third patient was hospitalized for severe worsening of cholecystitis following his second dose of study drug at the 500 mg level but investigators deemed that this was unrelated to study drug. The authors concluded that CK-2017357 merits further study and the potential next steps may include studies to explore whether the adverse events observed, such as dizziness, could abate with repeated dosing, alternate dosing regimens, and/or gradual dose titration.
Bilateral Heel Raise Poster Presentation
A second poster titled "Bilateral Heel Raise Test: A Novel Functional Endpoint for Early Stage Clinical Trials in Peripheral Artery Disease (PAD)," was also displayed and presented by Dr. Hirsch on Thursday, June 2, 2011. This poster described in more detail the bilateral heel raise test that was used in the Evidence of Effect trial reported above and evaluated its utility as a functional assessment in patients with calf muscle claudication. The parameters assessed from a single bilateral concentric heel raise test demonstrated modest reliability across baseline measurements during a 3-week period in patients with peripheral artery disease and claudication. Intra-class correlations by patient for time, number of repetitions, and work to the end of testing were 79%, 76%, and 75%, respectively. The authors concluded that bilateral heel raises performed according to a specified-protocol consistently elicited claudication in patients with a history of claudication associated with peripheral artery disease and thus may be a functionally relevant, easy-to-deploy, and cost-effective measure of calf muscle endurance and fatigue in patients with claudication due to peripheral artery disease. Consequently, the use of the heel raise test in early phase "proof of concept" clinical trials may facilitate demonstration of clinical efficacy in patients with claudication without requiring treadmill procedures. Comparison of bilateral heel raise tests with standardized treadmill testing will be needed to establish this test as a surrogate endpoint that parallels the current gold standard for functional exercise testing in the peripheral artery disease population.
YES,shame,SHAME!!!!
Cytokinetics to Present Clinical Data Relating to CK-2017357 at the 22nd Annual Sessions of the Society for Vascular Medicine
Press Release Source: Cytokinetics, Inc. On Thursday May 26, 2011, 4:00 pm
SOUTH SAN FRANCISCO, CA--(Marketwire - 05/26/11) - Cytokinetics, Incorporated (NASDAQ:CYTK - News) announced today that two posters relating to CK-2017357 are scheduled to be presented at the 22nd Annual Sessions of the Society for Vascular Medicine to be held June 2-4, 2011 at the Seaport Hotel in Boston, MA.
One poster will highlight the results from a Phase IIa Evidence-of-Effect clinical trial evaluating CK-2017357 in patients with claudication associated with peripheral artery disease and the other poster will provide support for the validation of a novel functional endpoint, bilateral heel raise test, in this patient population.
CK-2017357, the lead drug candidate from the company's skeletal muscle contractility program, is a fast skeletal muscle troponin activator and is in Phase IIa clinical trials. CK-2017357 selectively activates the fast skeletal muscle troponin complex by increasing its sensitivity to calcium, leading to an increase in skeletal muscle force. This mechanism of action has demonstrated pharmacological activity in preclinical models that may relate to the potential treatment of diseases associated with aging, muscle wasting or neuromuscular dysfunction.
Poster Presentations at the Society for Vascular Medicine 22nd Annual Scientific Sessions:
Abstract #25: A poster presentation titled "Efficacy and Tolerability Of The Novel Fast Skeletal Muscle Troponin Activator, CK-2017357, In Patients With Claudication" will be on display on Thursday, June 2nd and is scheduled to be presented by Alan Hirsch, MD, Cardiovascular Division and Lillehei Heart Institute, University of Minnesota, from 5:30 PM to 6:30 PM Eastern Time.
Abstract #23: A poster presentation titled "Bilateral Heel Raise Test: A Novel Functional Endpoint For Early Stage Clinical Trials In Peripheral Artery Disease (PAD)," will be on display on Thursday, June 2nd and is scheduled to be presented by Alan Hirsch, MD, Cardiovascular Division and Lillehei Heart Institute, University of Minnesota, from 5:30 PM to 6:30 PM Eastern Time.
http://finance.yahoo.com/news/Cytokinetics-to-Present-iw-4187318011.html?x=0&.v=1
POS-??????!!!!!!!
Just my luck,I'm scheduled to arrive in Cairo, Egypt Feb 22nd. So much for my dream cruise??!!
I was answering someone who had cashed in,I did not cash out any today. Long term holder here!
Nice profit! Over 10 Years ago I had CELG and CEPH,oh how I wish I would have kept just 1000 shares of either one! ARIA is trading very similar to those 2 stocks of my past,they both moved up steady on early PH III results,and on approval went to the moon(many 2-1 splits). I think I will keep my position on ARIA for awhile!!
BIG profit takers at EOD. I don't think these are shorts!
"IF the SUCCEED trial fails?" Ah,that would be a buying opportunity!
Oh yes, After making a bundle on HGSI,I took a large position on ARIA. Started buying aug 09 @ $ 1.81,bought more in $2 range. I have taken lots off the table,from the $3.60-$5.20. I still have a nice chunk left! GLTU
I have traded in biotechs for over 13 years now,and I am up over $3 on ARIA!!! So I also tend to get a little excited when I see a little GREEN!
Longs can care less about the daily movement. Let it come down more,I have more money. It's real easy to see which side of the trade a lot of people are on. Love your charts,Thanks
Page 1 of Clinical Trials for ridaforolimus, 28 Total Matches
http://clinicaltrialsfeeds.org/clinical-trials/results/term=ridaforolimus?pg=1
Thursday, January 6, 2011
RIP Tyler
Tyler Blesoe passed away at 6:25 this morning. I pray that he may finally rest in peace.
http://bledsoebattle.blogspot.com/
OH YES,OK!!! "You probably made a good move. It looks like it's heading lower for the time being. 4.75- 4.95"
You just gotta love shorters,sooner or later,they turn into BUYERS!!!
I follow Bledsoe blogs,and I say a lot prayer for him! He has many problems. PLEASE don't blame Ponatinib failure here!!
It's working,Thanks. Sorry you sold!!
That accounts for the big pop at 210pm. I check his thread quite often,but I always do my own DD!
That was a quick move up,shorts must be gasping!!!
$5.39,New high!!!!!!!!!!!!
MRK,With Avg Vol 13,751,400 Shares traded daily,I doubt any little buyers could move MRK up!
Another New high,volume picking up!!
$5.00!!!! Is it OK to get excited NOW!!!!!!
ARIAD Pharmaceuticals, Inc. (ARIA) After Hours Trading Pre-Market Charts | After Hours Charts Dec. 17, 2010 Market Close: $ 4.57
18:08 $ 4.5615 1,528 18:08 $ 4.57 654 18:00 $ 4.57 7,600 17:21 $ 4.5691 4,201 17:17 $ 4.569 230 17:16 $ 4.569 67,676 17:13 $ 4.5637 57,197 17:10 $ 4.5691 4,201 17:10 $ 4.5685 9,526 17:08 $ 4.5685 239,931 17:01 $ 4.57 24,252 17:00 $ 4.5685 239,931 16:48 $ 4.57 2,000 16:45 $ 4.57 21,433 16:40 $ 4.5685 5,728 16:39 $ 4.57 99,790 16:35 $ 4.569 5,984 16:32 $ 4.5655 4,490 16:31 $ 4.57 100 16:31 $ 4.57 555 16:31 $ 4.57 345 16:31 $ 4.57 138 16:30 $ 4.5735 25,095 16:28 $ 4.57 1,605 16:28 $ 4.57 129,995 16:28 $ 4.57 236 16:28 $ 4.57 65,482 16:19 $ 4.57 20,615 16:17 $ 4.57 4,850 16:16 $ 4.57 33,985 16:16 $ 4.57 6,620
Read more: http://www.nasdaq.com/aspxcontent/ExtendedTradingTrades.aspx?selected=ARIA&mkttype=after#ixzz18g12twgZ
Dec 21st 2007 $4.51 previous close high! Yes,new 3 yr high today.($4.66)! http://finance.yahoo.com/q/hp?s=ARIA&a=11&b=16&c=2007&d=11&e=16&f=2010&g=d&z=66&y=726
Kinda quiet today? Must not have met some expectations!!