PAION Eine Fledermaus lernt wieder fliegen

wenn die 88 fällt, dann kommt der EURO

noch alles ohne NEWS  

https://www.maxblue.de/de/...tml?symbol=PA8.ETR&isin=DE000A0B65S3

Ausgegebene Aktien 25 Mio. Stückaktien
Gezeichnetes Kapital 25,38 Mio. EURO

Stückaktien zu 1,00 (EURO)

Streubesitz (77,0%)
Varuma AG (5,88%)
Merrill Lynch & Co. Inc (3,10%)
IPSA (9,12%)
Dr. Mariola Söhngen und Dr. Wolfgang Söhngen (4,87%)

hier kann gut hoch gehen..

http://www.finanzen.net/dividende/PAION

schon mal so eine sause dann ging es ganz schnell wieder runter  

...damals vollkommen verständlich. die targets waren viel zu weit weg. jetzt kann es aber jederzeit kurstreibende news geben. wer will da schon gern den richtigen zeitpunkt für den einstieg verschlafen?  

Zitat aus WO-Threat
...

Bist noch nicht lange dabei;)
-Arcorda startet im 2. hj. Eine weitere ggf2 Studie (Meilensteine:))
-Die Rekrutierung der wichtigen PII/III u. PIII sind lange abgeschlossen (Ergebnisse jederzeit)
-Studierende der US Studie August 13
-Option für Korea soll bis ende 2013 gezogen werden.
-Studierende der EU PII von Paion Anfang 2014
-Deal für die USA ist in aller Munde:)
-Yichang China hat das Datenpaket erhalten, kann als jederzeit mit eigenen Studien beginnen.
-Interesse an dem Datenpaket von Solulin vorhanden.

....  

Neuer Abstract zu GGF2. Hier dürfte auch bald die Phase 2 starten. Sehr wahrscheinlich sind dann Zahlungen an Paion fällig

Intravenous glial growth factor 2 (GGF2) isoform of neuregulin-1β improves left ventricular function, gene and protein expression in rats after myocardial infarction.

Hill MF, Patel AV, Murphy A, Smith HM, Galindo CL, Pentassuglia L, Peng X, Lenneman CG, Odiete O, Friedman DB, Kronenberg MW, Zheng S, Zhao Z, Song Y, Harrell FE Jr, Srinivas M, Ganguly A, Iaci J, Parry TJ, Caggiano AO, Sawyer DB.

Source

Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

AIMS:

Recombinant Neuregulin (NRG)-1β has multiple beneficial effects on cardiac myocytes in culture, and has potential as a clinical therapy for heart failure (HF). A number of factors may influence the effect of NRG-1β on cardiac function via ErbB receptor coupling and expression. We examined the effect of the NRG-1β isoform, glial growth factor 2 (GGF2), in rats with myocardial infarction (MI) and determined the impact of high-fat diet as well as chronicity of disease on GGF2 induced improvement in left ventricular systolic function. Potential mechanisms for GGF2 effects on the remote myocardium were explored using microarray and proteomic analysis.

METHODS AND RESULTS:

Rats with MI were randomized to receive vehicle, 0.625 mg/kg, or 3.25 mg/kg GGF2 in the presence and absence of high-fat feeding beginning at day 7 post-MI and continuing for 4 weeks. Residual left ventricular (LV) function was improved in both of the GGF2 treatment groups compared with the vehicle treated MI group at 4 weeks of treatment as assessed by echocardiography. High-fat diet did not prevent the effects of high dose GGF2. In experiments where treatment was delayed until 8 weeks after MI, high but not low dose GGF2 treatment was associated with improved systolic function. mRNA and protein expression analysis of remote left ventricular tissue revealed a number of changes in myocardial gene and protein expression altered by MI that were normalized by GGF2 treatment, many of which are involved in energy production.

CONCLUSIONS:

This study demonstrates that in rats with MI induced systolic dysfunction, GGF2 treatment improves cardiac function. There are differences in sensitivity of the myocardium to GGF2 effects when administered early vs. late post-MI that may be important to consider in the development of GGF2 in humans.
 

Hintergrundartikel zu GGF2. Da jetzt ziemlich viel neue Leute Interesse an Paion zeigen. Neben Remimazolam entwickelt Acorda das von Paion auslizensierte GGF2. Ein Wirkstoff mit Blockbusterpotential, das demnächst die zweite Phase startet. Bis zur Zulassung sind noch ca 7,5 Millionen an Paion fällig. Bei Zulassung umsatzabhängige Beteiligung. Im Erfolgsfall dürften dies Zahlungen von ca 60-80 Millionen $ an Paion bedeuten.

http://www.mc.vanderbilt.edu/vanderbiltmedicine/...html?article=10019

The Accidental Drug Developer
Steady research trek leads from the bench to the bedside of patients with failing hearts

oug Sawyer wasn’t looking for a new treatment for heart failure when he started his research fellowship 15 years ago. As a cardiologist, he was interested in helping patients with the condition, to be sure, but as a scientist, he was more intrigued by the biology of heart muscle cells. He wanted to understand how these cells maintain themselves for a lifetime.

 

“How do constantly beating cardiac myocytes (muscle cells) withstand the wear-and-tear of contraction? And how do they survive for so many years?” wonders Sawyer, M.D., Ph.D., Lisa M. Jacobson Professor of Medicine and chief of the Division of Cardiovascular Medicine at Vanderbilt University Medical Center.


Sawyer and other investigators have zeroed in on a survival factor – a protein called Glial Growth Factor 2 (GGF2) – that protects cardiac myocytes from stressors in culture and enhances heart function and survival in animal models of heart failure. Now, Sawyer and colleagues at Acorda Therapeutics are poised to test GGF2 for the first time in human patients.


If the first trials show that GGF2 is safe and well tolerated by patients, the investigators will pursue further clinical trials.


GGF2 represents a potentially new approach for treating heart failure, a chronic condition in which the heart is unable to meet the body’s demands, leaving patients short of breath and unable to complete daily activities. Current medications address the symptoms of fluid build-up and aim to modify the heart’s workload, but GGF2 appears to enhance the repair of damaged heart muscle.


“I never expected to be so fortunate as to be involved with something that’s gone all the way from studies at the bench to the point where we’re going to give it to people to see if it might help them,” Sawyer says. “I feel very lucky in that regard.”



••••
Probing cardiac cell survival

As its name suggests, Glial Growth Factor 2 was first characterized for its growth-promoting actions on glia, cells that support and protect neurons in the nervous system. GGF2 is a member of a family of proteins called neuregulins, which themselves are part of an even larger family of epidermal growth factor (EGF) proteins. Vanderbilt’s Stanley Cohen, Ph.D., was awarded the Nobel Prize in 1986 for his discovery of EGF.


GGF2 landed in Sawyer’s hands by chance.


He was new to the research group of Ralph Kelly, M.D., and Thomas W. Smith, M.D., experts on cardiac myocyte biology, at Brigham and Women’s Hospital, where he had begun to study the effects of cancer drugs called anthracyclines (such as adriamycin) on cultured cardiac myocytes. These drugs were known to cause heart failure in cancer patients, and Sawyer was testing whether they killed heart cells the same way they killed cancer cells. He was also examining factors that might improve cell survival.


Mark Marchionni, Ph.D., at a company called Cambridge Neurosciences, had approached Kelly about looking at the effects of GGF2 on cardiac myocytes. Marchionni had cloned the gene for GGF2 and coined the term “neuregulin.”


“The GGF2 project was an orphan in the lab, and Ralph Kelly said to me, ‘why don’t you study GGF2 in the myocytes while you’re doing your other experiments,’” Sawyer recalls.


He included GGF2 in a panel of factors he was testing, and he found that GGF2 regulated myocyte survival – with GGF2 around, the cells lived longer, even after stressors like anthracyclines.


“That result made GGF2 much more interesting to me,” Sawyer chuckles.


GGF2 had been studied in other cell types and was known to work through the EGF family of erbB receptors. Sawyer used those previous reports as a starting point for his own examination of the receptors and signaling pathways activated by GGF2 in cardiac myocytes.


Findings were also emerging from other groups that neuregulins played critical roles in the developing heart. Mice missing neuregulin-1 (GGF2 is a version of this neuregulin) or its receptors erbB2 or erbB4 died in utero because of failures in heart development.


Sawyer and Kelly speculated that if GGF2 improved cell survival in the setting of heart failure, it might be a good therapy for the condition. So Cambridge Neurosciences patented GGF2 and other neuregulins as potential treatments for heart failure. Sawyer is an inventor on the patent, but he didn’t intend to continue his neuregulin research. Instead, after finishing his fellowship, he took a faculty position at Boston University and continued his studies of anthracycline toxicity, oxidant stress, and cardiac cell survival.
“I just went about my business,” he says. “I didn’t know what was going to happen with the neuregulins, but I figured I was better off pursuing my interest in cardiac myocyte biology and leaving the drug development to the company.”


Then chance intervened again. A new cancer drug – Herceptin – was introduced, and it caused heart failure in patients with breast cancer, particularly those who were also taking anthracyclines.


••••
Clues from the clinic

Herceptin was developed to block erbB2 receptors, which are activated by epidermal growth factor family members, including neuregulins. Breast cancers with increased levels of erbB2 receptors – also called HER2/neu receptors – are more aggressive and have a worse prognosis compared to breast cancers that do not overexpress erbB2.


“Herceptin’s cardiac effects demonstrated in humans that this neuregulin signaling system matters in the heart – if you interrupt it, it’s bad news,” Sawyer says.


Genentech, the manufacturer of Herceptin, invited Sawyer and others to submit grants to study the roles of neuregulins, anthracyclines and Herceptin in cardiac biology. Sawyer was awarded a Genentech grant.


“I basically dove back into neuregulin biology,” Sawyer says. “And we stayed focused on the biology, rather than the therapeutic development.”


Sawyer’s team learned which heart cells express neuregulins, and which neuregulin form is most potent in regulating cell survival. They discovered how neuregulins modulate cell metabolism and cell growth. And they explored how the body controls neuregulin expression and activity – and how that might go awry in heart failure.


Other groups found that erbB receptor expression drops in animal models of heart failure and in human tissues from patients with heart failure, further implicating the signaling system in the condition.


During this time, Acorda Therapeutics, a neurosciences-focused company, bought the neuregulin technologies from Cambridge Neurosciences/ Cenes and pursued development of GGF2 for a range of neurologic and cardiac conditions, including stroke and heart failure.


In 2006, data supporting the therapeutic potential of neuregulins in heart failure “reached a tipping point,” Sawyer says.


Researchers at Zensun, a company in China, reported that a version of neuregulin-1 (different from GGF2) improved cardiac function and survival in animal models of heart failure caused by ischemic injury (like a heart attack), cancer drugs and viruses.


“I was happy – and surprised – to see those results,” Sawyer says. “I honestly never believed neuregulin was going to go anywhere therapeutically because in cancer it could promote growth.”


Therapeutic development was never his mission, he says, rather, he was interested in maintaining a grant-funded basic science lab and in training new investigators to study cardiac myocyte biology.


But another chance occurrence – a new grant mechanism – brought Sawyer into the drug development arena.



••••
Back to the bedside

Just after the Zensun findings were reported, the National Heart, Lung and Blood Institute introduced the Cardiac Translational Research Implementation Program (C-TRIP) to advance research on promising new therapeutics for heart failure and arrhythmias.


Vanderbilt and Acorda received a C-TRIP grant in 2010, which is supporting additional studies of GGF2 in animal models of heart failure and a Phase I clinical trial to assess the safety of GGF2 in human patients with heart failure. Acorda is sponsoring another Phase I trial of GGF2 at Vanderbilt.


“C-TRIP has been a great mechanism for pulling academic and industrial groups together,” says Anthony Caggiano, M.D., Ph.D., vice president of Preclinical Development at Acorda and a co-principal investigator with Sawyer on the C-TRIP grant.


“Our collaboration over the years, and now with this grant, has been ideal in that our strengths are complementary and only somewhat overlapping. Acorda has strength in drug development science, while Dr. Sawyer and his colleagues have basic science and cardiology expertise.”


The Phase I trials of GGF2, being led by Daniel Lenihan, M.D., professor of Medicine, and Carrie Geisberg, M.D., assistant professor of Medicine, are designed to study GGF2 safety and dosing. The investigators also will be looking at measures of heart function – using blood biomarkers and non-invasive imaging including echocardiography – to gather information that would support further clinical testing.


“We’re really excited about these trials,” Lenihan says. “We have a lot of room for improvement in treating heart failure,” which he notes is the most common reason for hospital admission in the United States.


“We think that GGF2 is going to enhance the repair of damaged heart muscle, no matter what has caused the damage,” Lenihan says. “That’s really a whole line of therapy for heart failure that we haven’t investigated. There are no therapies that do that right now.”


“I think it’s a good experiment. It’s worthwhile to test GGF2 in people,” Sawyer says. “We know that the chances of success for any experimental therapeutic are small, but we’re hopeful that GGF2 will help patients with heart failure.”


Chance, after all, seems to be on Sawyer’s side.
 

Da kann noch diesen Monat etwas kommen
http://clinicaltrials.gov/ct2/show/study/NCT01790607
 

würde kurse um 5€ rechtfertigen. nicht auszumalen, wenn neben 7056 auch dieser wirkstoff erfolgreich vermarktet werden könnte.  

Selbst wenn Remimazolam nicht klappen würde(was ich nicht glaube), könnte Paion sich langfristig nicht gegen eine Verzehnfachung wehren . Voraussetzung wäre natürlich eine Zulassung von GGF2 und das Paion GGF2 vorher nicht verkauft.  Die Datenlage zu GGF2 ist schon verdammt gut. Paion brauchte nur die Tür zuzumachen und einige Jahre warten.    

Hier noch mal die Ergebnisse der Phase 1 Studie. Bemerkenswert, dass diese Ergebnisse schon nach einer einmaligen Gabe von GGF2 erreicht wurden.

Data from First Clinical Trial of GGF2 in Heart Failure Presented at the American College of Cardiology 62nd Annual Scientific Session
Study Identifies a Maximum Tolerated Dose of GGF2
Preliminary Efficacy Measures Show GGF2 Improves Heart Function
ARDSLEY, N.Y. & NASHVILLE, Tenn.--(BUSINESS WIRE)--Mar. 7, 2013-- Acorda Therapeutics, Inc. (Nasdaq: ACOR) and collaborator Vanderbilt University Medical Center today announced data from a Phase 1 clinical trial of Glial Growth Factor 2 (GGF2) designed to study safety, tolerability and exploratory measures of efficacy in people with heart failure who were already on optimized regimens of currently available therapies. The study evaluated the effects of a range of doses, with each participant receiving a single dose. Data from this trial, which enrolled patients at Vanderbilt and St. Joseph’s Hospital in Atlanta, GA, are being presented on Sunday, March 10 at the American College of Cardiology 62nd Annual Scientific Session in San Francisco, CA.

“We have completed the first in human trial with GGF2 in patients with heart failure, and especially want to thank our patients who volunteered for this important study. We are very encouraged by the results,” said Daniel Lenihan, M.D., Professor of Medicine and Director, Clinical Research at the Vanderbilt University Medical Center, Division of Cardiovascular Medicine. “It is notable that trends of long-lasting and dose-related improvement in cardiac function were seen following a single dose in patients who were already optimized on standard therapies. GGF2 warrants further investigation as a treatment for heart failure.”

“Preclinical studies have suggested that GGF2 may improve heart function through direct repair of cardiac muscle, a novel mechanism of action. This first clinical trial in patients with heart failure identified a maximally tolerated GGF2 dose and key safety parameters to be monitored in future studies. This information supports continued development of the compound as a potential treatment for heart failure,” said Anthony Caggiano, M.D., Ph.D., Vice President of Research and Development at Acorda.

This was a double-blind, placebo controlled, escalating single dose clinical trial that included 40 patients with advanced heart failure. Safety and exploratory efficacy were monitored for 90 days in patients randomized to receive various doses of GGF2 or placebo.

Safety Findings

In this study, a single dose of GGF2 in patients with heart failure was generally well tolerated up to 0.75 mg/kg. Among participants receiving GGF2, the most commonly observed adverse events were headache, site injection reaction and gastrointestinal symptoms. There were no notable effects of treatment on hematology or electrocardiogram, and no adverse events led to withdrawal from the study.

A dose-limiting adverse event of hepatotoxicity (liver injury) meeting Hy’s Law criteria (elevated ALT, AST and bilirubin) occurred in the highest-dose cohort. The patient’s liver function tests and bilirubin had returned to normal by two weeks after dosing. There was also one reported case of uroepithelial carcinoma, a form of cancer in the cells that line the bladder, which was diagnosed three months after dosing in the highest-dose cohort. The patient’s baseline urinalysis showed the presence of red blood cells, indicating that the tumor was likely present prior to dosing.

Ejection Fraction Findings

A left ventricle ejection fraction of 55% or higher is considered normal; all participants in the Phase 1 GGF2 trial had left ventricle ejection fraction of less than 40%. Trial participants receiving GGF2 showed a consistent and dose-responsive trend towards improving left ventricular ejection fraction over 28 and 90 days compared to placebo.

Mean ejection fractions at screening in the treatment and placebo groups were 27% and 29%, respectively. For the cohort receiving the maximally tolerated dose (0.75 mg/kg) of GGF2, the mean ejection fraction at screening was 28% and the absolute mean changes in ejection fraction at day 8, day 14, day 28, and day 90 were 5%, 12%, 12.0% and 9.0%, compared to absolute mean changes of -1%, -1%, 0% and 2% for the placebo group; thus, the mean ejection fraction for this GGF2 group at day 28 was 40%, versus 29% for placebo.

Acorda has discussed the findings from this initial study with the U.S. Food and Drug Administration (FDA) and has reached agreement on the next clinical study of GGF2 in heart failure. This study will primarily investigate further the safety profile of GGF2 across a range of doses, and will continue to explore efficacy outcomes.

The FDA has granted Fast Track designation for GGF2 for the treatment of heart failure.

About GGF2

GGF2 is the leading development candidate from Acorda’s neuregulin program. Neuregulins are a class of naturally occurring protein growth factors that have multiple effects on the nervous and cardiovascular systems.

Preclinical studies demonstrate that GGF2 acts directly to repair cardiac muscle and improve its contractile function. No currently available therapies do this, and GGF2 may therefore offer an important new treatment option for people with heart failure.

In addition to its clinical program in heart failure, the Company also has preclinical development programs for GGF2 in a number of neurological indications, including peripheral nerve injury and stroke.  

sollten im August wirklich NEWS aus USA kommen, da ist der € Geschichte,
habe deswegen heute entschieden wieder einzusteigen.

Nach unten sehr gut gesichert, EK und Finanzierungen bis 2015 gesichert

 

wahrscheinlich anlass, um imense fantasie in diesem wert zu entfachen. ich kann einfach nicht nachvollziehen, warum die aktivititäten paions, immer noch als eine art fake betrachtet werden. anders kann ich mir diese absurde, tiefe bewertung nicht erklären. selbst desmo, der einst hoch gehandelte und damals einzige wirkstoff in der pipeline, wurde gewinnbringend veräussert. das dies nicht gerade die erwartungen der aktionäre erfüllte, ist klar, zeigt aber, dass paion sofort reagierte und anders als viele biotechwerte, damit das überleben sicherte und sich jetzt durch den strategiewechsel, vorzüglich positioniert hat, um vollkommen stressfrei, bestmögliche deals auszuhandeln.  

Finale Vorbereitungen für den Start der Studie laufen, Erwartung der Studienergebnisse in H1 2014.

http://www.finanznachrichten.de/...der-indikation-anaesthesie-016.htm

wird die Geschiechte schreiben..

Über PAION PAION AG ist ein börsennotiertes biopharmazeutisches Unternehmen mit Hauptsitz in Aachen und verfügt über einen weiteren Standort in Cambridge (Vereinigtes Königreich). Das Unternehmen kann eine Erfolgsgeschichte in der Entwicklung innovativer Arzneimittel mit einem erheblichen, nicht gedeckten medizinischen Bedarf für den Krankenhausbereich vorweisen. PAION AG baut sein Geschäftsmodell von einer reinen Entwicklungsgesellschaft zu einem spezialisierten Pharma Unternehmen mit einem Schwerpunkt auf Anästhesie-Produkten aus, mit dem Ziel, Remimazolam als Basis seiner künftigen Vertriebsaktivitäten zu nutzen.

egal
http://clinicaltrials.gov/ct2/show/study/NCT01790607
kurzfristig Nachrichten


später mehr

EK ist gut und keine KE in Sichtweite

hier muss kein BB pushen, die Bewertung gewinnt von alleine, Insider vielleicht...  

ich mach mir keine sorgen. nicht über paion und auch nicht über evo. das sind 2 positionen in meinem depot, welche noch für furore sorgen werden ;))

ich kann bloss die lächerliche bewertung nicht nachvollziehen und das so wenige unsere überzeugung teilen, wo die fakten doch eine ganz andere sprache sprechen.  

quelle Paion HJ- Bericht 2013
http://www.paion.de/images/stories/investoren/...n/2013/en/q22013.pdf

S. 25/26   Ziele 2013 (incl 2. Halbjahr)



 

Ich habe eine kleine Sammlung zu allen wichtigen GGF2 und Remimazolam  Artikeln angelegt. Damit ihr nicht mühsam alles im Netz zusammen suchen müsst, bietet sich hier eine Recherche an.

http://www.ep.vm-elsig.de/yabb2/YaBB.pl?num=1268722260

Ich hoffe ihr könnt damit was anfangen.

Liebe Grüße
Gurke
 

der Beitrag auf S. 2 von heute morgen

"The FDA has granted Fast Track designation for GGF2 for the treatment of heart failure."

wenn das so stimmt, dann gibt es eine schnelle Genehmigung...

vielleicht erklärt das auch die steigende Nachrfrage....???  

es stabilisiert sich,
der kursanstieg hat die unterbewertung zum branchenvergleich etwas verkürzt
sollten news kommen :)

chart:
88 92 EURO

Unterstützung bei 80,5

bye  

Moin allerseits, ich bin auch wieder dabei. Die Ergebnisse zu GGF2 sind tatsächlich ein Kracher und bei weiterer positiver Phasen die Einnahmeerwartungen durch Umsatzbeteiligung vergleichbar stark wie durch Remimazolam einzuschätzen. Unterm Strich sehe ich das Unternehmen so stark aufgestellt wie seit langem nicht: finanziert bis 2015, beginnende auslizensierung von Remimazolam, starke Ergebnisse beim bereits auslizensierten GGF2. Auch wenn erstmal keine Nachrichten mehr kommen, sorgt das mMn für genug Phantasie.